1
……………. Part I: An Introduction To Integrative Physiology….………
Chapter 1: A New Paradigm of Bioenergetics ……………………...……………………….. Pg. 5
Chapter 2: Applied Physiology And Sports Informatics ………...…………..……………... Pg. 14
Chapter 3: Integrated Cardiovascular Control …………………...…………….…..………. Pg. 23
…….….…………….Part II: Energy System Training….….………………
Chapter 4: A Physiological Performance Paradigm ……………………………….…..….... Pg. 32
Chapter 5: Challenging Conventional Paradigms of Maximal Exercise Performance…....... Pg. 35
Chapter 6: Understanding Bioenergetic Limitations………………………………...………Pg. 45
Chapter 7: Understanding Sport Specific Limitations.…………………………….……...... Pg. 51
Chapter 8: Training Interventions For Delivery Limited Athletes…………………….….... Pg. 56
Chapter 9: Training Interventions For Respiratory Limited Athletes….………………..….. Pg. 67
Chapter 10: Training Interventions For Utilization Limited Athletes….……………........... Pg. 74
Chapter 11: Movement Classification For Energy System Training….………………......... Pg. 82
Chapter 12: Combining Strength And Energy System Training….………………..………. Pg. 85
………………...……...Part III: Resistance Training…….…....…..…..……
Chapter 13: Resistance Training Fundamentals….………………………………..……...... Pg. 91
Chapter 14: A Decision Making Algorithm For Muscle Hypertrophy …………..….…….... Pg. 97
Chapter 15: Auto-Regulation For Resistance Training….……………………………....... Pg. 104
…………..…..……..Part IV: Models Of Performance…..…..……………..
Chapter 16: Critical Power And Critical Metabolic Rate………...……………………...... Pg. 107
Chapter 17: Fitness-Fatigue Dynamics………………………………..………………....... Pg. 117
……………………..Part V: Integrated Biomechanics……………………..
Chapter 18: Variations Of Human Movement……………………………………….......... Pg. 121
Chapter 19: Tensegrity And Regional Interdependence………………………………....... Pg. 124
Chapter 20: Gait, Posture, And Locomotion…………………………………………........ Pg. 131
Chapter 21: Pain, A Complex Emotion ………………………………………….……....... Pg. 137
Chapter 22: Breathing And Autonomics……………………………………... ………....... Pg. 141
Chapter 23: Muscle Tension…………………………………………………………......... Pg. 148
Chapter 24: Load Management………………………………………………….……....... Pg. 151
……………..……...Part VI: Athlete-Centric Coaching……..……………..
Chapter 25: Exercise Adaptation………………………………………………...……....... Pg. 155
Chapter 26: The Limiter-Bridge-Performance Model…………………………………...... Pg. 158
Forward
If you were a high school student at any time in the last forty years, chances are that you
have been introduced to cell biology with a metaphor that compares cells to machines. If you
crack open Miller and Levine's best selling textbook, Biology, the cellular biology chapter begins
with an analogy comparing cells to factories. For example, DNA is the head of the factory
2
calling the shots, lysosomes are janitors removing waste from the factory, and the mitochondria
are the power plants or generators providing energy to the factory. The introduction then explains
how individual cells operate like machines, with each organelle performing its own discrete
function with clockwork precision.
Machine metaphors for the human body didn't begin with high school science curricula.
As far back as the 17th-century, scientists like Giovanni Alfonso Borelli dissected animals and
described muscles as "inert and dead machines", which says nothing about all of the other
machine-related analogies used in science. For example, Johannes Kepler famously discussed the
celestial "clockworks" of the moving planets in the night sky. These machine metaphors helped
guide early scientific thought, and to the extent that humans could understand machines, they
could also understand nature.
However, we seldom pause to consider how these ‘man as machine’ metaphors give rise
to perceptions about how the human body works that are anything but scientific. For example,
machines are simple — a given input will always provide the same output. This is how exercise
physiology is often taught as well. There are discrete set and rep protocols for building strength,
hypertrophy protocols for building muscle, and interval protocols written to confer a precise
adaptation. In this view, the training protocol is the point of control. However, anyone who has
coached human beings for a while knows that exercise adaptation is not straight forward. A
given protocol will not only lead to a different result for two individuals, but it may also lead to a
different result for the same individual at two different points in time. These ‘man as machine’
metaphors have also influenced how coaches view adaptation and periodization with
supercompensation theory and block periodization being the epitome of these outdated ideas.
As we move away from these outdated and broken ways of viewing the human body, we
need to rethink many concepts firmly rooted in training culture. By doing so, we can embrace the
inter-individual variations in training response and the non-linearity in exercise adaptation. We
can also modify the old ways of approaching training and incorporate new findings from
contemporary scientific insights. By doing so we can embrace the art and science of coaching in
order to make major breakthroughs in the performance world.
As you work through this book, you'll be exposed to concepts and ideas from fields such
as integrative physiology, molecular biology, rehabilitation science, and more. Of course, my
intent is to make these ideas practical, so rather than going an inch wide and a mile deep on any
of these topics, the aim is to extract and deliver key concepts while weaving in some narrative
along the way. The ultimate goal is to create a cohesive body of training knowledge that you can
apply to your coaching practice.
3
Part I: An Introduction to Integrative Physiology
Chapter 1: A New Paradigm of Bioenergetics
We can't have a nuanced discussion about energy system training, or conditioning more
broadly, without first discussing bioenergetics. Bioenergetics are the stimulation of metabolic
4
processes that result in the supply, transport, and utilization of energy in the body. Contrary to
popular belief, energy systems do not create energy. Instead, energy is transferred from one state
to another both inside and outside of our bodies. This harkens back to the law of energy
conservation which states that energy can neither be created nor destroyed - only converted from
one form of energy to another. For example, we get electrons from the sugars in the food that we
eat, and we breathe in oxygen from the environment around us. Electrons and oxygen meet in the
mitochondria to transform free energy into a form we can use in our body. The better the
capacity of our energy systems, the better we can transform this free energy into a usable form,
which in practice means restocking ATP, the energetic currency of the cell. For what sounds like
a straightforward process on paper, the details and intricacies of this process are incredibly
complex and are often poorly understood by athletes and coaches.
In figure one you’ll find a muscle oxygenation measurement from an athlete performing a
45-second sprint, captured with a NNOXX wearable device. Notice that the second the athlete
begins their sprint, oxygen is utilized instantaneously in the working muscle. In fact, oxygen is
consumed at a much greater rate than it is supplied to the active muscle, which is why muscle
oxygenation is declining. As soon as the athlete stops pedaling oxygen supply supersedes oxygen
utilization, and oxygen saturation rises rapidly.
Having worked with many physiologists, researchers, and high-performance-minded
physicians, it's always interesting to me that they're not surprised in the least when they see these
types of measurements. "Of course, oxygen is utilized immediately upon load" they'll say. Yet,
this fact is often lost among coaches. After all, a max effort sprint is an anaerobic event, right? I
write that facetiously, yet this is still the dominant viewpoint among strength and conditioning
coaches. If you pick up any given training book you'll see terms like anaerobic a-lactic capacity,
lactic endurance, and aerobic power thrown around liberally. Of course, some coaches will
acknowledge that the varying bioenergetic processes do overlap in time. Still, few appreciate the
speed at which these varying processes occur or the fact that they are overlapping on the
millisecond time scale.
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My belief is that all training is aerobic and all training is lactic. In vivo oxygen is always
part of the energy production process, whether direct or indirect, and lactate is always present as
well. You may have been shaking your head in agreement as you read the last sentence, or you
may have felt like the rug was pulled out from under your feet. Don’t worry if you’re in the latter
camp. You don't need to have any of this committed to memory to grasp the concepts presented
later in this book. I present this material because it opens the door for a more nuanced take on
training where we think in terms of limiting systems rather than thinking in terms or what energy
systems we need to train.
What is Wrong With The Old Model Of Bioenergetics?
Oftentimes, in discussions about energy systems, coaches and athletes will make a hard
distinction between two modes of energy production: anaerobic and aerobic. The anaerobic mode
of energy production is subdivided into the phosphagen and the glycolytic pathways which occur
in the absence of oxygen and the aerobic mode of energy production comes from the oxidative
pathway, which requires oxygen to function. This model proposes that aerobic and anaerobic
processes occur independent of one another — that is to say, that at any given time we are either
operating aerobically or anaerobically. There are a number of flaws with this framework.
You’re more than likely familiar with the image
shown in figure two. This image is often shown in
coaching manuals, strength and conditioning books,
and personal training courses and it attempts to depict
the relative energy contributions from the varying
energy systems over time. For example, figure two
shows that all of the energy systems are working in
tandem, with varying contributions, during work bouts
lasting under two seconds. From two to ten seconds it
shows that the phospen system is supplying the bulk
energy with moderate assistance from the glycolytic
since and small contributions by the oxidative system.
Then from ten seconds to two minutes it shows that the
glycolytic system is the primary contributor to energy production with a moderate contribution
from the oxidative system, and finally from two minutes onward a transition occurs where all
energy is supplied by the oxidative energy system.
Despite the model in figure two being widely reproduced it is not in agreement with
modern scientific findings. For example, this model shows that phosphocreatine supplies almost
all of the energy needed for sustained bursts of contractions lasting less than ten seconds, after
which it is replaced by glycogenolysis. This is not supported by contemporary biochemical
research findings. For example, in Robert Shulman and Douglas Rothman’s paper titled, The
6
glycogen shunt in exercising muscle: A role for glycogen in muscle energetics and fatigue 1, they
report the presence of the enzyme glycogen phosphorylase in its active form under conditions
where glycogen concentrations are constant. This seems paradoxical because glycogen
phosphorylase’s role is to break down muscle glycogen to release glucose and it’s the key
enzyme needed for utilizing both muscle and liver glycogen stores. The only reason why
glycogen phosphorylase would be found in its active form while glycogen concentrations are
stable would be if glycogen synthesis and breakdown were occurring simultaneously. This would
only make sense if the support of continuous muscle contraction requires continual
phosphocreatine breakdown and glycogen phosphorylase rapidly increases activity to restore
phosphocreatine, and in turn ATP. Through the classic lens of bioenergetics this would seem
contradictory since it is believed that phosphocreatine consumption falls after ten seconds.
Perhaps phosphocreatine is an important energy source during exercise bouts beyond ten
seconds.
In Yourgran Chung and colleagues' paper titled, Metabolic Fluctuation During A Muscle
Contraction Cycle 2, the investigators found that phosphocreatine consumption is approximately
forty times greater than previously believed. Traditionally phosphocreatine measurements were
recorded by counting the number of muscle twitches in a given time period and then dividing the
drop in phosphocreatine concentrations by said number of twitches. Yourgran Chung and
colleagues used a different approach to quantifying muscle phosphocreatine consumption called
phosphorus nuclear magnetic resonance imaging, or P-NMR for short. The P-NMR measurement
technique showed that the traditional method of calculating phosphocreatine consumption per
muscle twitch significantly underestimates the total amount of phosphocreatine utilized because
it fails to account for the continual depletion and restoration of the phosphocreatine pool that
occurs on the order of milliseconds. Chung and colleagues' experiments also show that
phosphocreatine cannot be the ultimate energy source in contracting muscle. At a cost of three
millimolar of phosphocreatine per twitch a muscle would rapidly deplete its energy supply unless
phosphocreatine were replenished between muscle contractions.
1
Shulman RG, Rothman DL (2001). The "glycogen shunt" in exercising muscle: A role for glycogen in muscle energetics and
fatigue. Proc Natl Acad Sci. 98:457-461.
2
Chung Y, Sharman R, Carlsen R, Unger SW, Larson D, Jue T (1998). Metabolic fluctuation during a muscle contraction cycle. Am J
Physiol. 27: 846-852.
7
Additionally, in Kevin McNully and colleagues’ paper, Simultaneous In Vivo
Measurements Of HBO2 Saturation and PCr Kinetics After Exercise In Normal Humans 3, we
see that phosphocreatine and oxygen kinetics are tightly coupled during exercise and following
exercise, which is demonstrated in figure three. There are also reports by Paul Greenhaff and
James Timmons where they state, “However, that PCr hydrolysis and lactate production do not
occur in isolation, and that both are initiated rapidly at the onset of contraction.” In order to make
sense of all of this information I'll introduce you to the contemporary model of bioenergetics.
The Contemporary Model of Bioenergetics
Figure four depicts a visual
representation of the most up to date
model of bioenergetics. You’ll notice
similarities with the traditional model. For
example, the phosphagen, glycolytic, and
oxidative energy pathways are still
included in this diagram. However, you’ll
notice that they are all overlapping in their
contributions to energy production. This
differs from the traditional model where
different energy pathways are shown to be predominant in each compartmentalized time frame.
Additionally, the time frame in figure four is from zero to one hundred milliseconds, versus the
traditional model which spans from zero seconds to multiple hours. Effectively, the
contemporary model acknowledges that energy transduction processes occur on much shorter
time scales than previously believed, and that all of the energy systems are working in tandem.
3
McCully KK, Iotti S, Kendrick K, Wang Z, Posner JD, Leigh J Jr, Chance B (1985). Simultaneous in vivo measurements of HbO2
saturation and PCr kinetics after exercise in normal humans. J Appl Physiol. 77: 5-10.
8
The contemporary model of bioenergetics can be summed up as follows: when a muscle
contracts ATP, the energetic currency of the cell, is depleted. In order to sustain continuous
muscle contractions a rapid, non-oxidative, energy source is needed to replenish ATP. However,
ATP must be replenished on the order of milliseconds, otherwise it will be depleted. This rapid
energy source comes from the breakdown of phosphocreatine, which is used to restore ATP
within 0-15 milliseconds of a muscle contraction. Now, phosphocreatine needs to be replenished,
otherwise the high energy phosphate stores in the muscle will be depleted. Restoring
phosphocreatine requires a non-oxidative energy source. An issue arises when you consider the
fact that the supply of glycolytic intermediates in the muscle, such as glucose, are limited.
However, biochemical evidence shows that the enzyme glycogen phosphorylase is in its active
form during exercise where muscle glycogen concentrations are held constant. This appears to be
contradictory at first though because glycogen phosphorylase’s role is to break down glycogen to
release glucose. The only explanation for why glycogen phosphorylase would be active while
glycogen concentrations are stable is that glycogen breakdown and synthesis are occurring
simultaneously. In fact this does occur. Glycogen phosphorylase is activated during exercise and
it continually breaks down muscle glycogen to restore phosphocreatine, which is needed to
maintain physical exertion levels. As this process continues, lactate is continuously produced and
oxidized to provide the ATP needed to re-synthesize and replenish glycogen pools in the muscle
and re-establish ion gradients. However, only a fraction of the lactate produced needs to be
oxidized to provide the necessary energy for the aforementioned processes. As a result, lactate
accumulates in the muscles. The accumulation of lactate does not mean that it is a fatigue
by-product as traditionally believed, but rather it demonstrates an inefficiency in the energy
transformation process.
A major takeaway from the contemporary model of bioenergetics is that all exercise is
aerobic, and all exercise is lactic. All exercise is aerobic because oxygen is always part of the
energy production process in-vivo, whether it plays an indirect or direct role. Additionally,
lactate serves as a necessary buffer that bridges the gap between fast and slow energy needs,
which explains the paradoxical generation of lactate in well oxygenated tissue. Another key
takeaway is that oxygen and phosphocreatine are utilized at the same rate during exercise, and
are replenished at the same rate following exercise, which is demonstrated in figure three. This is
contrary to the traditional view where phosphocreatine is utilized first and is depleted prior to the
initiation of oxygen consumption. It also points to a major difference between the traditional and
modern energy system paradigms. While both models demonstrate that the various energy
systems overlap in time, the traditional view is that these processes occur on the order of seconds
to minutes, whereas the modern view acknowledges that these processes are occurring on the
millisecond time scale.
Another important difference between the traditional and modern energy system
paradigms is that the traditional model contradicts observed muscle oxygenation trends whereas
9
the modern model does not. The modern model appreciates the fact that oxygen utilization
responds immediately to the body's energetic demands at the onset of loading. For example, at
the start of a maximal effort sprint muscle oxygen saturation will drop rapidly until it reaches a
nadir. When muscle oxygenation reaches a nadir oxidative metabolism is compromised, which
leads to a reliance on glycolysis to replenish phosphocreatine stores, and subsequently ATP.
Glycolysis, while always active, is much less efficient at supplying energy than oxidative
metabolism is and it comes with a greater cost. An overreliance on glycolysis is accompanied by
a rapid onset of fatigue and the employment of compensatory movement strategies in order to
maintain force output. As a result, muscle oxygenation and its rate of change can be used to
determine proximity to failure in live time, which only makes sense in light of the contemporary
model of bioenergetics.
Rethinking The Role of Lactate In Fatigue
The information covered in the preceding sections of this chapter forces us to reconcile
with different aspects of how we approach training. For example, knowing that all exercise is
both aerobic and lactic, we may wonder what ‘alactic anaerobic training’ is really doing
physiologically. When coaches prescribe ‘alactic power’ training for their athletes they assume
lactate isn’t generated because they do not observe elevated blood lactate levels with a blood
lactate analyzer. However, this is not an indication that lactate was not generated during exercise.
When a blood lactate measurement is taken from an ear or finger there is a time lag because the
measurement is taken in the systemic circulation rather than at the source of lactate generation in
the working muscle. Additionally, measured lactate levels reflect the balance of lactate
production and consumption, not how much lactate was produced in totality. In actuality lactate
production can be quite high during ‘alactic’ exercise intervals, but it’s consumed at such a fast
rate that it doesn’t appear on a blood test.
When we acknowledge that all exercise is both aerobic and lactic we can jettison
traditional ideas about bioenergetics, and energy system training, and come to new conclusions
that are better informed. For example, maximal effort sprinting has traditionally been classified
as a test of ‘anaerobic alactic power’ or ‘anaerobic alactic endurance’ spending on duration of
the sprint. In figure five we have a chart from a popular exercise science and training book with
the accompanying text above it: “As a rule of thumb, the closer the event's duration is to one
10
minute, the lower the aerobic contribution to overall performance will be. The opposite is also
true: the longer the duration is, the more dominant the aerobic system will be.” In truth, oxygen
is utilized immediately upon the start of a maximal effort sprint. In fact, oxygen is consumed at a
much greater rate than it is supplied to the working muscles, which is why muscle oxygenation
declines at a rapid rate during maximal effort exercise. Additionally, when muscle oxygenation
reaches a nadir power output decreases rapidly. Finally, when the exercise bout is finished
muscle oxygenation saturation will rapidly rise to baseline levels. Despite what the authors of
figure five would suggest, oxidative processes are dominant at the start of a sprint and decrease
over the course of the work bout as oxygen levels are depleted. This is the opposite of what is
suggested to occur in the traditional energy system models. Furthermore, when oxygen is
depleted we can infer that less fat is being oxidized for fuel, and that glycolysis is increasingly
being relied upon to power activities. However, glycolysis is an extremely inefficient means of
energy production and most athletes are quick to reach volitional failure when muscle
oxygenation levels are depleted.
When muscle oxygenation levels are
brought to a nadir, for an extended duration,
we’ll often observe elevated blood lactate
concentrations on a metabolic analyzer. The
reason this occurs is that the more sugars are
broken down for energy, during glycolysis, the
higher blood lactate levels will rise.
Additionally, lactate buffers acid hydrogen
ions that are produced during the glycolysis.
This is demonstrated in figure six, which
shows the relationship between muscle pH and blood lactate levels. In the past it was assumed
that lactate was the cause of fatigue since elevated lactate levels were frequently detected at the
point of volitional failure during maximal effort exercise trials. However, this was a classic error
of mistaking correlation for causation. Bruce Gladen said it best in his 2004 paper titled Lactate
metabolism: a new paradigm for the third millennium 4 where he said, “Lactate can no longer be
considered the usual suspect for metabolic ‘crimes’, but instead a central player in cellular,
regional, and whole body metabolism.”
You should now be able to see that maximal effort exercise is not only aerobic, but also
lactic. This may seem like a pedantic point to make, but there are real practical implications for
updating your understanding of exercise physiology. When we think in outdated terms such as
‘alactic power’ or ‘lactic endurance’ it leads us to make natural conclusions as to how we may
need to train to get better at certain types of workouts. For example, if a one hundred meter sprint
is believed to be a test of ‘anaerobic alactic’ power, then we’d be unlikely to consider that
4
Gladden LB (2004). Lactate metabolism: a new paradigm for the third millennium. J Physiol. 558: 5-30.
11
someone’s performance on that event may be limited by their maximal rate of oxygen utilization,
or their ability to supply oxygen to the working muscles. However, when we can look past these
outdated terms we can approach training through a new lens that is better informed. For example,
we can think in terms of rate limiting factors in an individual's ability to uptake, transport, and
utilize oxygen versus questioning what energy system is limiting someone. Rather than saying,
“my athlete needs to improve her lactic power to get better at a 200m sprint” we may identify
whether an individual should prioritize training their pulmonary, cardiovascular, or muscular
system to improve their performance.
A Unified Theory of Bioenergetic Demands in Sport
If you accept the ideas in the previous sections to be true, then it opens up a whole
dialogue about how to classify different work-capacity based sporting events. For example, it’s
common to classify football and hockey as anaerobic-alactic power and anaerobic-lactic
endurance sports respectively, or to call distance running events tests of aerobic endurance.
Given that all of these sports are in fact aerobic, it seems nonsensical to try and classify them
based on what energy systems they challenge. However, there is a utility in creating a
classification system that categorizes athletes that compete in work-capacity based sports with
differing physiological demands, despite all being ‘aerobic’ events. This is where the derivative
of muscle oxygenation becomes a useful metric.
Muscle oxygenation measurements reflect the balance of oxygen supply and demand in
the working muscles. If oxygen supply supersedes oxygen utilization, muscle oxygenation
increases and vice versa. The derivative of muscle oxygenation, termed ΔSmO2, expresses the
rate that muscle oxygenation is changing over time. If ΔSmO2 is positive then oxygen supply is
greater than utilization, and the more positive ΔSmO2 becomes the greater the rate oxygen is
being supplied to the muscle. If ΔSmO2 is negative then oxygen utilization is superseding
supply, and a more negative ΔSmO2 means oxygen is being utilized at a greater rate. Finally, if
ΔSmO2 is zero, then muscle oxygenation has reached a steady state and is not changing over
time. The rate of change of muscle oxygenation is an important measurement because it adds a
temporal component to oxygen utilization, which is typically only thought of in terms of sheer
magnitude.
Sprinters have maximal rates of oxygen utilization that far exceed those of distance
runners, and as a result ΔSmO2 can be used to delineate between athletes who specialize in
different work-capacity based events. An elite sprinter may start a one hundred meter race with a
muscle oxygenation level of 75% and they may finish their race with a muscle oxygen saturation
level of 10%. That means that their maximal rate of oxygen utilization during their race was
approximately 7% per second. An elite ten thousand meter runner on the other hand may start
their race with the same muscle oxygenation level as the sprinter, but after clipping off multiple
miles at 4:30 mile pace they may finish their race with a muscle oxygenation level of 25%. In the
later case the runner would have an oxygen utilization rate of roughly 0.5% per second. Both the
12
sprinter and distance runner are aerobic athletes, but they differ substantially in their rates of
oxygen utilization. The sprinter trains to utilize oxygen at as fast of a rate as possible while the
distance runner trains to extend their oxygen supply in order to maximize their average speed
over many miles. Mixed sport athletes, like Crossfit competitors for example, fall somewhere in
the middle of that spectrum.
Now that we’ve shifted the focus from what energy systems an individual needs to train
to improve in their sport towards their rate of oxygen utilization we can start to think in terms of
limiting systems. For example, the pulmonary system, cardiovascular system, and muscular
system work in concert to uptake, transport, and utilize oxygen. The maximum integrated
capacity of these systems represents the upper limit of performance in work-capacity based
sporting events, and by identifying which of these systems limits an individual's performance on
their event you can approach training with a high degree of precision.
13
Chapter 2: Applied Physiology & Sports Informatics
The human body is a repository of physical patterns: heartbeats, muscle movements,
neural activity, cyclic temperature changes, and more. These patterns contain information rich
messages that can be excavated, refined, and decoded. To do so we need sophisticated tools and
interfaces to effectively access and evaluate such information. The multidisciplinary team and
NNOXX has developed a novel wearable device that enables exercisers to collect and convert
physical patterns into beneficial forms in order to gain insights into the human body and
ultimately enhance performance.
This chapter provides a broad overview of the different types of measurements that can
be derived with NNOXX’s wearable technology. NNOXX has developed an all-in-one wearable
equipped with state of the art biosensors and AI-powered analytics to interrogate exerciser’s
physiology in a way that was previously unimaginable. This makes NNOXX’s wearable an
irreplaceable tool for assessing two of the major determinants of exercise capacity, oxygen
delivery and oxygen utilization respectively. Since the NNOXX biosensor uses a non-invasive
optical technique to record its measurements it’s appealing for a wide range of training and
competition scenarios.
In addition to helping guide athlete’s training, and identify key performance indicators
NNOXX’s wearable provides a lens through which you can understand exercise bioenergetics
and energy system training. It’s one thing to discuss abstract concepts, such as oxygen kinetics,
and it’s another thing to watch these processes occurring in live time. Even if you have no
intention of using NNOXX’s biosensor technology I believe there is utility in understanding the
material presented in this chapter since it will provide requisite context for other topics in this
book that you can practically apply to your own exercise routines.
Muscle Oxygenation (SmO2)
Muscle oxygenation is a measurement of the percentage of total hemoglobin that is
carrying oxygen in the capillaries of a muscle tissue and the subsequent transfer of oxygen to
myoglobin, the oxygen carrying molecule located in said muscle. Muscle oxygenation is a
localized oxygen saturation measurement that is influenced by muscle blood flow, exercise
intensity, and alterations in hemoglobin’s oxygen dissociation curve. Muscle oxygenation is
measured with a non-invasive optical technique that allows an exerciser to determine the relative
amount of hemoglobin and myoglobin that are oxygen bound. The resulting muscle oxygenation
measurement, called SmO2, is expressed as a percentage of a zero to one hundred scale.
It is important to note that muscle oxygenation is measured in the microvascular capillary
beds whereas pulse oximetry which measures oxygen saturation in the arteries. While SmO2 and
peripheral oxygen saturation, termed SpO2, are both measures of a tissue's oxygenation level
they are recorded in different regions of the circulation and as a result cannot be used
interchangeably. For example, muscle oxygenation reflects the dynamic balance between oxygen
14
delivery to the working muscles and oxygen consumption in the capillary beds of said muscles.
Peripheral oxygenation on the other hand reflects the function of the pulmonary system, and as a
result there are very small variations in SpO2 in healthy individuals.
The benefit of muscle oxygenation measurements is that they allow quantitative
measurements to be made in the skeletal muscles, which provides a means for assessing two of
the major determinants of exercise capacity: oxygen delivery and oxygen utilization. The
non-invasive nature of muscle oxygenation measurements makes them appealing for use in
dynamic environments and for activities of daily living.
There are currently a handful of companies selling muscle oximeters to consumers.
However, the quality of said devices and the accuracy of their muscle oxygenation measurements
vary. The NNOXX wearable is equipped with state-of-the-art muscle oxygenation measurements
and AI-powered analytics. This allows coaches and athletes to investigate their muscle
physiology and transform those findings into practical insights without needing to have a
comprehensive educational background in exercise physiology.
One of the key differentiating
factors between NNOXX’s muscle
oxygenation measurements and their
competitors is that the NNOXX
biosensor is capable of recording
measurements at a greater frequency
as compared with other muscle
oximeters. This allows exercisers to
see the full variation in the muscle
oxygenation measurements on a
muscle contraction by muscle contraction basis whereas competing devices cannot capture this
variation, as shown in figure seven. As a result, NNOXX’s biosensor device is the only one
capable of quantifying the oxygen cost per muscle contraction, which allows an exerciser to
quantify their movement economy and how their muscle coordinates the contraction-relaxation
cycle. Additionally, the NNOXX biosensor can combine muscle oxygenation measurements with
location data, such as GPS or accelerometer, in order to understand the relationship between
muscle metabolism and external measurements of speed, power, or distance. This allows
exercisers to track progress on key performance indicators, identify exercise limitations, and
quantify both internal and external workloads in an unprecedented fashion.
Mechanical, Metabloc, and Neurological Mediates of Skeletal Muscle Blood Flow
The primary function of skeletal muscle is to contract and produce movement of the
joints, which is an incredibly energy intensive activity. As a result, the skeletal muscles demand a
15
considerable amount of blood flow in order to provide oxygen and remove metabolic waste
products in an efficient manner. The delivery of oxygen and removal of metabolic waste products
is the responsibility of the circulatory system, which is laid out in a highly organized fashion
with the muscle. Arterioles give rise to capillaries that run parallel to muscle fibers with each
muscle fiber being surrounded by three to four capillaries. At rest the skeletal muscle’s need for
oxygen is minimal and as a result only a fourth of capillaries are open and actively perfused with
blood. In contrast, during high intensity exercise all of the capillaries may be perfused with
blood, which increases the total number of open and active capillaries surrounding muscle fibers.
The arrangement of capillaries around individual muscle fibers and the ability to open capillaries
when needed minimizes the distance that oxygen must travel when it diffuses into the skeletal
muscle cell. This allows for an efficient exchange of gasses between blood in the microvascular
capillaries and the muscle cells, especially when oxygen demand in the muscle is high.
During maximal effort full-body exercise muscle blood flow can increase by more than
twenty fold above resting levels. Therefore, skeletal muscle has a very large flow reserve, which
is made possible by alterations in blood vessel tone between resting and exercise conditions. At
rest blood vessel tone is high, which limits skeletal muscle blood flow, and vice versa during
exercise. Blood vessel tone at any moment is determined by the interplay between sympathetic
vasoconstrictor activity, which decreases muscle blood flow, and metabolic vasodilator activity,
which increases muscle blood flow. At rest vasoconstrictor activity dominates, leading to an
increase in blood vessel tone, whereas metabolic vasodilator activity dominates during exercise,
exerting the opposite effect. There are additional factors impacting blood flow as well, such as
skeletal muscle contraction.
The blood flow response to skeletal muscle contraction depends on both the type and
strength of muscle contractions. During rhythmic muscle contractions below 30% of an
individual’s maximum voluntary contraction strength, blood flow decreases during the
contractile period and increases during the relaxation periods between muscle contractions.
When the force of a muscle’s contraction rises above 30% of maximum voluntary contraction
strength, as is often the case during resistance training, it can lead to venous occlusion. During
venous occlusion muscle blood volume will increase significantly since blood is capable of
entering the muscle through the arterioles, but cannot leave the muscle through the venules and
veins. As a result, blood pools in the capillary beds. If maximum voluntary contraction strength
exceeds 70% an arterial occlusion can occur, which means both arterial inflow and venous
outflow are restricted. In this case oxygenated blood cannot enter the muscle, nor can metabolic
waste products leave the muscle.
In addition to mechanical factors impacting muscle blood flow, there are also local
metabolic mechanisms that are responsible for dilating skeletal muscle blood vessels during
exercise. For example, when blood flow is compromised during sustained high force muscle
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contractions, muscle oxygen saturation will plummet and the tissue will become hypoxic. Tissue
hypoxia then provides a signal for the blood vessels to dilate. The precise mechanism for how
tissue hypoxia induces vasodilation is complex and involves an acute increase in interstitial
adenosine and potassium ions upon the start of muscle contraction, followed by endothelial nitric
oxide release and red blood cell mediated active nitric oxide release, among other factors such as
dissolved carbon dioxide. Collectively, these factors that increase muscle blood flow during
exercise make up the active hyperemic response.
Until recently it was not possible to differentiate between the neural, mechanical,
metabolic regulators of muscle blood flow with a wearable device. The previous generation of
muscle oximeters do not measure blood flow directly. Instead, they measure a surrogate measure
called total hemoglobin, or THb short. Total hemoglobin is a measure of muscle blood volume,
not blood flow, which poses a number of challenges. For example, during exercise you the
aforementioned muscle oximeters will display a simultaneous decrease in muscle oxygenation
and an increase in total hemoglobin. Because these devices measure blood volume, and not blood
flow, it’s not possible to discern if that increase in blood volume is due to venous occlusion,
hypoxic vasodilation, or some combination of the two. Similarly, if total hemoglobin goes down
during exercise they cannot discern whether that is due to a compression of blood vessels during
muscle contraction, sympathetic vasoconstriction, or a left shift in hemoglobin dissociation curve
from over-expelling carbon dioxide. In order to differentiate between the various factors that
regulate muscle blood flow NNOXX has developed a novel measure of active nitric oxide
release called personal nitric oxide, or PNO for short. PNO is a dynamic measurement of active
nitric oxide release from the red blood cells during exercise. To fully appreciate the range of
applications for measuring an individual's PNO level it’s important to understand the varying
roles that nitric oxide and S-nitrosothiols play in human biology, which will be discussed in the
next section.
Personal Nitric Oxide (PNO)
Nitric Oxide is one of the most important molecules for promoting health, fitness, and
performance, yet few people are aware of its role in the body because our traditional
understanding of the respiratory cycle is incomplete. We've all been taught the classic view of the
respiratory cycle. We breathe oxygen in, and we breathe carbon dioxide out. This classic depicts
blood as a passive substance that simply carries oxygen and carbon dioxide to and from tissues
respectively, while the heart is the primary regulator of systemic blood flow. After blood leaves
the heart it flows into large arteries that fan out into progressively smaller arteries that eventually
reach individual organs and tissues. As hemoglobin packed into red blood cells travels through
the body it flips back and forth between two distinct shapes. When hemoglobin is loaded with
oxygen it takes on shape A, and after it releases oxygen it changes to shape B, then picks up
carbon dioxide. In other words, hemoglobin’s shape changes depending on its oxygen supply.
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The classic two-gas respiratory cycle accounts for oxygen and carbon dioxide, but there's
a third lesser known gas, called nitric oxide, that completes the cycle. Ordinary nitric oxide is
produced in the inner lining of blood vessels and is scavenged from tissues by hemoglobin as the
red blood cells travel through the tissue's vasculature. When ordinary nitric oxide is picked up by
hemoglobin, it binds to the heme-iron center in the hemoglobin molecule. On the way back to the
lungs the red blood cells, which have already delivered oxygen to the tissues, are loaded with
carbon dioxide and nitric oxide. Once the red blood cells enter the lungs they release carbon
dioxide, which is expelled as a waste product. Then hemoglobin picks up oxygen in the
pulmonary capillaries and the nitric oxide moves from the hem- iron in hemoglobin to the
93-cysteine amino acid site, forming S-nitrosohemoglobin, or SNO-Hb for short. Importantly,
SNO-Hb is the bioactive form of Nitric oxide that controls blood flow to tissues. After leaving
the lungs, many red blood cells are packed with hemoglobin carrying oxygen and SNO-Hb. They
then travel to the heart and are pumped out to the rest of the body to nourish tissues including the
brain, heart, and exercising muscles.
When oxygen and SNO-Hb laden red blood cells reach the microvascular arterioles and
capillaries of the tissues, such as muscle, hemoglobin senses how much oxygen is present. If the
oxygen level in the tissue is low, hemoglobin responds by changing its shape, causing oxygen
and SNO-Hb to be released. Oxygen nourishes the surrounding tissues whereas SNO-Hb signals
for the blood vessels to widen, resulting in even greater blood flow and oxygen delivery to the
tissues. When oxygen levels in the tissue are high, hemoglobin doesn’t change its shape and
oxygen and SNO-Hb are not released. This system makes sense when you consider the need to
regulate blood flow at the level of individual tissues. For example, when you exercise you must
deliver more blood to working muscles to nourish them with oxygen. But when you stop
exercising you want to slow blood flow back down. Each tissue has its own blood flow
requirements and hemoglobin regulates blood flow to individual tissues on an as needed basis.
Doctors have long known that there is a significant disconnect between the amount of
oxygen carried in the blood and the amount of oxygen delivered to the tissues, such as exercising
muscles. Therefore, the current generation of wearables that measure blood O2 levels lacks a key
ingredient for giving you a better biomarker of health or fitness. While the aforementioned devices
tell you how much oxygen is carried in the blood, they still leave you in the dark as to how much
oxygen is delivered to tissues.
Active nitric oxide increases blood flow to tissues; without active nitric oxide the ability
to nourish tissues with oxygen is significantly impaired. Thus, by measuring both active nitric
oxide levels and the amount of oxygen in muscles, NNOXX provides a powerful health and
fitness index.
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It’s well known that consistent and routine exercise can improve active nitric oxide levels
over time. But the type, intensity, and duration of exercise that best increases those levels will
vary from person to person. Traditional measurements of active nitric oxide require a blood
sample from the macro-vasculature, as well as complex laboratory procedures, and cannot
directly predict oxygen delivery to tissues. As a result, scientists have previously been limited in
their ability to discover optimal and individualized methods to increase active nitric oxide
(SNO-Hb) levels in order to improve brain and cardiovascular health, fitness, and exercise
performance.
NNOXX is redefining human health and performance with the world’s first and only
non-invasive active nitric oxide activity measurement. NNOXX combines state-of-the-art
biosensors and AI-powered analytics to help people boost their active nitric oxide levels through
exercise. By doing so, exercisers can increase blood flow to their brain, heart, and working
muscles. Additionally, NNOXX gives athletes a competitive edge by providing the most
sophisticated tool for holistic performance enhancement.
Sports Informatics & Data Analytics
Data analytics is the process of discovering insights from data in order to make better
decisions more quickly. In business data analytics are relied upon to guide an organization in
developing their strategies. Similarly, elite sports can benefit from such a framework in order to
streamline the effective use of data, which can be used to evaluate training progress, determine
next steps in the training process, and reduce injuries. Figure eight provides an example data
analysis framework that sports teams, coaches, and individual athletes can use to guide the long
term athletic development process. The aforementioned framework combines descriptive,
diagnostic, predictive, and prescriptive analytics in order to transform data driven insights into
actionable decisions. Fortunately, NNOXX has considered these various factors when designing
an AI-powered analytics platform. By automating the processing, analysis, and interpretation of
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data coaches and athletes can make better-informed decisions without having to spend time and
effort sifting through data. Furthermore, they can spend their limiting time focusing on the
training variables within their locus of control.
The first level in the analysis framework shown in figure eight is descriptive analytics.
Descriptive analytics explain what has already happened and can be used to compare an athlete's
actual training progress with the expected results. For example, a coach may write a training
program intended to increase a cyclist's VO2max and time trial performance by a specified
margin. Descriptive analytics can compare the cyclists actual improvements in VO2max and
performance with the coaches expectations, allowing the coach to monitor progress and assess
the effectiveness of their program. However, descriptive analytics fail to explain why the athlete
progressed as well as they did, or alternatively why they failed to progress on a well written
training program. In order to glean insights about causality we look to the second level in the
framework, diagnostic analytics, which answers the question “Why did it happen?”. For
example, using diagnostic analytics we can look at the aforementioned cyclists training volume,
intensity, workload distribution, and key performance indicators. By drawing causal relationships
between these different factors we can better understand which training variables are most
strongly associated with the observed performance improvements.
Whereas the first two levels of analytics framework rely on simple statistical techniques,
predictive analytics rely on advanced statistics and machine learning techniques such as
regression and decision trees. Through the use of predictive analytics we can create forecasts that
give us insight into the probability that a specific training outcome will occur. This isn’t
dissimilar from forecasting the weather. A series of data points are used to make a prediction,
like a thirty percent chain of rain next tuesday, and as additional data points are gathered the
forecasts may change. For example, a coach may look at a forecast about an athlete’s injury risk
or probability of improving their max deadlift. These forecasts are based on historical data points
and can be used to guide future training decisions, which will in turn alter future forecasts.
The final step of the analytics framework is prescriptive analytics which attempts to
answer the question “what should we do next?”. For example, our predictive forecast may
indicate that an athlete has a high chance of improving their time trial performance the following
week. However, that athlete still needs to know the most effective strategy they should take to
optimize their long term progress while simultaneously keeping injuries at bay. Prescriptive
analytics can help identify the most effective and efficient training method for an athlete to use
today, which can be taken at face value or modified to fit the overarching context of the training
plan and the athletes preferences.
It’s important to keep in mind that the analytics framework presented in this section is not
a full-fledged substitute for a human coach. Coaches and exercisers are still the primary driver of
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decision making. The role of data is to help these individuals avoid the different types of
cognitive biases that cloud human judgment and enhance the overall training process. In the next
section you’ll learn how human-machine interaction can elevate the field of human performance.
The Role of Artificial Intelligence In Sports Science
On the best days working with elite athletes is like operating a well run railway station.
Things happen according to rules, generalization, and principles. We can forgive a two minute
delay in the train's arrival as an exception to the rule because it almost always runs on time, and
it’s sure to arrive shortly. Similarly, an unexpected PR in the gym doesn’t derail our sense of
control over an athletes training program because there were clues that it would happen
eventually. However, there are other times when the training floor in an elite sports performance
facility is like a multi-car pileup on the freeway. We may understand the physics of the collision,
but there are so many things happening simultaneously that we never could have predicted it, nor
can we stop it from happening again in the future. These are the days where two athletes hit huge
personal records, four of them have moderately productive workouts, and one limps out of the
gym with a torn ACL. What is true of the athlete who achieves a personal best or has an
uneventful workout is also true of the individual who has a season ending injury. All of these
scenarios were influenced by interdependencies among an uncountable number of factors that
overwhelm the explanatory power of the rules we use to guide our decision making progress. We
may applaud one athlete for their success and curse another’s terrible luck, but it’s unlikely we
could have predicted either of them through our own senses of perception. In fact, modern
artificial intelligence algorithms are revealing how many of our everyday experiences are more
random than they are governed by discrete rules. Artificial intelligence gains a considerable
amount of its predictive power by ditching the types of generalizations that we humans tend to
understand and apply. Some coaches are concerned about the ‘black box’ nature of AI systems
for the simple fact that they excel at predicting things that we cannot. However, these same
systems can help coaches redefine the world of high performance athletics and what is
achievable.
Machine learning works differently than traditional computer programs, which are the
epitome of rule-based systems. For example, let's take a standard program that aims to recognize
handwritten numbers. The computer programmer instructs the computer that a ‘1’ is drawn as an
upright straight line and that a ‘0’ is an upright oval with perfectly symmetrical sides. The
aforementioned program would work well in some cases, but its reliance on perfect examples of
hand-drawn numbers means it will misidentify a high percentage of numbers written by humans
with imperfect handwriting. A machine learning program on the other hand could be shown
thousands of handwritten numbers with each correctly labeled with the number they represent.
The system will then discover the relationship between the pixels composing the images that
share a given label and over time it will correctly identify handwritten numbers, whether they are
drawn by someone with perfect penmanship or a kindergartener. This is a simple example of how
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machine learning can be used. So simple in fact that we can accomplish this type of image
recognition task ourselves.
There are many real-life scenarios where the amount of incoming data is so great, and the
relationships between the data are so complex, that we could never understand it ourselves. For
example, human physiology is influenced by an incredibly complex set of interacting and
interdependent variables. Now, imagine someone creates a machine learning system, named
Deep Physiology, that can accurately predict how the human body will respond to different
environmental conditions, ingested compounds, and circumstances. Deep Physiology could
conceivably become the most important source of knowledge about the human body, even if we
have no idea how it produces its answers. Additionally, Deep Physiology may become the go to
place for exercise scientists, sports physicians, and coaches to explore ideas and ask questions
about how the human body will adapt to specific stimuli. Over time many coaches would
become reliant on Deep Physiology and two camps would form among those individuals. One
camp believes that the inexplicability of Deep Physiology is a problem that they need to put up
with in exchange for useful information. The other camp sees the inexplicability of Deep
Physiology as a profound truth. They believe that Deep Physiology works so well for the precise
reason that it can perform more computations per second than they can without having to worry
about explaining itself in a way that a human being can understand.
It’s easy to believe that machine learning models are absent of rules, principles, and
generalizations. This couldn’t be further from the truth. Machine learning works as well as it
does because of its ability to make generalizations and predictions from an overwhelming
amount of information. The crux is that the types of generalizations that machine learning
models make are unlike our own. People like traditional generalizations because we can
understand them and apply them in our everyday lives. Machine learning on the hand makes
generalizations that are not always understandable. Instead, they are statistical, inductive, and
probabilistic. These very things are what make machine learning models so useful to coaches and
sports science practitioners. Rather than being fearful that machines will steal our jobs we should
embrace the use of artificial intelligence in sport because it perfectly compliments our own
strengths and weaknesses. This relates to Moravec’s paradox which states that it’s relatively easy
to create machines with superhuman analytical abilities, but nearly impossible to give the same
machines the perceptual skills of a toddler. This paradox is explained by the fact that humans
have evolved over millions of years to develop powerful, though largely unconscious, perceptual
skills. In Hans Moravec’s book titled Mind Children: The Future of Robot and Human
Intelligence he says, “We are all prodigious olympians in perceptual and motor areas. So good
that we make the difficult look easy. Abstract thought, though, is a new trick, perhaps less than
100,000 years old. We have not yet mastered it. It is not all that intrinsically difficult, it just
seems so when we do it.” By equipping coaches, possessing a keen ‘coaches eye’, with
AI-powered analytics we can usher in a new era of high performance athletics.
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Chapter 3: Integrated Cardiovascular Control
Blood flow regulation is one of the most interesting aspects of human physiology. When
an exerciser performs high intensity exercise oxygen is consumed at a greater rate than it can be
supplied to the working muscles, and as a result there is a net deoxygenation of the skeletal
muscle. In response to skeletal muscle hypoxia, exerciser’s working muscles will undergo
metabolic vasodilation, resulting in increased muscle blood flow. This process is simple during
single joint or small muscle mass exercise, like a bicep curl for example. However, it becomes
increasingly complex when we progress to regional exercise using multiple muscle groups in
close proximity to one another or during full body exercise. The reason for this is that we have a
finite ability to metabolically vasodilate tissue before we outstrip our cardiac output and cannot
maintain our arterial blood pressure. As a result our body has built in protective mechanisms to
ensure that we never vasodilate so much that it threatens our arterial blood pressure, which
would lead to a loss of consciousness. One mechanism by which this occurs is an increase in
sympathetic nervous system activity, termed sympathetic vasoconstriction. This sympathetic
regulation of peripheral blood vessel tone guards against the extreme vasodilator capacity of
skeletal muscle invoked by exercise and protects us from hypotension or low blood pressure.
The fine regulation of skeletal muscle blood flow is never more apparent than when
doing full-body, all-out, exercise like Crossfit or Nordic Skiing. During these full body
endurance sports the demand for oxygen by skeletal muscle can be increased by multiple orders
of magnitude and as a result skeletal muscle blood flow is very high. This creates some problems
during full body exercise where there are two potentially competing physiological needs. First,
skeletal muscle blood flow needs to be matched to meet the metabolic costs of muscle
contraction. Second, blood pressure needs to be regulated to ensure there is adequate perfusion
pressure to all organs. The idea that these two important needs compete arises when we consider
the total mass and vasodilator capacity of skeletal muscle compared to the maximal pumping
capacity of the heart. With enough skeletal muscle vasodilation there exists a risk that cardiac
output is outstripped and blood pressure regulation will be threatened, resulting in an inability to
maintain blood flow to the brain and vital organs. So, in addition to considering the heart as a
pump, the blood vessels as an oxygen delivery system, and the muscle as an end user of oxygen,
we also need to consider the overall need of the human body to maintain arterial blood pressure
in order to ensure the brain and vital organs get enough blood flow. One way that arterial blood
pressure is regulated is that the sympathetic nervous system restrains blood flow to the
contracting skeletal muscles. This was first explained by Loring B. Rowell in his sleeping giant
hypothesis which reflects the idea that the vast ability of skeletal muscle to vasodilate can
outstrip the ability of the heart to generate adequate cardiac output and arterial blood pressure. If
the sleeping giant awakens and blood flow to the skeletal muscle is not restricted, then
autonomic failure will ensue and blood pressure will fall so low that an individual will quickly
lose consciousness.
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In addition to blood flow to the working muscles being restrained, there is also a
diversion of blood flow away from less active skeletal muscle and other tissues so that the vast
majority of cardiac output, after the brain and vital organs are perfused, is directed to active
skeletal muscle. This adaptation is most impressive in elite endurance athletes. In these
individuals vasodilating factors in the skeletal muscle outcompete sympathetic vasoconstriction
in the arterioles closest to the contracting muscle while allowing for continued vasoconstriction
upstream, which is called functional sympatholysis. This process allows for high degrees of
oxygen extraction while maintaining high flow rates and simultaneously protecting cardiac
output. In this way, elite athletes straddle the line between supplying the muscle with sufficient
oxygen while keeping cardiac output as high as possible without threatening the ability to
maintain consciousness.
The Second Heart
If an aeronautical engineer were to analyze a bumblebee they would quickly
conclude that it could never fly. Yet, it does. Similarly, if a hydrodynamic analysis were done on
the human circulatory system it would lead to the conclusion that human beings cannot stand
upright, Yet, they do. We partly owe this ability to our ‘second heart’. While the heart acts as the
master pump in our bodies, it’s just one part of an integrated system and it could not function
without a secondary pump, called the muscle pump. The muscle pump acts as a secondary heart
on the venous side of circulation. Without this second heart an exercising human could not force
enough blood back to the right ventricle of the heart to maintain an adequate level of cardiac
output to keep them upright and conscious, let alone exercising.
If you’ve ever stood up for an extended period of time, without the slightest movement,
you’re familiar with the sensation of teetering on the bring of unconsciousness. Thankfully, even
the most modest muscle contractions of the leg muscles are enough to act as an effective pump
driving blood back to the heart and preventing you from blacking out. The reason for this is that
these muscles contract rapidly to restore ventricular filling pressures and stroke volume.
However, cardiovascular control is extremely complex, and there are instances where we can’t
rely on the second heart to help control cardiac output. For example, when exercising in high
heat conditions. Exercising in high temperatures forces humans to cope with two of the most
powerful regulatory demands they can face: the competition between the skin and muscle for
large fractions of cardiac output and blood flow.
The cutaneous circulation is second only to the skeletal muscle in its capacity to receive
large amounts of blood flow and can therefore seriously compete with skeletal muscle for cardiac
output during exercise. Simply put, we can’t increase blood flow to a great extent in one highly
compliant region without decreasing it somewhere else. This means that at some level of
physical output, in high heat conditions, cardiac output just can’t rise enough to supply both the
skin and muscle with necessary blood flow. This competition between the skin and muscle for
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blood flow provides a perfect example of how peripheral circulation determines the performance
of the heart and lines up with the mid twentieth century physiologist August Krogh’s beliefs that
the distribution of cardiac output determines the volume of blood available to the heart at any
moment. When we shunt more blood to the skin's surface to dissipate heat it means that a lower
fraction of blood volume is passing through the skeletal muscle pump and as a result less blood
is being driven back to the heart between contractions.
The price we pay for pumping more blood through the skin circulation, or any
non-pumping circuit, during exercise is a fall in ventricular filling pressure, cardiac preload,
stroke volume, and consequently cardiac output. We cannot sacrifice cutaneous blood flow for
the sake of maintaining ventricular filling pressure and cardiac output, otherwise disabling
hyperthermia would quickly ensue. This is one of the reasons why our performance is lowered
when we exercise in very high temperatures, and it is also a cause of cardiac drift. Cardiac drift is
a consequence of progressive increases in the fraction of cardiac output directed to vasodilated
skin as body temperature rises. This causes decreases in thoracic blood volume, and
consequently stroke volume with an upward ‘drift’ in heart rate at a fixed work bout.
Local, Regional, and Systemic Exercise
Have you ever wondered what the physiologic differences are between regional and
systemic exercise? For example, if you wanted to do an interval session have you wondered if
there is a meaningful difference between using a watt bike where only your legs are involved
versus an airdyne bike that incorporates both lower and upper limb activity? If so, you’ve
pondered questions about cardiovascular control mechanisms. When intense upper body
movement is added to intense lower body movement blood flow to the legs at a given work rate
will reduce by up to 10%. So, for example, if an exerciser is pedaling on an airdyne bike with
only their legs, then starts using both their arms and legs, blood flow to their lower body would
be reduced. A similar effect also occurs in the upper body, as would be the case if an exerciser
was powering the airdyne bike only using their arms and then started using their legs as well.
These reductions in blood flow to the extremity muscles are a product of peripheral
vasoconstriction, which is caused by the arterial baroreflex. The arterial baroreflexes key
function is to support and maintain blood pressure.
Reductions in skeletal muscle blood flow can be observed when an exerciser is limited by
the maximal pumping capacity of their heart during high intensity exercise and is incapable of
increasing cardiac output to cope with an increased work demand. In these cases cardiac output
is not sufficient to maintain blood pressure and the arterial baroreflex increases peripheral
resistance by augmenting sympathetic nervous system activity and restricting blood flow to
working skeletal muscles. This is an effective strategy because very small changes in the radius
of a blood vessel have huge impacts on blood vessel resistance and subsequently blood flow. The
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aforementioned scenario is common for Crossfit athletes who carry a meaningful amount of
muscle, and have good local muscle oxidative capacity, but lack sufficiently high levels of
cardiac output. These athletes often end up in a scenario where the demand for blood flow is
higher than the cardiac system is capable of supplying and as a result blood flow to the working
muscles is constrained. This phenomena is best observed during ramp incremental exercise tests
where progressive restrictions in blood flow can be observed as an exerciser travels through the
moderate, heavy, severe, and extreme exercise intensity domains.
Full-body endurance sports like Crossfit pose additional constraints in that discrepancies
between local and systemic energy reserves occur. Traditional endurance sports like running, on
the other hand, involve regional muscle groups working in concert with one another or large
muscle groups across the body working harmoniously, as is the case while rowing. Crossfit
workouts certainly have movements that individually fall into these categories, but are
complicated by the liberal sprinkling of small muscle mass exercises added in. For example, a
crossfit athlete may be asked to row a fixed distance, then string together a set of rebounding box
jumps before performing strict handstand pushups. These movements are systemically,
regionally, and locally taxing respectively. Since Crossfit metcons exercise a large percent of an
individual's total skeletal muscle mass a muscle oxygenation measurement captured on a single
muscle group can misrepresent the status of their systemic energy reserve. As a result I advocate
for measuring multiple muscles simultaneously which can be accomplished with one device on
the largest primary working muscle, a second sensor on a secondary working muscle, and a third
device on an intercostal muscle to assess the work of breathing. This allows an exerciser to
determine whether they are systemically or locally limited. If an individual is systemically
limited then they should aim to improve their VO2max which represents the maximum
integrated capacity of the pulmonary, cardiovascular, and muscular system to uptake, transport,
and utilize oxygen respectively. If an individual is locally limited on the other hand they should
train to improve local muscle strength, coordination, or edurace. Understanding which of these
factors is limiting an athlete is critical in order to retrieve the lowest hanging fruit to improve
performance.
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Oxygen Transport In Deep and Superficial Muscles
In addition to understanding how the total amount of exercised muscle impacts systemic
cardiovascular control it's also worth exploring the differences in oxygen kinetics between deep
and superficial muscles. Figure nine includes muscle oxygenation data from a collegiate rower
while they perform a maximal effort two-thousand meter row in six minutes and twenty-two
seconds. The red trend line represents muscle oxygenation from the rectus femoris, a deep
muscle, whereas the blue trend line represents muscle oxygenation from the vastus lateralis
muscle, a superficial muscle. Deep muscles have greater capillary than superficial muscles, and
as a result they receive greater blood flow during exercise. Deep muscles also tend to be more
oxidative than superficial muscles, which explains why deep muscles have slower rates of
oxygen desaturation than superficial muscles at a given power output as observed in figure nine.
Additionally, deep and superficial muscles have different oxygen transport strategies. Deep
muscles rely on perfusive oxygen transport whereas superficial muscles rely on diffusive
transport. These differences are an underappreciated aspect of local muscle metabolic control and
can account for many of the differences in muscle oxygenation between adjacent muscles during
exercise.
In addition to varying oxygen transport strategies, differences in coordination and
recruitment will impact muscle oxygenation trends in adjacent muscles during exercise. For
example, a rower may begin a two-thousand meter time trial with a knee flexion dominant slide
pattern and as the knee flexors fatigue they may rely more on hip extension to power their stroke.
This transition would result in less oxygen consumption in the vastus lateralis muscles and
greater oxygen extraction in the rectus femoris. Knowing this, it’s clear that only monitoring one
working muscle can misrepresent the status of overall systemic energy reserves, which is of
practical importance when trying to reach the utmost pinnacle of endurance performance.
In figure nine you can observe muscle oxygenation decreasing in both the rectus femoris
and vastus lateralis muscles as soon as exercise begins. Within six hundred meters muscle
oxygenation in both muscles reaches a local low point, which is maintained up to
thirteen-hundred meters. This maintenance of muscle oxygenation from six-hundred to
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thirteen-hundred meters indicates that the rower is working at a maximum steady state output.
However, after the thirteen-hundred meter mark an inflection point occurs and muscle
oxygenation in the vastus lateralis begins to increase while rectus femoris muscle oxygenation
simultaneously decreases. This indicated a change in movement coordination and muscle
recruitment, which is an unconscious strategy employed as primary locomotor muscles fatigue.
Individual Variations In Skeletal Muscle Vasodilator Capacity
There are local feedback mechanisms within exercising muscles that respond to
imbalances in oxygen supply and demand and adjust vascular conductance, the ease with which
blood flows through a muscle, accordingly. For example, during high intensity exercise muscle
oxygenation will decrease as oxygen consumption increases, and in response to that
deoxygenation there is a vasodilatory process that increases muscle blood flow. This vasodilatory
process is called blood flow autoregulation. Under normal circumstances there is a proportionate
compensatory increase in muscle blood flow per unit of oxygen consumed. However, there are
individuals in which this response is absent. That is, certain individuals present with a
‘non-compensator phenotype’ and lack the ability to metabolically vasodilate a tissue in response
to deoxygenation. Individuals with the non-compensator phenotype have lower than average
exercise tolerance and experience greater reductions in performance during high intensity
exercise due to their inability to increase muscle blood flow by an appropriate margin.
The existence of exercisers with a non-compensator phenotype speaks to the importance
of understanding interindividual differences in the mechanisms that govern the relationship
between oxygen supply and demand. These mechanisms include changes in potassium ions,
osmolarity, the partial pressure of oxygen, and adenosine which all play a role in the initiation of
exercise induced increase in blood flow. However, the aforementioned factors lack a sustained
influence as exercise continues as the varying molecules mentioned are cleared from the active
working muscles within minutes of starting exercise. It is suggested that the sustained
vasodilatory response during exercise, and compensatory vasodilation in response to
deoxygenation, are more closely related to the red blood cells ability to sense muscle
oxygenation. The red blood cell oxygen sensor hypothesis popularized by Dr. Jonathan Stamler
has gained widespread recognition as a potential mechanism for matching muscle oxygen supply
to demand. As an exerciser increases their workout intensity and red blood cells oxygen
saturation decreases there is a conformational change in hemoglobin’s structure, which results in
the release of bioactive nitric oxide. The release of bioactive nitric oxide in the microvasculature
evokes a local vasodilatory response that aids in the supply of oxygenated blood to the working
muscles. It has been speculated that the lack of compensatory vasodilation in exercisers with the
non-compensator phenotype may indicate compromised active nitric oxide release in the red
blood cells.
28
Figure ten shows muscle oxygenation and PNO trends, captured with the NNOXX
biosensor, for two different athletes performing a ramp incremental exercise test consisting of
four minute work bouts at 12.5%, 15%, 17.5%, 20%, 22.5%, 25%, 27.5%, 30%, and 32.5% of
their respective maximum sprint speeds with one minute rest between each set. Athlete ‘A’ has
an optimal vasodilatory response and is able to increase bioactive nitric oxide levels in direct
response to deoxygenation. As a result, there is a large upward trend in their PNO levels during
each work bout. Athlete ‘B’ presents with a non-compensator phenotype and has a blunted
vasodilatory response during each work bout. Additionally, Athlete ‘B’ reported much higher
ratings of perceived exertion in each work bout. I have also found that athletes with the
non-compensator phenotype have significantly compromised work capacity when exercising at
intensities above their critical power. To improve non-compensator athletes performance they
need to improve their ability to vasodilate, which is accomplished by selecting training
modalities that increase peripheral circulation and muscle capillarity. Additionally, these
individuals may benefit from implementing interventions to improve blood sugar control,
vascular health, and circulation.
Genetic Influences on Muscle Oxygen Kinetics & Cardiovascular Control
It’s well accepted that genetics play a meaningful role in an individual's adaptability to
training, recovery, and subsequently performance. Yet, coaches and exercisers rarely consider
individual genetic variations when designing a strength and conditioning program. The reasons
for this are likely two-fold. First, direct to consumer genetic tests are of varying quality and
many of the insights gained from these services are based on genome wide association studies
which often have little predictive value for individual consumers. The second reason is that the
influence of specific genetic markers on athletic performance is not abundantly clear. This
relationship is muddied by the fact that superior genotypes do not guarantee a superior
phenotype. It’s then further complicated by the fact that sports performance is so multifaceted
that the effects of specific genes can easily be overshadowed by other factors that influence
performance such as an individual's environment, their mental wellbeing, and the specifics of
their training plan. That said, SNP genotyping may still be a useful tool when used in the context
of a larger, more nuanced, athletic screening process.
29
SNP genotyping is a measurement of genetic variability in a person's single nucleotide
polymorphisms, which are the most common types of genetic variations between individuals of
the same species. The first SNPs to capture exercise physiologists' attention were those that code
for variations in the ACE gene, which codes for the angiotensin converting enzyme that converts
angiotensin-I to angiotensin-II. The angiotensin converting enzyme plays an important
component of the renin-angiotensin-aldosterone system, which regulates fluid volume and blood
pressure. There are three broad categories of ACE genotypes than an individual can possess. The
DD genotype is associated with high plasma levels of the ACE protein and as a result individuals
with this genotype have the highest capacity to produce angiotensin-II. These DD genotype
individuals experience a premature and excessive increase in blood pressure during exercise,
which results in a lower than average max heart rate and VO2max. Individuals with the DI
genotype have intermediate levels of the ACE protein and compared to DD genotype individuals
they have a high maximal heart rate and VO2max. Additionally, individuals with the DI
genotype have enhanced endurance performance compared to individuals with the DD genotype.
The DII genotype is associated with the lowest levels of the ACE protein and individuals with
this genotype often present with enhanced oxygen consumption and endurance performances.
It shouldn’t be a surprise that DI and DII ACE genotypes are found with an increased
frequency among elite endurance athletes. However, we can’t chalk up an exerciser’s
performance to one gene alone. For example, it’s well established that variations in the ACTN3
gene, which codes for the alpha-actinin-3 protein, has a meaningful influence on an individual’s
strength and endurance performance. There are also known synergistic effects associated with
different combinations of ACE and ACTN3 genotypes. For example, possessing
endurance-associated alleles in both genes predisposes an exerciser to excel in endurance sports
whereas having strength-associated alleles in both genes predisposes an exercise to excelling in
strength and power sports. One potential explanation for these findings is that particular
combinations of ACE and ACTN3 genes can influence muscle fiber composition.
In a paper titled, Influence of muscle fiber composition on muscle oxygenation during
maximal running 5, the investigators identified a strong association between an individual's
muscle fiber composition and the minimum muscle oxygenation level they reach after a maximal
effort running exercise. Exercisers who are more slow-twitch, and have a higher percentage of
oxidative muscle fibers, have higher muscle oxygenation levels after maximal effort running as
compared to exercisers with a higher percentage of fast-twitch glycolytic muscle fibers. A
potential explanation for this finding is that oxidative fibers have greater capillary density and
vascular conductance when compared to glycolytic fibers which enhances oxygen delivery. On
the flip side, glycolytic fibers have greater oxygen extraction when compared to oxidative fibers.
5
Kitada T, Machida S, Naito H. Influence of muscle fiber composition on muscle oxygenation during maximal running (2015). BMJ
Open Sport Exerc Med.
30
Knowing an exerciser's ACE and ACTN3 allele variation can give a strong indication of
whether they are likely to excel in strength or endurance sports. Additionally, knowing an
exerciser's genotype can help inform what type of training protocols will be most beneficial for
them. For example, if one athlete presents with a DD ACE allele and an RR or RX ACTN3 allele
we would want to train them differently than an athlete with a DI or DII ACE allele and an XX
ACTN3 allele. If both of these athletes wanted to gain muscle they would likely fare best with
different total set volumes, repetition schemes, and intensity distributions. The first athlete may
benefit more from high load, low repetition, resistance training whereas the latter athlete may
benefit most from moderate load, high repetition, resistance training. One reason for this is that
exercisers with a XX ACTN3 allele are deficient in the a-actinin-3 protein and as a result they
have impaired skeletal muscle function which lessens their ability to recover from high intensity
training. This paints an abundantly clear picture that the same exercise protocol will not affect
two different people in exactly the same way. George Brooks expressed this idea well when he
said, “It is wise to note that we are all individuals and that whereas physiological responses to
particular stimuli are largely predictable, the precise responses and adaptations to those stimuli
will vary among individuals. Therefore, the same training regimen may not equally benefit all
those who follow it”.
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Part II: Energy System Training
Chapter 4: A Physiological Performance Paradigm
Imagine we have two runners, John and Steve, who are to race one another. Both John
and Steve have a VO2max of 80 millimeters of oxygen consumed per minute per kilogram of
muscle mass. This VO2max value represents the maximum integrated capacity of their
pulmonary, cardiovascular, and muscular systems to uptake transport and utilize oxygen
respectively. Despite these athletes having identical VO2max values, John ends up beating Steve
in a 5,000m foot race when they toe the line against one another. How do we reconcile this?
I’ve often heard one camp of coaches make the argument that a high VO2max is
everything, and that the results of races are predetermined before they start. I’ve heard a different
camp of coaches make another argument entirely, which is that VO2max is meaningless because
it can’t predict finishing places among elite runners. In reality, both of these camps are right to a
degree. If two runners show up to a race and one of them has a VO2max of 50 ml/kg/min, and
the other has a VO2max of 80 ml/kg/min, we can make a surefire bet that the later runner will
win. But, when two athletes with high, but similar, VO2max values race against one another it’s
a toss up who will win. That is, unless we account for other factors outside of VO2max. This
relates to Simpson’s paradox which refers to the fact that correlations that exist within a
heterogenous group often break down within homogenous groups. For example, while VO2max
may be a strong predictor of performance at a population level, it is a very weak predictor in a
group of athletes at a similar fitness level.
One reason why VO2max is not predictive of performance in a homogeneous group of
exercisers is that VO2max is a functional criteria and not a performance criteria. The following
analogy uses cars to express this concept. The functional criteria of a car establishes how much
power it’s engine can produce. However, it says nothing about how far the car can go, how
quickly it can go from zero to sixty miles per hour, or how many miles it gets per gallon. These
are all performance criteria. In the same way, VO2max tells us something about the maximum
integrated capacity of major organ systems, but it doesn’t tell us how exactly an athlete will
perform in a foot race. In order to understand why John beat Steve in the 5,000m footrace, we
need to look past VO2max and start to consider certain performance criteria like critical speed,
which represents the fastest pace an individual can sustain before their rate of oxygen utilization
outstrips their oxygen supply. This has less to do with the maximal rate of energy turnover, and
more to do with an individual's ability to transfer energy into mechanical work. For example,
while John and Steve have the same VO2max, John may be able to sustain a 5:28 mile pace
before his oxygen consumption outstrips his oxygen supply, and Steve can only sustain a 5:32
mile pace before the same thing occurs. In this case, John can run at a 5:30 mile pace without
depleting his finite oxygen reserves, since he is running slower than his critical speed, while
Steve depletes himself in order to hang on. However, when we’re dealing with the highest level
32
athletes things can get even more complex. Let's take another scenario, where we have two
runners, Raina and Alexa. Both of these runners have a VO2max of 55 ml/kg/min, and they both
have a critical speed of 7:45 per mile. Yet, when they go head to head in a 10k Raina ends up
beating Alexa to the finish line. We know that both runners have the same rate of maximal
energy turnover, as well as the same ability to transfer energy into mechanical work, yet one still
wins the race while the other loses. This can be explained by differences in their running
economy, which defines their energy expenditure per unit of output. Traditionally, one’s running
economy is calculated as the rate of oxygen consumption for running at a specific submaximal
velocity. Improvements in running economy allow athletes to run at a faster velocity for the same
oxygen consumption, and thus achieve superior performances.
The importance of running economy is demonstrated in a famous case study published by
professor Andy Jones titled, The Physiology of the World Record Holder for the Women's
Marathon 6. This study shows that over a five year period Paula Radcliff’s fastest 3,000m race
time went from 9:22 down to 8:36 while her VO2max simultaneously decreased from 72.8
ml/kg/min to 66.7 ml/kg/min. Paula Radcliff’s drastic performance improvement can be
attributed to a substantial improvement in her running economy, which is demonstrated by the
fact that her oxygen cost while running sixteen kilometers per hour dropped from 53 ml/mk/min
down to 47 ml/kg/min while her running speed at VO2max increased from 19 km/hr upto 20.4
kg/hr. In other words, Paula Radcliff not only improved her running speed at VO2max, but also
consumed less oxygen at the greater speed. Using the earlier car analogy, this would mean the
car's engine got smaller while simultaneously producing more horsepower and having better fuel
efficiency. This is akin to trading a 1950’s muscle car for a Tesla Roadster.
By accounting for multiple different functional and performance criteria it's possible to
create a robust model of endurance performance that can accurately predict an individual's
capability in real world racing scenarios. The first tier of this model is VO2max, which acts as an
upper ceiling constraining an individual's performance potential. The next tier is lactate
threshold, which is the fraction of an individual's VO2max they can sustain before lactate
accumulates in the blood at a faster rate than it is consumed for fuel. While lactate levels
themself are not an indicator of fatigue or performance, the lactate threshold is a good proxy
measurement reflecting an individual's reliance on glycolysis to provide energy. The third tier in
the performance model is critical power, which is the highest power output, or velocity, that an
individual can sustain indefinitely before they begin to deplete their finite oxygen reserve. The
fourth and final tier is movement economy, which describes the oxygen cost of performing a
given activity at a submaximal intensity.
6
Jones AM (2006). The Physiology of the World Record Holder for the Women’s Marathon. International Journal of Sports Science
& Coaching. 2:101-116.
33
Collectively the four aforementioned factors can be used to develop a comprehensive
model of bioenergetic competence. In essence, this model states that whoever has the highest
sustainable rate of energy turnover, the greatest ability to transfer that energy in mechanical
power and the greatest ability to apply power to the task of running with the greatest efficiency
and for the longest duration will win an endurance event when all other factors are equal. The
crux is that there are metabolic tradeoffs between some of these traits, such that the individual
with the highest VO2max will not have the highest economy and vice versa. It is up to each
individual to determine which of the aforementioned factors should be prioritized over others in
order to maximize their own performance. Increasing one’s VO2max requires improving their
energetic limiter, and subsequently raising their ceiling for performance, which will be discussed
in length over the next two chapters. Increasing critical power not only requires improving the
maximal rate of energy turnover, but also increasing the percentage of maximal power output
that can be sustained during steady-state exercise. Finally, improving movement economy will be
a recurring theme throughout the next few chapters on understanding both energetic and sport
specific limiters.
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Chapter 5: Challenging Conventional Paradigms of Maximal Exercise
Performance
Loring B. Rowell, the late physiologist, once said, “Exercise more than any other stress
taxes the regulatory ability of the cardiovascular system. The advantage to the investigator is that
more is learned about how a system operates when it is forced to perform than when it is idle.” In
simple terms, this means that exercise can be used to push the human body to its limits, which
provides scientists with an understanding of human physiology that couldn’t have been gained
otherwise. One reason for this is that it’s exceptionally difficult to record uniform and consistent
measurements of an individual’s physiology at rest. Joseph Barcroft understood this as early as
1934 when he wrote, “scaling from measurements at rest suffers from the marked random
variation characterizing that loosely defined state” in Features in the Architecture of
Physiological Function. Joseph Barcroft’s key point was that the term rest is too seemingly
arbitrary to be useful. For example, am I resting as I sit upright in a chair? Or, am I only resting
if I lay supine without moving a single muscle? These questions may seem pedantic, but they
have real consequences in research where conditions need to be standardized to the utmost
degree.
Rather than grappling with the aforementioned issues physiologists have adopted a
different method of collecting uniform measurements. It’s long been known that the most
uniform and consistent measurements of human physiology occur at an individuals’ maximal
exercise capacity. The most common test used to interrogate an exerciser’s maximal work
capacity is the ramp incremental VO2max test, which is a measurement of the entire
cardiovascular system’s functional capacity. You can think of an exerciser’s VO2max as the
maximum integrated capacity of their pulmonary, cardiovascular, and muscular system to uptake,
transport, and utilize oxygen respectively.
Despite VO2 being a relatively simple measurement of total body oxygen consumption
there is a bit of nuance as to how a true VO2max is attained. For example, attaining a true
maximum VO2 measurement requires that a certain fraction of an exerciser’s total muscle mass
is engaged during activity. As a result, the term VO2max only applies to the highest attainable
VO2 value an individual can reach, independent of exercise modality. On the other hand, the
term VO2peak is contextual and refers to the highest VO2 value achieved during a given
exercise bout. If you were to exercise a small fraction of total muscle mass by using an arm
ergometer your VO2peak would be much lower than your VO2max. However, if you were to
perform a full body exercise, like rowing, your VO2peak would be equal to your VO2max.
Interestingly, you do not need to exercise your full body to reach a true VO2max. You only need
to cross a critical mass of engaged skeletal muscle and past that point engaging even more
muscle will not lead to greater whole body oxygen consumption.
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Determinants of Maximal Oxygen Consumption
The whole idea that there is a finite rate that oxygen can be transported from the
environment to the mitochondria of exercising muscles began in the early 1920’s with the Nobel
prize laureate Archibald Hill’s work. Since then VO2max has become one of the most ubiquitous
measurements in exercise science.
VO2max is calculated with the Fick equation, which states that the volume of oxygen
consumed at any given time is the product of an exerciser’s cardiac output (which is itself the
product of heart rate and stroke volume) and the difference in oxygen concentration between
their venous and arterial blood, also known as the arteriovenous difference. Using the Fick
equation one can derive that there are two ways that an individual can increase their VO2max.
The first is increasing oxygen supply and the second is by increasing oxygen utilization.
However, the traditional viewpoint is that interindividual differences in VO2max are almost
entirely due to differences in stroke volume and cardiac output between exerciser’s. The idea is
exemplified in Lundby, Montero, and Joyner’s paper titled Biology of VO2max: looking under
the physiology lamp 7 where they state, “The dominant and deterministic physiological pathways
that account for a vast majority of interindividual variability in VO2max are well known and
center on total body hemoglobin content and peak cardiac stroke volume and as a result cardiac
output.”
It makes sense that an exerciser’s stroke volume would play a large role in determining
their VO2max when you consider the fact that an enlargement of the heart’s ventricles, enhanced
cardiac contractility, and increases in blood volume are all common adaptations from endurance
training. These adaptations all allow for an increased filling of the ventricles between heart beats,
and in turn they increase stroke volume. Additionally, it's well known that endurance training
increases hemoglobin concentrations in blood, which can increase stroke and VO2max. Per-Olof
Åstrand was the first to demonstrate this relationship when he showed that the differences in
VO2max values between adults and children, and between adult men and adult women, are
primarily due to differences in hemoglobin concentrations. Since then it has been shown that
acute reductions in hemoglobin concentrations result in decreased endurance performance and
oxygen carrying capacity in the blood, even when blood volume is maintained. Conversely,
increases in hemoglobin concentration and blood volume are associated with enhanced
endurance performance. The reason is that increases in blood volume cause end-diastolic
volume, ejection fraction, and stroke volume to go up, which are all associated with increased
VO2max values.
Collectively, the aforementioned factors provide evidence for the existence of a
cardiovascular oxygen supply limitation. However, this evidence does not mean that VO2max
cannot be limited by other factors such as oxygen utilization in the working muscles, or
7
Lundby C, Montero D, Joyner M (2017). Biology of VO2 max: looking under the physiology lamp. Acta Physiol. 220: 218-228.
36
pulmonary oxygen supply. In other words, the existence of one phenomenon does not disprove
another. For example, elite endurance athletes with very high maximal cardiac outputs will often
present with pulmonary diffusion limitations because of the red blood cells moving through the
pulmonary capillaries so quickly that they cannot adequately pick up oxygen. This form of
pulmonary diffusion limitation was first observed in Peter Snell, the former world record holder
for the fastest mile run. Peter Snell performed a maximal effort step test on a treadmill, and
finished with an peripheral oxygen saturation of 80%, systemic oxygenation. Additionally, this
finding was later confirmed by Jerome Dempsey, Scott Powers, and colleagues, when they
showed that arterial deoxygenation occurs in some high trained endurance athletes and that when
these subjects breath in hyperoxic gas mixtures their hemoglobin saturation and VO2max
increase. It’s also common for elite Crossfit competitors to experience significant decreases in
peripheral oxygen saturation after competition intensity work bouts. This suggests that
pulmonary gas exchange can limit total body oxygen consumption in highly trained athletes who
exhibit exercise-induced reductions in peripheral oxygenation at sea level. It also suggests that a
healthy pulmonary system can become a so-called limiting factor to oxygen transport and
utilization as well as carbon dioxide transport and elimination during maximal effort exercise in
the highly trained.
According to the Fick equation, an increase in VO2max must be accompanied by a
concomitant improvement in maximal cardiac output or a widening of the arteriovenous oxygen
concentration difference. Knowing this, it’s clear why a pulmonary diffusion limitation would
decrease VO2max and impair performance. If an exerciser’s peripheral oxygen saturation
decreased, it would minimize the concentration difference between their arterial blood, which
should be highly oxygenated, and their venous blood, which has a lower oxygen concentration.
In these cases improving pulmonary function would widen the arteriovenous concentration
difference, thus increasing VO2max. However, oxygen utilization limitations may also be
present, which would truncate the arteriovenous concentration difference by increasing the
oxygen content of venous blood. In these cases improving an exerciser’s oxygen extraction and
utilization would widen the arteriovenous difference, increasing VO2max as a consequence.
Redefining VO2max
Traditionally VO2max has been defined as the maximal rate of oxygen consumption
measured during intense exercise, and it’s long been believed that stroke volume is the dominant
and deterministic limiter of VO2max. However, there are well-established cases where VO2max
is limited by other physiologic factors. As a result, It’s more appropriate to define VO2max as
the maximum integrated capacity of the pulmonary, cardiovascular, and muscular systems to
uptake, transport, and utilize oxygen, respectively.
It’s now clear that VO2max can be limited by a range of physiological factors such as an
exerciser’s pulmonary diffusion capacity, maximal cardiac output, peripheral circulation, and the
37
oxidative capacity of skeletal muscle. However, most coaches and physiologists still do not hold
this view. Instead, they believe that the cardiovascular system’s capacity to transport oxygen to
the working muscles is the principal determinant of VO2max. This idea emerged as a result of
Archibald Hill’s research in the early 1900’s.
While Archibald Hill’s work undoubtedly contained many partial truths, its partial
validity shouldn’t mask its clear shortcomings. It is crucially important to realize that Archibald
Hill formulated his hypotheses based on a small number of measurements of expired respiratory
gasses. He did not include any measurements of cardiovascular function, pulmonary function, or
any measurements of skeletal muscle contractile and metabolic function. An unfortunate
consequence is that generations of exercise physiologists have been taught that respiratory gas
analysis, in the absence of other biomarker measurements, can give you answers about the
factors that limit human performance. I believe this is false. For example, in Archibald Hill’s
quantitative estimates he calculated that arterial blood would be 90% saturated during all-out
exercise and that mixed venous blood would be 10-30% saturated. He also assumed that these
values would generalize to all exercising individuals. If this were true, and the arteriovenous
concentration difference were fixed, it would lead to the natural conclusion that cardiac output is
the primary determinant of VO2max, as Hill and generations of physiologists after him asserted.
However, we know these values are not only not fixed, but vary considerably between exercising
individuals. Thus, opening the door for a more nuanced understanding of the limiting factors for
maximal exercise performance.
How Does VO2max Increase?
The cardiovascular system has a profound ability to adapt and change when it is
repeatedly exposed to exercise-induced stressors. Physical conditioning, from exercise, increases
the functional capacity of the cardiovascular system in two distinct ways. First, physical
conditioning increases maximal cardiac output by increasing heart rate and/or stroke volume.
Second, conditioning can lead to adaptations that widen the arteriovenous oxygen concentration
difference during exercise which is accomplished by increasing arterial oxygen saturation or
increasing fractional oxygen extraction.
In healthy young adults who are previously untrained VO2max can increase by upwards
of 20% after three months of training. Approximately half of the increase in VO2max can be
attributed to increases in maximal cardiac output and oxygen extraction respectively.
Additionally, the exercise induced increases in cardiac output are due almost entirely to increases
in stroke volume, and not heart rate. However, in advanced athletes who have undergone years of
training 30% of improvements in VO2max are attributed to increases in stroke volume, 10% are
attributed to increases in maximal oxygen extraction, and the remaining 60% of improvements
are attributed to enhanced movement economy and pulmonary diffusion.
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Based on the broad body of exercise physiology literature it’s apparent that the peripheral
adaptations that lead to increased oxygen extraction occur rapidly in response to exercise. For
example, improvements in oxygen extraction and muscle oxygen utilization have been observed
in as little as two to three weeks of dedicated training. Cardiovascular and circulatory
adjustments, on the other hand, occur over much longer time scales. The rates of adaptation in
different bodily systems helps explain why oxygen extraction limitations are less common
among elite athletes.
Increasing Stroke Volume
There are three proposed mechanisms contributing to exercise-induced increases in stroke
volume. These include changes in the myocardial contractile state, changes in ventricular
afterload, and changes in ventricular preload.
Although it has traditionally been believed that changes in the myocardial contractile
state lead to exercise-induced increases in stroke volume that theory can be quickly dispensed
with. While it is true that the myocardial contractile state increases as exercise intensity
increases, additional enhancements to the myocardial contractile state over time with training are
small because left ventricular ejection fraction is already high at 85%. Additionally, end-systolic
volume is low at peak exercise. As a result, it’s unlikely for exercise to yield further
improvements in the myocardial contractile state.
Ventricular afterload is the amount of pressure that the heart must work against to eject
blood during systole, which is the phase of the heartbeat when the heart muscle contracts and
pumps blood into the arteries. While it has been proposed that changes in afterload account for
some of the observed increases in stroke volume with physical conditioning I find this to be
implausible. There is little evidence demonstrating significant effects of training on ventricular
afterload. Additionally, cross sectional studies show that highly trained athletes and sedentary
individuals have similar mean arterial pressure at their respective maximal cardiac outputs. This
suggests that physical training is accompanied by peripheral adjustments that match total
vascular conductance to maximal cardiac output, without significant changes to ventricular
afterload.
Collectively the aforementioned information suggests that the bulk of increases in stroke
volume as a product of physical conditioning are attributed to changes in ventricular preload.
Ventricular preload, also known as end-diastolic volume, is the amount of stretch that the cardiac
muscle cells experience at the end of ventricular filling between heart beats. Based on cross
sectional studies, it’s been shown that ventricular preload is significantly elevated at rest and
during exercise in athletes as compared to sedentary individuals. It is also believed that structural
changes in the heart allow for increased ventricular preload, which is supported by medical
imaging and autopsy studies showing that chronic physical training increases ventricular volume
39
and ventricular wall thickness and that there is a significant correlation between heart size, stroke
volume, cardiac output, and VO2max. Additionally, long term-training results in meaningful
increases in blood volume, which can have a small but noticeable positive impact on ventricular
preload.
Arterial Oxygen Saturation During Exercise
It’s important to remember that the circulatory system is a closed loop where oxygen
travels from the heart to the working muscle and back along the following route: heart → artery
→ arteriole → capillary → venule → vein → heart. When we record arterial oxygen saturation,
often referred to as SpO2 or SaO2, we are measuring at the location of the artery. Arterial
oxygen saturation depends both on hemoglobin concentration as well as its oxygen binding
capacity, pulmonary diffusion capacity, and alveolar ventilation.
It’s commonly assumed that both arterial oxygen content and hemoglobin saturation are
well maintained during exercise. However, during maximal effort exercise arterial hemoglobin
concentration and oxygen carrying capacity can both rise by up to 10%. This occurs when
plasma water is lost into the active muscle cells and interstitial fluid as the concentration of
osmotically active particles in the muscles rise.
Insofar as an individual’s arterial oxygen capacity rises, while their oxygen content
remains constant, their arterial oxygen saturation will fall. This is why you’ll often see a
meaningful decrease in peripheral oxygen saturation during very high intensity exercise.
Additionally, the aforementioned decrease in peripheral oxygen saturation during high intensity
exercise is partly attributable to reductions in arterial pH and a rise in temperature, both of which
lower arterial oxygen saturation at a given oxygen binding capacity. In very extreme cases you
may see peripheral oxygen saturation fall below 90%, though this is much more common in elite
endurance athletes. In these cases the extreme drops in peripheral oxygen saturation are caused
by a pulmonary diffusion limitation.
Skeletal Muscle Oxygen Extraction During Exercise
The Fick equation states that the volume of oxygen consumed at any given time is the
product of an exerciser’s cardiac output and the difference in oxygen concentration between their
venous and arterial blood. Muscle oxygenation, as recorded with the NNOXX biosensor, is
measured in the microvascular capillaries, which approximates mixed venous oxygen content.
The two populations where the lowest muscle oxygenation values are observed are high training
athletes with enhanced oxygen extraction capabilities, and heart failure patients who have very
low cardiac output due to an insufficiency of the heart as a pump.
Highly trained athlete’s enhanced oxygen extraction capabilities are explained by a range
of factors. Unlike cardiac muscle where moist capillaries are open at all times, only a small
fraction of capillaries are perfused in skeletal muscle during rest. As a result, the diffusion
40
distance between capillaries and muscle fibers is large. When you consider these large diffusion
distances and the fact that the mean transit time of red blood cells through the muscle capillaries
are very short, there is little time for oxygen extraction and uptake by the skeletal muscle at rest.
However, during exercise the number of open capillaries increases, which reduces the diffusion
distance and increases capillary blood volume significantly. As a result, the mean transit time of
red blood cells increases, which allows for more oxygen to be unloaded from the blood to the
working muscle. As a consequence of increased capillary recruitment during exercise, each
muscle fiber is supplied by more capillaries than at rest. Therefore, to maintain high oxygen
extraction across the muscle there needs to be a balance between optimal rates of muscle blood
flow, capillary blood volume, and the minimum mean transit time of red blood cells to release
oxygen for skeletal muscle uptake. This balance is well preserved during intensity exercise
where both muscle blood flow and oxygen extraction increase significantly, thus increasing
whole body VO2 as well. In these cases capillary blood volume and red blood cell mean transit
time are large enough to allow oxygen to be released from hemoglobin and diffuse all the way
from the capillaries to the mitochondria of muscle cells.
Oftentimes exercises with low training ages will present with oxygen extraction
limitations as a result of low mitochondrial and capillary density. Additionally, there are
instances where athletes with very high maximal cardiac outputs will present with oxygen
extraction limitations as well, particularly when they eschew high intensity training for extended
time periods. In both cases increasing muscle mitochondrial and capillary density, and improving
vascular conductance, will lead to enhanced skeletal muscle oxygen extraction.
Mitochondrial DNA, Maximal Oxygen Consumption, and Metabolic Efficiency
For decades mitochondria have been seen as nothing more than microscopic cellular
powerhouses. However, mitochondria also play critical roles in regulating cell death and
survival, aging, and various physical adaptations to endurance training. It’s well known that
mitochondria are the only organelles in animal cells with their own discrete genome, which is
attributed to their endosymbiotic origin. Thus, while we inherit our chromosomal DNA from
both our parents, our inherited mitochondrial DNA comes exclusively from our mothers. This
maternal inheritance of mitochondrial DNA, combined with the high mutation rate of
mitochondrial DNA, allows us to track our maternal lineage back through generations. You can
envision these mitochondrial DNA lineages as a giant tree, where the clustered groups on the
different branches make up different haplogroups. These haplogroups arose in geographically
localized populations, and their distribution across the world has allowed researchers to
reconstruct the ancient migrations of women across the globe.
It is well accepted that one of the main determinants of the individual variation in
endurance performance is the metabolic properties of skeletal muscle, particularly its
mitochondrial oxidative potential, which is coded by mitochondrial DNA passed down through
the maternal lineage. This material DNA codes for some of the most essential polypeptides of the
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mitochondrial energy generating system, most notably OXPHOS, which generates cellular
energy by the oxidation of dietary calories. As electrons move down the electron transport chain
the energy released pumps protons out across the inner mitochondrial membrane to generate a
proton electrochemical gradient, which the ATP synthase enzyme can employ to drive ATP
synthesis. Therefore, the mitochondrial genome provides a few candidate genes for the study of
elite endurance athletic status.
Since mitochondrial DNA genes have a central role in OXPHOS expression, different
haplogroups and functional variants in mitochondrial DNA can have massive impacts on human
physiology and exercise performance. For example, the efficiency with which the electron
transport chain generates the proton gradient and by which the proton gradient is converted into
ATP is referred to as the coupling efficiency. Humans can differ substantially in their coupling
efficiency due to mitochondrial DNA polymorphisms. Since a dietary calorie is a unit of heat,
every calorie burned by the mitochondria generates one calorie of body heat. Tightly coupled
mitochondria generate the maximum ATP and minimum heat per calorie burned and thus could
be beneficial in warmer climates, while loosely coupled mitochondria must burn more calories
for the same amount of ATP, generating more heat, and could be of benefit in colder climates.
The importance of heat generation per unit of energy created will be discussed shortly.
As previously mentioned, aerobic ATP generation by OXPHOS is a vital metabolic
process for endurance exercise. Notably, mitochondrial DNA codifies 13 of the 83 polypeptides
implied in the respiratory chain. As such, there is a strong rationale for identifying an association
between mitochondrial DNA variants and endurance phenotypes. In the context of endurance
performance, high sustained ATP synthesis is one of the most important competitive advantages.
It is increasingly recognized that there is a conserved evolutionary trade-off between
maximum-power output using fermentative pathways and maximum metabolic efficiency using
complete oxidative phosphorylation, which is rooted in differences in the catalytic capacity of
the different pathways. The phenomenon is known as overflow metabolism. The reason that
metabolic overflow occurs stems from a bottleneck deep inside the mitochondria termed
complex-I. At lower power outputs such as during long slow distance training, the muscles
energy stores are burned efficiently using complex-I. When power output is increased, complex-I
reaches its full capacity, so to be able to match the energy requirements mitochondria start to
bypass complex-I choosing a metabolic strategy with a higher capacity but a lower efficiency.
This allows the muscles to produce more power, but also more heat. Going into power mode
thereby means that your energy stores are zapped faster and the athlete risks hitting the wall
before reaching the finish line.
This becomes relevant when we think of rate limiting factors for increasing an
individual’s VO2max. While many athletes use VO2max as a measuring stick for performance
improvement, they seldom consider that improving VO2max may come at the cost of decreased
efficiency. For example, Oskar Svendson has been recorded as having the highest VO2max of all
42
time. Naturally, this leads to the question of why wasn’t he a faster cyclist? Mikael Flockhart and
Filip Larsen offered a suggestion to this question in their 2019 paper in the Journal of Applied
Physiology titled, Physiological adaptation of aerobic efficiency: when less is more 8. In essence,
they suggest that Svendson has a massive engine but poor fuel efficiency and that this is no
coincidence. Michael Joyner has made a similar suggestion in a paper titled, Modeling: optimal
marathon performance on the basis of physiological factors 9, where he stated, "It may be that
high VO2max values are incompatible with an excellent running economy."
Interestingly, in the early 1990’s Michael Joyner had posited that the first runner to run a
sub 2-hour marathon would have a high but realistic VO2max, running economy, and lactate
threshold without any of these individual variables being off the charts. He was clear that the
individual with the highest VO2max value would be an unlikely candidate. The reason for this is
that it’s physiologically implausible for someone with a very high VO2max to have a world-class
running economy in the same way that it’s unlikely to hit the mega millions jackpot twice.
Interestingly, Eliud Kippchogee perfectly fits this bill. He has a high VO2max at 78
ml/kg/minute, but it is by no means off the charts. However, his economy sets him apart, which
allows him to use 0.2 ml/kg/minute of oxygen per minute than his competitors at a top speed. He
has struck the perfect balance between power and efficiency. Research suggests that between two
elite runners with equal race times, the individual with the higher VO2max will have a lower
economy and vice versa. This surely applies to Oskar Svendson and is a topic of discussion in
Bent Ronnestad and colleagues' paper titled, Case Studies in Physiology: Temporal changes in
determinants of aerobic performance in an individual going from alpine skier to world junior
champion time trial cyclist 10. Interestingly, Oskar Svendon’s data suggests that his gross
efficiency (the power delivered to the bike pedals divided by the rate he burned calories) was
highest before he began science training and as his VO2max progressively increased, his
efficiency dropped at a disproportionate rate. A potential mechanism for this lies in Avlant
Nilson and colleagues' paper titled, Complex-I is bypassed during high intensity exercise 11,
which hammers home the aforementioned concept that at very high intensities mitochondria
bypass complex-I and rely on metabolic strategies that allow for higher capacity, but with lower
efficiency. This strategy will enable muscles to produce more power, but also more heat. It stands
to reason that the individuals with the highest VO2max values in the world, also have some of
the most loosely coupled mitochondria and vice versa. Remember, loosely coupled mitochondria
are beneficial in colder climates, whereas highly coupled mitochondria benefit in warmer
climates. Interestingly, some of the highest VO2max values have been recorded by athletes of
northern European descent, whereas individuals living closer to the equator tend to have lower
than average VO2max values when adjusted for age and body mass. While investigators have
8
Flockhart M, Larsen FJ (2019). Physiological adaptation of aerobic efficiency: when less is more. J Appl Physiol.
Joyner MJ (1991). Modeling: optimal marathon performance on the basis of physiological factors. J Appl Physiol.
10
Rønnestad BR, Hansen J, Stensløkken L, Joyner MJ, Lundby C (2019). Case Studies in Physiology: Temporal changes in
determinants of aerobic performance in individual going from alpine skier to world junior champion time trial cyclist. J Appl Physiol
11
Nilsson A, Björnson E, Flockhart M, Larsen FJ, Nielsen J (2019). Complex I is bypassed during high intensity exercise. Nat
Commun
9
43
begun to identify mitochondrial haplotypes associated with both of these adaptations, more
research is needed before consumer DNA tests can be used for talent identification.
Chapter 6: Understanding Bioenergetic Limiters
44
I suspect that many of you, reading this book, came here to learn more about bioenergetic
limiters. For one reason or another, this is one of the concepts I've become best known for, and it
always seems to drum up interest. While I do think this is a useful concept for profiling athletes
and identifying low hanging fruit that you can go after in their training, it's not the only thing we
should be concerned with when trying to optimize performance on a given task. We can’t neglect
sport specific limitations, or the fact that an individual’s bioenergetic limiter is just one part of an
integrated system that should be trained in all its capacities.
A common misconception about limitation based training models is that exercisers
should only train to improve their bioenergetic limiter in order to enhance their performance. For
example, this would mean that a delivery limited athlete only trains to improve their ability to
transport oxygen to the working muscles, which is an obvious mistake. It’s important to realize
that an exerciser’s bioenergetic limiter is the rate-limiting process for increasing their
VO2max.There are instances where increasing an individuals’ VO2max will result in a direct
performance improvement, but that isn’t always the case. For example, an exerciser’s maximal
rate of oxygen consumption may be limited by their pulmonary systems ability to uptake oxygen.
However, if this same exerciser wants to compete in a 100m sprint it’s unlikely that their
pulmonary system will be the rate-limiting factor for performance improvements. Instead, they
are more likely to be limited by their maximal rate of oxygen utilization in the working muscles.
Similarly, if the same athlete decides to compete in an ultramarathon their event specific limiter
will be different. In the latter case they are likely to be limited by their ability to deliver
oxygenated blood to the working muscles, regulate their blood pressure, or they may even be
limited by central fatigue and glycogen depletion.
Finally, it’s important to understand that an athlete will not fail to perform when their
limiter can no longer cope with the demands of maximal effort exercise. They will fail when they
have exhausted all of their available compensatory strategies. It’s not a matter of if an athlete’s
limiter will fail to cope with the demands placed on it during maximal effort exercise, but when.
Enhancing the capacity of an exerciser’s limiter will get them further before they are forced to
rely on compensatory strategies, but they still need to strengthen the compensating systems
nonetheless. While it’s important to train known limitations and always aim to grab the ‘lowest
hanging fruit’, that doesn’t mean there isn’t a time and place to climb a bit higher and grab the
next highest piece up in the tree. After all, when the lowest hanging fruit is exhausted, the next
highest is effectively the new lowest.
Functional Systems Theory
A functional system is a collection of biological components that work in unison to
achieve a useful adaptation for an exerciser. Inclusion, or exclusion, of a given training quality or
biological component in a functional system is predicated on its usefulness for aiding in the
achievement of an exerciser’s goals. In practical terms, we can think about this from a systems
45
standpoint. In our body we have varying organs systems like muscular system, pulmonary
system, cardiovascular system, and so forth. All of the aforementioned systems will need to
function for survival, and as a result they will all be developed to a given degree. But, when we
undergo a specific type of physical training for years on end we start to develop some systems
more than we do others. For example, if you’re an olympic weightlifter your functional system
will exclude very high degrees of cardiopulmonary system development. But, you’ll develop the
muscular system to a greater extent. As a result, your physiology will self organize according to
those principles and you will develop adaptations that are useful to your goal, and neglect those
that are not, which is the development of a functional system. On the other hand, if you are a
cross country skier, then your functional system will include very high degrees of
cardiopulmonary system development. This is important so far as it ties into the concept of
limiters, which is the backbone of the energy system training model that I'll discuss in the next
few chapters. No limiter is inherently good or bad. Different sports select for different limiters.
So, knowing this, we need to understand the energetics of the goal, and athletes' limitations, and
how to best train them for that task. Anytime I work with an athlete in a work capacity sport I
ask myself the following questions:
1. What result are we trying to achieve? This can be broad or highly specific. For
example, the desired result can be improving cardiac output, or it can be rowing two
thousand meters in six minutes and fourteen seconds.
2. What is the physiological disposition of the athlete? Are they limited by their ability to
uptake oxygen, transport oxygen to the working muscles, or utilize oxygen in the
working muscles?
3. What mechanisms or training qualities will support the desired result? The answer to
this question will be derived from our answers to the two questions above. For example,
if we have two athletes who both want to row two thousand meters in six minutes and
fourteen second, but one of them is limited by their ability to delivery oxygen to the
working muscle and the other is limited by their rate of oxygen extraction they will need
to take very different paths to achieve the same end result.
Global Adaptation Trends
When you take a diverse group and have them train in a similar manner over time, you’ll
find that they adapt in unique, but somewhat predictable, ways depending on their bioenergetic
limiter. These defined patterns of adaptation are called global adaptation trends.
Global adaptation trends are easiest to spot in work capacity based sports like Crossfit,
mixed martial arts, and tactical strength and conditioning where you have athletes from very
diverse backgrounds, physiological makeups, and bioenergetic limiters all training to accomplish
46
similar tasks. The first global adaptation trend, discussed below, pertains to respiratory limited
athletes.
Respiratory limited athletes most often present with above average maximal cardiac
output, high mitochondrial density, and high capillary density. As a result, these individuals have
well developed oxygen transport systems and a high maximal rate of oxygen utilization in the
primary working muscle groups for their sport. However, these athletes are limited by the
strength or fatigue resistance of their inspiratory muscles, expiratory muscles, and diaphragm.
During high intensity exercise the diaphragm has a large energy requirement and will be required
to contact with high force and frequency. When the diaphragm muscle begins to fatigue
locomotor muscle oxygenation will decrease, as will expelled carbon dioxide. In extreme cases
exercises will present with hypoxemia, defined by a large decrease in arterial oxygen saturation
levels as measured with a pulse oximeter. I’ve previously observed arterial oxygen saturation
levels as low as 15% below resting resting values during maximal effort exercise, which is
indicative of a pulmonary diffusion limitation and lack of respiratory muscle endurance.
It’s common for respiratory limited athletes to have a low forced vital capacity, and
functional lunge volume, relative to their body mass. Additionally, basic spirometry
measurements can be used to discern between inspiratory and expiratory muscle limitations. An
athlete with weak inspiratory muscles will have a lower forced vital capacity (FVC6) and a low
forced expiratory volume (FEV1), but the ratio between the two will be between 76-80%. An
athlete with weak expiratory muscles will also have a low FVC6 and FEV1, but the ratio
between the two measurements will be below 76%.
Among elite endurance athletes, respiratory limitations are the most common
bioenergetic limiter. While most systems in the body undergo substantial adaptations to intense
exercise, this doesn’t appear to be the case for the respiratory system. For every increase in
VO2max we should expect to see an increase in hemoglobin mass, left ventricular volume, and
mitochondrial density in the working muscles, among other adaptations. Given the adaptability
of various organ systems we would expect the airways, pulmonary vasculature, and lungs to
adapt to exercise as well. However, recent research has revealed multiple circumstances in which
one or more parts of the respiratory system are shown to be anatomically underbuilt or incur high
biological costs during maximal effort exercise. For example, even highly trained athletes with
high VO2max values may not have enhanced pulmonary diffusion or lung volumes compared to
the average sedentary adult.
The lack of training effects on lung structure is shocking given how well the
cardiovascular and muscular system adapt to exercise. In addition to lacking clear signs of
adaptation, several components of the respiratory system can be negatively impacted by intense
exercise. For example, elite endurance athletes have an elevated risk of airway narrowing during,
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or immediately following, high intensity exercise. Additionally, high intensity training can lead
to maladaptive remodeling and hypersensitivity in the airways of elite endurance athletes. The
reason this occurs is that the high ventilatory demands of maximal effort exercise require flow
rates in excess of ten times resting levels, which can injure the airways. The aforementioned
phenomenon is most prevalent in female elite endurance athletes, though it also occurs at a
higher than average frequency in male elite endurance athletes as well. High resolution computed
tomography has shown that airway cross-sectional areas are comparable between the sexes
throughout the maturation process, but post-pubescent females show a 20–30% reduction in the
diameter of the trachea and main stem bronchi. A smaller lung size in adult females accounts for
much of these differences in airway size, but even when a limited number of comparisons were
made at equivalent lung volumes adult females had narrowed trachea and bronchi compared to
males of an equal body mass. Resting diffusion capacity and lung volumes are also lower in
women versus men, even when adjusted for age, height, and hemoglobin concentration.
According to Jerome Demsey, we can interpret the aforementioned data to mean that adult
women over a broad range of fitness levels gave hormonally determined trachea, bronchi, and
lung sizes that are underbuilt for the flow rates demanded by maximal intensity exercise.
Additionally, because the consequences of airway dysanapsis are likely to exist in the majority of
adult women we should expect to see a higher susceptibility to respiratory limitations during
high intensity exercise compared to men at any given fitness level.
In addition to respiratory limitations, which limit the rate of oxygen uptake,
cardiovascular limitations can also limit oxygen supply to the working muscles. From here out
I'll refer to cardiovascular limitations as delivery limitations, since they limit an individual's
ability to deliver oxygenated blood to the working muscles. Exercisers with delivery limitations
often have high maximal rates of oxygen extraction and are limited by the maximal pumping
capacity of their heart during exercise, which limits their peripheral blood flow. As a result,
oxygen utilization in the working muscle supersedes oxygen supply, resulting in very low muscle
oxygenation levels when volitional failure occurs.
Strong, heavily-muscled, athletes with great local and regional muscular endurance often
present with delivery limitations and as a result they struggle with tests of systemic work
capacity that utilize a large percentage of total skeletal muscle mass. For example, among
competitive Crossfit athletes you’ll often find individuals who can perform very large unbroken
sets of ring muscle-ups, handstand pushups, and chest to bar pullups in isolation and when
non-fatigued. However, when they pair the aforementioned movements with other full body
exercises in a metcon they’ll often struggle to complete even the smallest sets unbroken without
getting ‘pumped up’. This occurs because delivery limited athletes have lowered maximal
cardiac outputs, and as a result they are limited in the total amount of skeletal muscle they can
vasodilate at any given moment. This is problematic when they are forced to alternate exercising
muscle groups and it results in severe extremity muscle deoxygenation.
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Oxygen utilization limitations differ from both respiratory and delivery limitations in that
exerciser’s with this form of limitation are able to supply a sufficient amount of oxygen to the
working muscles. It's difficult to create a representative avatar of a utilization limited athlete
because the underlying causes of utilization limitations are so broad. For example, utilization
limitation can be caused by insufficient mitochondrial or capillary density, excessive muscle
damage, impaired muscle coordination and requirement, or changes in blood chemistry.
Additionally, exercisers with utilization limitations may be limited by their maximal rate of
oxygen utilization, the magnitude of oxygen utilization in the working muscles, or both. Given
the range of ways that utilization limitations can present themselves, there are few broadly
applicable global adaptation trends. However, some commonalities among utilization limited
athletes are poor rate of force development, a low maximal power output relative to their critical
power, poor skeletal muscle recruitment, and impaired metabolic activity in peripheral tissues.
Applications for Interval Training
Interval training is most often performed with repeated series of work bouts done at a
fixed speed. For example, an exerciser performing rowing intervals may repeat back to back sets
of a 1k row while maintaining a 2:00/500m average split across each of them. However,
manipulating intra-interval pacing can significantly impact how an athlete adapts to the exercise
bout, even if these alterations do not impact the total time it takes to complete each interval. For
example, if we wanted to prescribe 500m row repeats at race pace to an individual who can row
2,000m in seven minutes we could have them perform fixed pace intervals at 1:45/500m, we
could use a gradual ramping structure where they start at a 1:55/500m pace and increase in speed
by 0:05/500m every 100m increment, or we could have them perform a hard start interval where
they start at a 1:40/500m pace and gradually decrease their speed to 1:50/500m. Each of the three
aforementioned approaches will result in the rower finishing the intervals in the exact same time.
Yet, the respective adaptations to these three interval approaches will vary.
The athlete who performs the hard start interval will stress the pulmonary system the
most. Hard start intervals induce higher mean oxygen consumption levels than traditional
intervals despite similar average speeds, indicating that hard start intervals are a good strategy
for accumulating volume at a high percentage of an individual's VO2peak while controlling for
total training volume. On the flip side, the athlete performing intervals with a gradual ramping
pace structure will slowly build in pace in order to overcome cardiac lag and balance oxygen
supply and utilization in the working muscle. This approach will create a larger stress on the
cardiovascular system, with less stress to the pulmonary system, and as a result it’s more suitable
for a delivery limited athlete.
None of the three aforementioned approaches are superior to the others. However, there
are circumstances where one choice is better suited to achieving a specific outcome than the
other two. For example, if I were training a respiratory limited athlete I'd preferentially use a
49
hard start interval if their goal was to increase their VO2max. Knowing how to manipulate
intra-interval pacing structure is a useful skill when you want to alter a training stimulus without
meaningfully adjusting total training volume. Additionally, these types of adjustments can be
exceptionally useful when you’re coaching a team of athletes and everyones working needs to
conform to a specific time table, but you still want to add a dimension of individualization to
their training.
Chapter 7: Understanding Sport Specific Limiters
Having a high VO2max is necessary, but not sufficient for elite level endurance
performance. In other words, an individual is unlikely to be an elite endurance athlete if they do
50
not have a high VO2max, but having a high VO2max alone is not enough to compete at the
highest levels of sport. This same concept broadly applies for other work capacity works, like
Crossfit for example. The broader the demands of a given sport, the more factors that are
necessary, but not sufficient, for high level performance. For example, being able to complete
thirty ring muscle-ups in under four minutes is necessary, but not sufficient to be an elite Crossfit
competitor. As is being able to snatch one hundred twenty-five kilograms and row two thousand
meters in under six minutes and twenty seconds, among many other metrics. This concept
reminds me of a quote by Marilyn Strathern where she states, "When a measure becomes a
target, it ceases to be a good measure.” If sufficient rewards are attached to some measure,
people will find ways to increase their scores on that measure one way or another, and in doing
so will undercut the value of the measure in assessing what it was originally intended to assess.
In order to be a competitive Crossfit athlete we know there are some minimum strength
metrics that need to be achieved, certain paces an individual need to be able to sustain for a given
duration on the rower, and some ballpark estimates they should be able to hit on workout such as
thirty muscle-ups for time, one hundred strict handstand push ups for time, and so forth.
However, being able to achieve all of these milestones does not necessitate that an individual
will be a great Crossfit athlete. It’s a matter of necessity versus sufficiency. Being able to
compe;te these metrics is the equivalent of being accepted to study at a university. Just because a
student has been admitted through the doors does not mean they are automatically eligible to
graduate.
I’m always hesitant to put athletes through generic sport specific testing batteries. At
best, I can check a few boxes and see where they stack up relative to the field, which is helpful
for determining what they need to prioritize in their training. However, improving on specific
skills in isolation won’t necessarily translate to improved sports performance. Furthermore, it can
create the illusion that improving on the test metrics is the goal in and of itself. As a result, I take
a different approach and approach sport specific assessments from a bottom-up standpoint.
Conceptually I think about Crossfit, or any other work-capacity based event, as a cyclical
endurance sport. Like any cyclical endurance sport, the goal for a Crossfit athlete is to move
continuously, in effect turning a metcon into a cyclic activity. When an athlete is incapable of
performing a metcon in a cyclic manner I'll investigate why that is the case and after identifying
their rate-limiting factor I will train them to overcome that limitation. For example, instead of
having an athlete perform a classic test such as thirty ring muscle ups to see how they stack up
against their competition, I'll assess whether or not they can perform ring muscle ups in a cyclic
fashion during a sport specific event. If not, my aim is to understand why. A beginner athlete
may lack the requisite strength to perform consecutive muscle ups. An intermediate athlete may
struggle with their breathing mechanics and coordination under fatigue. Finally, an advanced
51
athlete may be limited by their ability to supply oxygenated blood to the working muscle at a fast
enough rate.
Science Backed Wisdom
Prior to the 2016 Crossfit games an organization I was working for hosted an athlete
camp with a handful of top competitors. One of the competition simulations at the camp included
a high volume of kettlebell snatches, box jump overs, and rope climbs. During the event a
colleague of mine made a comment that one of the athletes was able to complete the metcon as if
it was a cyclical event. It wasn’t intended to be a profound statement. Rather, he was
acknowledging the fact that the athlete did not stop moving for more than a split seconds
whereas a lot of the other competitors were breaking up their kettlebell snatches, using more time
for their transitions, and generally looked like they were approaching the metcon as a circuit with
defined work and rest periods.
The aforementioned observation
really struck a chord with me because it
matched my observations from
conducting physiological tests on
Crossfit competitors. In my
observations, the best Crossfit athletes
can turn the majority of metcons into
cyclical workouts whereas the rest of
the pack cannot. For example, the top
athletes have steady blood flow to the
working muscles, a linear rate of
oxygen utilization from start to finish, and their VO2 kinetics look similar to what you’d expect
during a two thousand meter row versus a circuit style workout. This is demonstrated in figure
eleven, which depicts two crossfit games athlete’s muscle oxygenation trends during a metcon
that includes thrusters, burpees, and rowing.
At the time of the aforementioned workout the athlete whose data is on bottom was a top
ten individual games competitor, and the athlete whose data is on top was a sanctional level
competitor who later qualified for the games as an individual. Note that the athlete on bottom has
a near linear oxygen desaturation trend across the workout without any major dips or peaks.
They were able to move through the workout unbroken with minimal rests and transitions, thus
allowing for a very high rate of energy turnover. The athlete on top, on the other hand, had less
steady blood flow to the working muscles and as a result they were forced to stop, rest, and
complete the workout in small chunks of intervals interspersed with rests and long transitions.
Interestingly, the total amount of work time for the athlete on top is actually slightly less than the
athlete on bottom, indicating a faster rep speed, but it was so broken up so much that they ended
52
up taking over two minutes longer to finish the workout. This raises the question, Why can some
athletes turn metcons into cyclical work but others cannot? The rest of this chapter will be used
to answer this question, as well as to provide some practical takeaways for how we can get an
athlete to make metcons more cyclical in nature based on their individual sport specific limiters.
Understanding Local Muscle Fatigue
Among hybrid athletes like Crossfit competitors, and mixed martial artists, local muscle
endurance is a commonly cited exercise limiter. However, the cause of local muscle fatigue is
poorly understood, and as a result training interventions intended to improve local muscle
endurance have mixed results.
One of the leading causes of local muscle fatigue is a restriction of muscle blood flow
due to high intramuscular mechanical pressure. Under ordinary circumstances there are two
different mechanisms by which muscle blood flow increases. During muscle contraction muscle
blood flow is diminished, and during muscle relaxation blood flow increases. This process is
known as active hyperemia, and it regulates blood flow on a contraction by contraction basis.
Across many muscle contractions there is another process called auto-regulation that increases
blood flow in response to muscle deoxygenation. Both of these processes occur simultaneously
and their combined effects determine the net change in blood flow moment to moment. However,
there are cases where both of these responses are blunted, thus decreasing muscle blood flow and
oxygen availability. For example, when
individuals employ high threshold
movement strategies, contract their muscles
with excessive force, or have elongated
muscle relaxation times they will impede
muscle blood flow, which will quickly lead
to local muscle fatigue limitations and an
inability to sustain work-output.
The aforementioned phenomenon
was observed in a study titled, Assessment of
lower-back muscle fatigue using electromyography, mechanomyography, and near-infrared
spectroscopy 12, where the investigators observed mechanical pressure decreasing muscle blood
flow during muscle contraction due to a compression of the blood vessels. In figure twelve you’ll
find a muscle blood volume measurement recorded from a biosensor placed on an athlete’s spinal
erectors. At the start of muscle contraction, delineated with the leftmost arrow, the capillaries in
the muscle are compressed, thus driving muscle blood volume down. Then upon the cessation of
contract, marked by the right arrow, muscle blood volume returns back to baseline. When the
12
Yoshitake Y, Ue H, Miyazaki M, Moritani T (2001). Assessment of lower-back muscle fatigue using electromyography,
mechanomyography, and near-infrared spectroscopy. Eur J Appl Physiol. 84: 174-179.
53
capillaries in a muscle are compressed the muscle will deoxygenate as oxygen utilization
supersedes oxygen delivery. This will manifest as local muscle fatigue, which is exacerbated
during high density bouts of exercise where the muscle cannot fully reoxygenate between
repeated contractions. Now you know the underlying cause of local muscle fatigue. However,
that still leaves the question of how an individual can improve their local muscle endurance and
performance.
In order to determine which protocol will be most effective for improving local muscle
endurance, we need to identify the rate limiting factor for increasing muscle blood flow. For
example, one athlete may have poor intramuscular coordination, resulting in a blunted active
hyperemic response. Another athlete may have poor breathing mechanics and mobility, which
puts excess tension on the working muscles and impairs muscle blood flow. Finally, a third
athlete may lack strength in a specific movement and as a result they are contracting their
muscles with such a high percentage of their maximum voluntary contraction force that they are
creating an arterial occlusion. All three of these individuals will need to use different training
methods to improve their local muscle endurance. In figure thirteen you’ll find an algorithm for
determining the lowest hanging fruit for improving an athlete's muscular endurance.
If I were to apply the algorithm in figure thirteen, I'd first start by determining if an
athlete's local muscle endurance on a specific movement is limited by strength. For example, let's
say an athlete is struggling with their lower back fatiguing during a Crossfit metcon with high
rep thrusters at ninety-five pounds. If this load is greater than thirty to forty percent of the
aforementioned athletes one rep-max front squat they may benefit from improving their absolute
strength. However, if this athlete is already quite strong, it is very unlikely that additional
increases in absolute strength will improve their muscular endurance. If we identify that strength
54
isn’t the limiter, I would then ask the athlete if they are able to perform ninety-five pound
thrusters for high reps in isolation without their lower back fatiguing, or if they are always
limited by lower back fatigue. In the former case the athlete may be limited by diaphragm
muscle fatigue, which is exacerbated under fatigue when their respiration rate is elevated. In the
later case I would ask the athlete if they are able to perform a thruster without any mobility
restrictions. If they are unable to perform the movement without restriction they should aim to
address that limitation before looking elsewhere. If they are not limited by their mobility I’d
assess their breathing mechanics while doing thrusters to see if they are able to inhale with
sufficient depth and exhale fully between breaths. Finally, if breathing is not an issue, I’d assess
their coordination at high contraction speeds and under fatigue.
After identifying an athlete’s individual limitation I would track improvements with the
NNOXX biosensor to ensure they are adapting to the new training stimulus. For example, lets
say the athlete is limited by strength and their one rep max front squat load is two hundred
thirty-five pounds. On week one I would have them perform a set of twenty unbroken thrusters
and while observing their muscle oxygenation levels. As this athlete improves their front squat
strength I’d repeat the aforementioned assessment. If they are able to perform the same number
of thrusters, in the same amount of time, with a higher finishing muscle oxygenation level they
have lowered the metabolic cost of that movement. At some point additional gains in strength
will not be accompanied by improved thruster performance, and at that point we’d look to
identify a new rate limiting factor. We could also track this athlete's max unbroken set of
thrusters during this process as well to ensure that it is increasing simultaneously as we train the
identified limiter.
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Chapter 8: Training Interventions For Delivery Limited Athletes
When working with delivery limited athletes I break their training down into a few
different sub-categories including foundations, general adaptations, tier one energy system
training interventions, and tier two energy system training interventions. Starting with
foundations, these are what I tend to consider to be prerequisites that need to be met before
someone can start performing high volume or intensity training. Though reductionist, the three
types of foundations I consider are movement capabilities, coordination, and breathing. If an
athlete cannot comfortably perform all of the relevant movements for their sport, they lack
coordination in said movement patterns, or they have trouble breathing with movement
appropriate mechanics they need not spend time hammering out intensive energy system
training. There is no sense in climbing all the way up a tree to pick the hardest to reach fruit
when you can easily reach overhead and pick a few apples without exhausting much time or
energy.
During the writing of this book I began coaching a late stage intermediate Crossfit
competitor who believed they were limited by their maximal cardiac output and their reasoning
that their lower back and quadriceps always ‘blows up’ during metcons. They surmised that
when performing high intensity workout the pumping capacity of their heart was not sufficient to
allow for steady blood flow to the working muscles, resulting in an occlusion. However, after
putting this athlete through testing and identifying their absolute power outputs, and their
maximal rate of oxygen utilization, I felt fairly confident that this athlete was most limited by
their ability to utilize oxygen in the extremity muscles. Yet, we can’t neglect the fact that this
athlete was experiencing their lower back and quadriceps getting ‘pumped out’. So, instead of
jumping to early conclusions I did a big picture assessment and one of the things I noticed early
on was that this individual had an utter lack of ankle and hip mobility. As a result they would
dump their torso forward anytime they were doing wall ball throws, thrusters, overhead squats,
snatches, or cleans. In these cases they were using their lower back musculature to stabilize
themselves, resulting in a restriction of blood flow to those issues, rapid muscle deoxygenation,
and an early onset of fatigue. In this case the athlete presented with a localized delivery
limitation, but it was less related to their maximal cardiac output and more so due to their
inefficient movement patterns.
After a few weeks of working on this athlete's mobility and movement capabilities, the
‘pumped out’ phenomenon disappeared. Had we neglected the foundations and moved straight to
flashy energy system protocols we would have missed out on this straightforward, and low cost,
opportunity to improve their performance. As a result, we always need to start with the
fundamentals and only when these are taken care of do we move to more advanced methods of
addressing delivery limitations.
In addition to making sure an athlete has sufficiently mastered the basic movement
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capabilities needed for their sport, we also need to ensure that their coordination and breathing
are not limiting their ability to deliver oxygenated blood to the working muscles. The former is a
particularly large concern when athletes are frequently limited from performing a greater work
density due to getting ‘pumped out’ or ‘blown up’ during workout. This is a common occurrence
in string, well-muscled, athletes who have a long history of strength and power training, but lack
a wide base of conditioning. As muscles contract with increasing force the demand for oxygen in
those muscles increases. However, that increase in the force of muscle contraction necessitates
an increase in intramuscular pressure as well, which can impede blood flow. Even as little as
twenty to thirty percent of an individual's maximum voluntary contraction can cause a restriction
in venous outflow in some individuals. What separates the good athletes from the great athletes
is how quickly they can relax between muscular contractions and restore blood flow to the
working muscle. Novice athletes can contract a muscle in ~0.3 seconds and relax in about ~0.45
seconds. Elite athletes on the other hand can contract in ~0.25 seconds and relax in ~0.20
seconds. Think about that for a second - elite athletes can contract a working muscle in ~80% of
the time as novice athletes, but they can relax in less than 50% of the time. So, is the separator
between the two a slightly faster rate of force production, or the ability to relax between
contractions much faster? If athletes who can relax quicker can clear waste products from the
muscle at a faster rate, and they will have steadier blood flow and tissue oxygenation. This would
constitute an improvement in intramuscular coordination, which is the coordination of motor unit
recruitment and synchronization within a muscle. However, we cannot neglect intermuscular
coordination, which is the coordination of multiple muscles during an activity.
When athletes have phenomenal movement capabilities, intramuscular coordination, and
intermuscular coordination they make movement look effortless. But, in order to maintain this
fluid chain of movement, they need to master the third fundamental which is breathing. Not only
is coordinated breathing a requirement for sustaining efficient movement, but being able to
breath with sufficient volume and with a high enough frequency is needed to maintain cardiac
output. Cyclical changes in intrathoracic pressure upon inspiration have significant effects on the
cardiovascular system, partly by influencing central venous pressure, venous return and cardiac
filling. This is called the 'thoracic muscle pump' or simply the 'respiratory pump'. When we take
a deep breath there is an immediate decrease in intrathoracic pressure, which decreases central
venous pressure. When central venous pressure decreases there is an increase in driving pressure,
which promotes greater venous return. This increase in venous return then increases
end-diastolic volume, stroke volume, and subsequently cardiac output. Because the
cardiovascular system is a closed-circuit the same volume of blood that leaves the heart needs to
enter the heart after going through our systemic circulation. Any increases in venous return will
ultimately increase cardiac output. What this means is that proper breathing mechanics, depth,
and frequency can be leveraged to improve venous return and cardiac output and poor breathing
mechanics can have a substantial negative impact on cardiac output and subsequently
performance.
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Improving your breathing, as a skill, is essentially low hanging fruit for any athlete in a
work-capacity sport. If you cannot breath in the bottom of a squat, hanging from a pullup bar, or
with a barbell over your then you're leaving a lot of progress on the table. Once you master these
basic skills in addition to the other fundamentals discussed in this chapter you can move on to
tier one energy system training interventions for improving delivery. These include
methodologies intended to elicit the following adaptations: improved blood flow and peripheral
circulation, cardiovascular adaptations including increased end-diastolic volume and stroke
volume, morphological changes to the heart including increased left ventricular hypertrophy, and
improved cardiac-pulmonary coordination.
Tier One Energy System Training Interventions
The tier one energy system training interventions for delivery limited athletes can
collectively be bucketed together and referred to as ‘basic endurance training’ or ‘basic delivery
training’. In this subchapter I am going to lay out general guidelines for basic delivery training
categories, which include D0, D1, D2, and D3 training respectively. Classically, these training
categories fall under the classification of structural endurance training, though I classify them as
oxygenating training due to the fact that one’s rate of oxygen delivery supersedes their rate of
oxygen utilization when performing this type of work. However, there are subtle differences as to
the physiological adaptations and magnitude of stress imposed by the basic delivery categories
D0 to D3.
The first delivery training category, D1, is a staple of many endurance training programs. The
purpose of D1 training is to develop basic cardiovascular adaptations to support future training
loads. When you begin exercise from rest your cardiovascular, pulmonary, and muscular system
all respond to the imposed stressor, but they cannot ramp up to full capacity instantaneously. It
can take a few minutes for cardiac output to rise to a meaningful degree, for blood vessels to
begin dilating, and for skeletal muscle oxidative enzymes to begin catalyzing reactions. The time
it takes for these processes to occur are referred to as your oxygen uptake kinetic rate, which is
sped up and improved by this form of training. Additionally, performing this type of training will
accelerate recovery from training by decreasing vagal tone, heart rate, and sympathetic
vasoconstriction at rest, which will allow for steady blood flow to the skeletal muscle as well as a
faster removal of waste products. As far as training guides go, D1 training is best done within
the following constraints:
1. Long duration continuous work bouts lasting twenty minutes on the low end up to three
to five hours on the high end. For powerful, heavily muscled, athletes I often advise using
short intervals at a low intensity with short rests interspersed in between rather than one
long continuous interval. For example, instead of doing a thirty minute row at 2:30/500m,
I may have them perform a forty second row at that speed, rest for twenty seconds, and
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repeat for forty total work sets.
2. Performed at low, sustainable, intensities. This type of training should be both easy and
very tolerable. For individuals recording biometric data we may want to see heart rate
values in the ballpark of 50-65% of an individual's maximum heart rate, and no blood
lactate accumulation above baseline concentrations. Additionally, muscle oxygen
saturation should be steadily increasing across the interval, or it should be stabilized at a
local maximum.
Multiple D1 training sessions can be performed in a twenty four period, or on back to
back days, without negative consequences to the athlete.
3. So far as exercise selection goes, D1 training is best done using cyclical modalities
including cycling, rowing, running, swimming, or skiing to name a few. This assumes an
individual has the requisite skill, movement capabilities, coordination, and breathing
mechanics to perform said movement without restricting blood flow to the working
muscles.
Example D1 Training Sessions:
60 Minute WattBike at
15-17.5% of maximum power
output. Modulate power and
RPM in order to reach a
maximum SmO2 steady state.
3 Rounds at 50-55% of
HRmax:
5:00 Row (20-24 SPM/ 5
damper)
5:00 Echo Bike
5:00 Run on Treadmill (2%
incline)
60 Minute EMOM:
1st - :30 Walking Lunge
2nd - :30 Skierg
3rd - :30 Erg Bike
4th - :30 Jacob's Ladder
5th - :30 Ground based flow
6th - :30 Erg Bike
*Module work rate so SmO2
never dips below 50% during
work, and recovers >70%
during all rest periods. Heart
rate should not exceed 60%
HRmax at any point.
Finally, some important considerations when prescribing D1 training for athletes are as follows:
1. Performing D1 training is ‘stimulative’ in nature, whereas D2 and D3 training can be
thought of ‘developmental’ due to the greater magnitude of stress imposed by the latter
training categories. As a result, D1 training is best used to maintain adaptations as well as
active recovery.
2. Athletes almost always overestimate their paces while performing D1 training. As a
result, monitoring biometric data such as heart rate, muscle oxygen saturation, or blood
lactate can be valuable for keeping intensity within check. However, when such measures
are not available a simple talk test can be applied. If an individual is incapable of holding
a fluid conversation during D1 training then they are working too hard.
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3. D1 training can be used to replace D2 or D3 training during deload weeks or during
training weeks where an athlete is performing a higher volume of sport specific training
and may not be able to tolerate the stress imposed by higher intensity delivery training
sessions.
Whereas D1 training is intended to improve the cardiovascular systems function at low
intensities, D2 training is used to improve the function and efficiency of the cardiovascular
system at moderate intensities. The target adaptations for D2 training are to develop
cardiovascular efficiency without the influence of local muscular limitations, as well as to create
morphological and structural adaptations to the cardiopulmonary system and mitochondria.
While D1 training is generalizable in the sense that it can play a role in any athletes training the
inclusion criteria for performing D2 training is more specific since it generates more fatigue per
unit of volume than D1 training. As far as training guides go, D2 training is best done within the
following constraints:
1. Long duration continuous work bouts lasting between twenty minutes on the low
end and one hundred eighty minutes on the high end. D2 training can also be
performed in an interval format using ten to thirty minute intervals for a total of
two to six sets and resting between thirty second and ninety seconds between sets.
2. Performed at moderate, sustainable, intensities. This style of training should
require focus on the part of the athlete while still being tolerable. For individuals
recording biometric data we should expect to see heart rate values between
~65-75% of an individual's maximum heart rate, very little blood lactate
accumulation above baseline concentrations, and muscle oxygen saturation levels
stabilized between roughly forty to seventy percent. For those without biometric
data, D2 training should be done at ~70-75% effort and if asked an athlete should
be able to speak a full sentence.
3. Multiple D2 training sessions can be done within twenty hour hours on one
another, or on back to back days, with little to no negative consequences for the
athlete.
4. Ideally, D2 training is done using cyclical modalities such as rowing, cycling, or
running. However, other regional and global movements such as kettlebell
swings, burpees, and thrusters, for example, can be implemented as well. In these
instances the total repetition counts, cycle time, and loading of these movements
all need to be tightly monitored so as to not cause any restrictions of blood flow to
the skeletal muscle or excess local muscle deoxygenation.
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Example D2 Training Sessions:
20 Minute WattBike at
40-55% SmO2 holding as
high of a wattage as possible
while staying in this range x4
Sets, Rest 1:30 between sets.
30 Minute Row at 65-75%
maximum heart rate (5
damper). Hold as high of an
output as possible while
staying in this HR range. If
power output needs to drop
by more than 10% to stay
within this range then stop,
rest for up to ninety seconds,
and then resume your
workout.
5 Rounds at 70-75% effort:
500m Row (5 damper)
6-12 UB Thruster (95lb)
6-12 Bar Facing Burpee
1 Mile Echo Bike
*You should be able to speak
in full sentences on the Row/
Echo Bike. If you experience
any local muscle burning
between six and twelve reps
on the thruster or BFB cut the
set and go on to the next
movement.
Additional considerations when prescribing D2 training for athletes are as follows:
1. An important factor when programming D2 training is that the goal is to elicit
cardiopulmonary adaptations with as little recovery cost as possible. In other words, we
want a high stimulus to fatigue ratio.
2. Some athletes will be able to use running as a trainable modality here, while others may
see their heart rate jump out of the desired range, or their muscle oxygen saturation
plummet to undesirable levels, too quickly. In these cases the athlete should either select
a different cyclical modality, or start with shorter running intervals and build up their
intraset duration over time. The same concept applies when adding regional and global
movements like thrusters, burpees, and pullups to D2 training intervals.
3. As with D1 training, heart rate, muscle oxygen saturation, and blood lactate monitoring
can all be invaluable tools for ensuring athletes properly regulate their intensity. It can be
mentally challenging for athletes unaccustomed to these types of sessions to work at such
low relative power outputs. Having objective data to help regulate an athlete's output can
help an athlete pull back on the reins until they are fit enough to work at faster paces
without outstripping their oxygen supply or until they get a feel for this type of training.
4. For advanced athletes with a history of performing long duration steady state training, D2
training can replace the bulk of D1 training that is regularly prescribed to them.
The final delivery training category, D3, has the highest relative intensity associated with it than
all of the other delivery training categories. Whereas the goals of D1 and D2 training are to
improve the efficiency of the cardiovascular system and low to moderate intensities, D3 training
improves the efficiency of the cardiovascular system at moderate to moderately high intensities.
D3 training can also be used to improve an individual's ability to tolerate greater volumes of high
intensity training, and as a result it’s often used as a bridge between basic endurance work and
higher intensity threshold and VO2max style training. My guidelines for performing D3 training
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are as follows:
1. Medium to long duration continuous work bouts lasting between fifteen minutes to sixty
minutes. D3 training can also be performed in an interval format using sixty second to ten
minute long intervals resting between half as long as the interval duration upto the same
length as the interval duration.
2. Performed at moderate to moderate high, sustainable, intensities. This style of training
ranges from moderate to hard, but it should remain tolerable throughout. For individuals
recording biometric data we should expect to see heart rate values between ~75-85% of
an individual's maximum heart rate, little blood lactate accumulation above baseline
concentrations, and muscle oxygen saturation levels stabilized between roughly thirty to
fifty percent. For those without biometric data, D3 training should be done at ~75-85%
effort and if asked an athlete should be able to speak five words without gasping for
breath afterwards.
3. D3 training sessions can be done within twenty hour hours on one another with little
negative consequence, though they should not be performed with this frequency on a
regular basis. This style of training is not as physically demanding as threshold or
VO2max style training, but it still poses a meaningful recovery demand on the athlete.
4. Unlike the other delivery training categories, D3 training can be performed equally well
using both cyclical and mixed modalities. However, this assumes an individual can
maintain a high cycle rate and turnover while employing mixed movements. Most global
movements can elicit an appropriate training response during D3 sessions and some
regional movements can be utilized as well as long as they are paired with cyclical
movements to ensure that local muscular endurance limitations do not occur.
Example D3 Training Sessions:
6 Minute WattBike at 35-45%
SmO2 holding as high of a
wattage as possible while
staying in this range x5 Sets,
Rest 3:00 between sets.
60 Minute Run at 75-80%
maximum heart rate. Hold as
high of an output as possible
while staying in this HR
range. If average speed needs
to drop by more than 10
second/ mile to stay within
this range then stop, rest for
up to three minutes, and then
resume your workout.
5 Sets at ~80% effort:
15 Wall Balls (20lb)
12 Toes to Bar
30 Double Unders
750m Row
Rest 4:30 Between Sets
Additional considerations when prescribing D2 training for athletes are as follows:
1. The most important consideration when writing D3 training is that the goal is to improve
an athlete’s tolerance to higher intensity training and to seamlessly bridge the gap
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between lower intensity delivery training and threshold or VO2max training.
2. Often athletes push too hard on D3 training and have a challenging time straddling the
line between the upper end of sustainable power outputs and unsustainable power
outputs. As a result biometric data can be useful for objectively determining the
‘goldilocks’ range of power outputs that are not too low, or too high, but just right.
3. For those familiar with the MAP model of energy system training, that entire model fits
within the D3 training category. I mention this to help reconcile your current knowledge
base with what I am presenting here.
​
Before moving on to tier two delivery training interventions there is one last basic
delivery training category to cover. D0 training is unlike all of the other delivery training
categories in that it is not intended to produce a target adaptation. The purpose of D0 training is
to stimulate the lymphatic system, reach a maximal oxygen saturation in the working muscle,
and drive the body into a parasympathetic state, all with the goal of accelerating recovery and
bolstering the body's restorative capabilities. In essence, D0 is similar in many facets to D1, but
it differs in one major way which is that D0 is performed at a local maximal muscle oxygen
saturation level. This means that the intensity used needs to be kept within a very tight range,
which is achieved with a Moxy muscle oxygenation monitor. In order to elicit maximal
oxygenation in the muscle tissue blood volume needs to be elevated, which requires a degree of
intensity, but if taken too far muscle oxygen saturation will start to decrease. As a result, D0
training requires one to ride a fine line.
Tier Two Energy System Training Interventions
Imagine you are coaching a strength athlete, and they come to you with the goal of
driving their one rep max back squat up. There are plenty of effective strategies we can employ
in this athletes program to get the job done, but ultimately if we were to distill this program
down to its most basic components we’d likely have this athlete doing some combination of
assistance exercise and heavy squat training. I can’t think of any coaches who would make the
mistake of filling this athletes program with single leg exercises, leg extensions, and hamstring
curls, but neglecting heavy squat training entirely. Yet, coaches often make that mistake when
aiming to improve a delivery limited athlete's performance. Long slow distance training and high
volumes of ‘zone two’ training without higher intensity training inputs are akin to training leg
extensions and leg curls, but neglecting to squat heavy. In essence, the tier two energy system
training interventions for delivery limited athletes are the ‘heavy squats’ that accompany the tier
one delivery training interventions, which are the ‘assistance work’ in this analogy.
Generally, my tier two energy system training interventions are either composed of
combo workouts or blended workouts. Combo workouts are when two or more workout
intensities are performed within a single session. Blended workouts, on the other hand, are when
two or more training intensities hit within a single interval or work bout. Most programs abruptly
move from one intensity to another over the course of a training phase, and the use of blended
workouts helps to integrate training in a more seamless fashion. Blended workouts can also be
used to target specific physiological adaptations, or systems, as a means of addressing certain
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limitations.
Let’s say we had a delivery limited athlete who’s best 2,000m row performance is seven
minutes flat, which averages out to 1:45/500m. If we had this athlete use a traditional interval
structure where they perform 500m repeats at their 2,000m row pace, their rate of oxygen
utilization would quickly outstrip their oxygen supply and they would perform the majority of
the intervals in a hypoxic state. This is fine when the goal is to peak or prepare for a competition,
but it is hardly an effective means for improving their energetic limiter. Instead we would want to
use a gradual desaturation interval structure where we gradually build in pace at a rate where
oxygen supply matches oxygen utilization. For example, we could have them do a 500m row
repeat where they build in speed every 100m starting at a 1:55/500m split and cutting the pace
down every 100m to 1:50/500, 1:45/500m, 1:40/500m, and 1:35/500m. If you calculate the
average speed of this interval, it still comes out to 1:45/500m, but the adaptation is quite different
from the traditional interval structure. Additionally, if you were recording NIRS data, you would
find that the correlation between muscle oxygen saturation and total hemoglobin is inverse-linear
in the latter workout example (-0.9 to -1), whereas it will be much weaker in the former example
(-0.2 to -0.7). This indicates that the THb signal in the former example is primarily influenced by
hypoxic vasodilation during gradual desaturation training, where it is dominated by occlusion
and sympathetic vasoconstriction during traditional intervals meaning that oxygen supply and
utilization are not being effectively coupled in the latter scenario. In essence, this is one of the
reasons why tempo runs are such a valuable tool for middle distance and long distance runners.
Example Cyclical Sessions:
1k Row building from 2k PR
pace -10 seconds ---> 2k PR
pace across the interval. Rest
to recovery x6 work sets.
Gradually build in speed so
you’re pulling 2k PR pace -5
seconds at the 500m mark,
then over the last 500m drop
the pace down to 2k PR pace.
20 Minute WattBike building
from 50% effort to 85% over
the course of the interval. At
the ~10 minute mark you
should be roughly at your
FTP pace, then the last 3-5
minutes should be hard, but
tolerable. If you’re holding
composure and not
experiencing any pooling of
blood in the last 1-2 minutes
you can finish with a strong
surge.
6 Minute Echo Bike
Rest 4:00 x4 Sets
*Start each interval at 225
watts and gradually increase
in speed across the interval
such that you’re finishing
with your SmO2 between
25-35%. There is some
gamification that will happen
here. You can trace out 6:00
on the screen and try to
impact what a linear
desaturation trend will look
like, and then modulate your
pace in live time to achieve
that.
While it is recommended that blended energy system training protocols aimed at
improving delivery are done cyclically, advanced mixed sport athletes can benefit immensely
from doing them in a mixed modal format. However, this requires a high degree of
cardiopulmonary development to ensure that the muscular contractions from regional and global
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movements do not create outflow restrictions, which will decrease venous return and impair
cardiac output. It should also be noted that these protocols are best done by alternating between
upper and lower body movements to challenge blood pressure regulation and the ability to
redistribute cardiac output between involved and non-involved muscle groups.
Example Mixed Sessions:
3:00 Minute Assault Bike
building from 50-85% of
HRmax. No rest, straight
into….
15 cal Skierg
20 Unbroken Wall Ball (20lb)
15 Unbroken CTB Pullup
400m Run
Rest 4-6 Minutes
x4 Sets
*Alter the order of
movements each set, while
adhering to the upper-lower
alternation pattern.
10:00 AMRAP With
Spectrum Pacing:
10 Thruster (95#)
10 Bar Facing Burpee
10 Toes to Bar
20 cal Echo Bike
(Rest 10:00)
X2 Sets
*First ~2:00-2:30 at ~75%
effort gradually building in
effort across the workout such
that you’re hitting an ~85%
effort at around the 6:00-7:00
mark, and finishing the last
1:00-2:00 at ~90-95% effort
intensity.
2:00 AMRAP:
5 OHS (95#)
5 Lateral Bar Burpee
5 Toes to Bar
6 BJ Step Down (24”)
12 cal Row
(Rest 1:00)
x8-10 Sets
*Pick up each set where the
previous left off. This should
not be a hard effort - the goal
here is to focus on movement
quality, rhythmic breathing,
and deliberate transitions.
Move from one station to the
next at a steady pace. This
should feel like a ~275-300
watt echo bike (for an
advanced athlete) where
you’re just cruising along
steadily.
Reference Charts
When prescribing energy system training the two questions I always ask myself are:
1. What result am I trying to achieve with this session?
2. What style of training will best facilitate me achieving said result?
Figure fourteen is intended to take the guessing out of this question for you. On the top of
the chart we have a multitude of different physiologic adaptations to adaptations to energy
system training and on the left hand side we have our four basic delivery training categories
listed out. Next to each energy system training category you will see boxes with ‘X’s’
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corresponding to a range of different adaptations. The number of ‘X’s’ represents the magnitude
of adaptation for a given dose of training. The more ‘X’s’, the greater the magnitude of
adaptation is conferred by that form of training.
Chapter 9: Training Interventions For Respiratory Limited Athletes
As with training delivery limited athletes, we can also sub-categorize respiratory limited
66
athletes training into a handful of classifications including foundations, tier one energy system
training interventions, and tier two energy system training interventions.
When I think about the foundations for improving a respiratory limited athlete's
performance, the first things that come to mind are structural foundations. The reason when
anatomy and physiology are traditionally paired together in higher education curricula is that
anatomical structures dictate physiological functions. The four primary structural points I’m
concerned with for respiratory limited athletes are the position of the pelvis, the position of the
thoracic spine, the orientation of the ribcage, and the width of the infrasternal angle of the
ribcage. Addressing the structural foundations need not be overly complicated and there are
plenty of resources for navigating this area. However, we do need to consider the fact that there
is a ‘chicken or egg’ relationship between said structural limitations and respiratory muscle
strength. For example, some athletes who are stuck in thoracic extension may be in that position
because they have an expiratory muscle strength limitation. In these cases they present with a
hyperinflation pattern, which is a state of excess inhalation with inadequate exhalation. This
hyperinflated pattern can be asymmetric or symmetric. In the former scenario it’s common for
the left side of the rib-cage to be more flared out than the right side, whereas in the latter scenario
both sides of the rib cage are flared out. This is a case where function, specifically strength,
impacts structure. On the other hand, we can have a scenario where structure impacts functions,
which is the case when a kyphotic athlete presents with an inspiratory muscle weakness.
After addressing the aforementioned foundational structures, I start to think about how
these structures move as well as the capacity of these structures. Collectively, this compromises
the functional foundations for respiratory limited athletes. These functional foundations include
the strength of inspiratory and expiratory muscles including the diaphragm, external obliques,
and abdominal muscles. These functional foundations alone include the fatigue resistance of the
respiratory muscles, breathing coordination, as well as the ability to breath with an optimal
depth and frequency in sport specific movement patterns and scenarios.
Once these structural and functional prerequisites are met a respiratory limited athlete can
begin redistributing their training volume to spend more time on tier one and tier two energy
system training interventions. These include methodologies intended to elicit the following
adaptations: improved capacity and efficiency of the cardiopulmonary system, improved
respiratory muscle strength and endurance, increased VO2max, and increased output at one’s
maximum metabolic steady state.
Tier One Energy System Training Interventions
The tier one energy system training interventions for respiratory limited athletes can
collectively be bucketed together and referred to as balanced delivery and utilization training. In
this subchapter I am going to lay out general guidelines for balanced delivery and utilization
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training categories, which include B1 and B2 training respectively. Classically B1 and B2
training would be referred to as threshold and VO2max style training and would fall under the
umbrella of functional endurance training or maximal aerobic endurance training because these
categories comprise the highest intensities that can elicited before oxygen utilization begins to
outstrip oxygen supply.
Any time we discuss compartmentalized energy system training categories we are really
drawing proverbial lines in the sand. In truth, these different categories lie on different areas of
the spectrum between very low intensities when we are delivering oxygen at a much faster rate
than it is utilized up to very high intensities where oxygen utilization greatly supersedes oxygen
supply. Practically, B1 and B2 training fall somewhere in the middle of this spectrum where
oxygen delivery and utilization are closely matched to one another. The difference between said
categories is that B2 training is done at the highest output that can be achieved before oxygen
utilization begins to outstrio oxygen supply whereas B1 training is done at a slightly lower
intensity than that.
Traditionally B1 training is referred to as threshold training. The purpose of B1 training is
to decrease the amount of lactate that accumulates above baseline concentrations while working
at moderate to high intensities, increase the rate of lactate transport and consumption, as well as
to create an individual's power output that can be sustained before they begin to utilize oxygen at
a faster rate than it can be supplied to the skeletal muscle. Typically athletes whose sports require
them to operate above or near their critical power for an extended period of time, whether that is
in one continuous effort or multiple repeated efforts, can benefit from B1 training. This includes
field sport athletes, middle to long distance endurance athletes, and mixed sport athletes like
Crossfit competitors. My guidelines for performing B1 training are as follows:
1. B1 training is best completed in an interval format using roughly forty second to ten
minute long intervals and resting between one fourth as long as the interval duration upto
the same length as the interval duration. However, B1 training can also be performed in a
continuous format with work bouts lasting between ten to forty five minutes.
2. Performed at high, but tolerable, intensities. This style of training is hard, but should be
sustainable for extended durations. For individuals recording biometric data we should
expect to see heart rate values between ~85-90% of an individual's maximum heart rate,
small to moderate blood lactate accumulation above baseline concentrations, and muscle
oxygen saturation levels stabilized between roughly thirty to forty percent. For those
without biometric data, B1 training should be done at ~85-90% effort and if asked an
athlete should be able to speak three to four words without gasping for breath afterwards.
3. B1 training is much more demanding than any of the basic delivery training categories,
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and as a result roughly forty eight hours are needed for optimal recovery between B1
training sessions.
4. As with D3 training, B1 training can be performed equally well using both cyclical and
mixed modalities. However, this assumes an individual can maintain a high cycle rate and
turnover while employing mixed movements and that they can tolerate high contraction
volumes of these movements without accruing meaningful muscle damage. The majority
of global movements can elicit an appropriate training response during B1 sessions, but
the loads will need to be scaled appropriately to ensure that local tissues are not
overloaded. Regional movements, like kipping pull ups or push presses, can also be used
during B1 training sessions as long as they are combined with a cyclic modality to ensure
local muscular endurance limitations do not occur.
Example B1 Training Sessions:
1k Row at 30-40% SmO2
holding as high a wattage as
possible while staying within
this range and maintaining a
Delta ΔSmO2 of 0% per
second. Rest = ½ Work x6
Sets.
40 Minute Wattbike at
85-87% of maximum heart
rate. Hold as high of an
output as possible while
staying in this HR range. If
sustained power needs to drop
by more than 8-10% to stay
within this range then stop,
rest for up to three minutes,
and then resume your
workout.
6:00 AMRAP at 85-90%
effort:
20 cal Echo Bike
12 KBS (24kg)
14 Wall Ball Throws (20lb)
10 Burpee
(Rest 4:00)
X3 Sets, picking up each
where the previous one left
off.
Additional considerations when prescribing B1 training for athletes are as follows:
1. The goal is B1 training to increase the power output or pace that an athlete can sustain
before their oxygen demand supersedes their oxygen supply. Many athletes will have a
tendency to push this type of training too hard to the extent that they ‘spillover’ into an
unsustainable intensity domain. As a result, monitoring biometric data can be extremely
useful for helping athletes regulate their work rates.
2. As athletes become more advanced, and accustomed to this form of work, you can
decrease the rest times below ½ their work time to further challenge their ability to match
their rate of lactate transport and consumption with lactate production. Elite swimmers
are able to perform thirty to sixty minute B1 training sessions with no more than twenty
second rest periods interspersed throughout the workout.
3. The amount of fatigue generated per unit of stimulus for B1 training is quite high, and as
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a result this style of training needs to be used sparingly. Additionally, this form of
training has a tendency to lower active muscle tension, so it must be implemented in a
strategic manner when working with mixed sport athletes who are not only trying to train
their energetic limiters, but are also required to perform resistance training throughout the
training week.
The second, and final, tier one training category for respiratory limited athletes is B2
training, which is often referred to as maximal aerobic endurance training or VO2max style
training. This type of training can be utilized for a wide range of athletes including track and
field competitors, field sport athletes, mixed martial artists, and crossfit competitors. In fact, this
training quality will be one of the primary ceilings for performance in 1,600m to 5,000m running
specialists as well as open level Crossfit athletes. My guidelines for performing B2 training are
as follows:
1. B2 training is best done in an interval format with set durations lasting between thirty
seconds to ten minutes. The rest intervals between intervals should be complete, and
approximately matched to the previous sets work time.
2. B2 Training should be done at a very high, to near maximal, intensity for the interval
duration. This style of training is very challenging, and uncomfortable to sustain for the
interval duration. For individuals recording biometric data we should expect to see heart
rate values between ~90-95% of an individual's maximum heart rate, moderate blood
lactate accumulation above baseline concentrations later into the workout, and muscle
oxygen saturation levels stabilized between roughly twenty to forty percent. For those
without biometric data, B1 training should be done at ~90-95% effort and if asked an
athlete should be able to speak two to three words without gasping for breath afterwards.
3. While B2 training is not performed at a maximal effort, it is quite taxing on athletes both
physically and mentally. As a result, it is advised that athletes do not complete this form
of training more than once every seventy two hours. However, there are times of the year
when this may not be avoidable as is the case during a pre competition phase for a
Crossfit athlete or during championship racing season for a middle distance training and
field competitor.
4. B
​ 2 Training is most effective when performed in a cyclical modality, however advanced
athletes may be able to combine cyclical and mixed elements effectively and still get the
appropriate training response. Most global movements can elicit an appropriate training
response as long as an athlete can maintain a very movement cycle rate with a high
relative power output. If the load gets too heavy or if an athlete is forced to rest due to a
local muscular endurance limitation then the relative intensity will drop too low to be
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effective.
Example B2 Training Sessions:
60 second WattBike at
125-130% of FTP pace, Rest
60 seconds x15 work sets. *If
SmO2 drops below 15% on
any of these work sets, or
cannot recover above your
resting baseline, then reduce
your loading by 10%.
1,000m Row at 90% effort,
Rest = Work x4-6 Sets. Note
your finishing heart rate and
SpO2 on all work intervals. If
HRmax exceeds 95% and/or
SpO2 drops below 94%, end
the workout.
5:00 AMRAP at 92.5-95%
effort:
8 Thruster (95lb)
10 Lateral Bar Burpee
18 cal Skierg
(Rest 5:00)
x3 Sets
Additional considerations when prescribing B2 training for athletes are as follows:
1. This style of training is extremely potent. Most athletes will see benefits from 1-2
exposure per week at most, and this style of training should not be performed year round.
2. Rest intervals should be held close to 1:1 or 2:1 work to rest. It’s important to rest enough
such that power output can be sustained from set to set without meaningful deterioration.
Tier Two Energy System Training Interventions
One of the most important considerations I take into account when training respiratory
limited athletes is that the amount of work accumulated at a high percentage of their peak oxygen
consumption is a primary determinant of performance. However, the amount of training volume
that an athlete’s muscles, bones, and joints can tolerate week after week is finite, which puts a
limit on how much work they can conceivably do at a high percentage of their peak oxygen
consumption. This is especially true in mixed sport athletes who can only dedicate so much time
to performing energy system training given all of the other sport specific qualities that need to be
trained year round. As a result, it’s crucial that we find ways to elicit these adaptations with as
little volume as is necessary to do so.
One way to add training precision is by manipulating intrainterval pacing structures to
stress some systems more than others. For example, let’s say we had a respiratory limited athlete,
and we wanted to train at a high percentage of their VO2peak. We could either have them do a
traditional interval training session where they complete a series of fixed pace intervals or we
can use a ‘hard start’ interval method. The latter entails starting at a very fast pace and
descending in speed across the interval. Numerous studies have shown that hard start intervals
induce higher mean oxygen consumption levels than traditional interval structures despite similar
average speeds, indicating that hard start intervals are a good strategy for interval sessions
aiming to accumulate more time at a high percentage of VO2peak with less wear and tear.
Practically, this could entrail replacing fixed pace 500m rowing intervals where the average pace
71
equals 1:40/500m for a 500m rowing interval where an athlete perform the first 125m at
1:34/500m, the next 125m segment at 1:38/500m, and the next two 125m segments at 1:42/500m
and 1:46/500m respectively. In addition to hard start interval methods, we can also utilize
blended energy system training protocols designed to stress the respiratory system in a more
targeted fashion, as demonstrated with the workout examples below.
​
Example Cyclical Sessions:
NNOXX Guided:
Row @1:32/500m (+/- 1
second) until SmO2 stops
declining and starts to level
out at the same %. Rest until
SmO2 stops going up and
reaches a recovery baseline.
Repeat x2-5 total times.
500m Row @decreasing
speed every 125m
(1:32-1:36-1:40-1:44/500m).
Rest 2:00 x6 Sets
Auto-Regulated:
Row - as long as
"comfortable" @~5-10
seconds faster than 2k pace.
Rest for 2:00 in a quadruped
position focusing on
breathing mechanics and
coordination. Rest to recovery
x2-4 sets. I want you hitting
your respiratory threshold on
each of these repeats, sitting
there until you start to feel
either local fatigue or
HR/breathing are reaching the
limit of control and then
resting until you're ready to
repeat the same effort agai
6:00 WattBike at FTP pace
(+/- 15 watts), Rest 4:00-6:00
x4-6 Sets. Start with what
feels like normal relaxed
breathing for this effort. If
you feel like you're not
getting enough air in, then
aim to increase your
respiratory rate (RR) while
maintaining your depth of
inhale and exhale.Over time
we can push the intensity and
get you comfortable breathing
at high RR's while
maintaining depth.
In addition to the aforementioned tier two energy system training interventions,
respiratory limited athletes can also benefit from using respiratory muscle trainers such as the
Spirotiger or Idiag-P100.
Strength
Endurance
Coordination
72
Set the ST or P100 to a
respiration rate of 0 breaths/
min so you can concentrate
on the depth of breathing
instead of speed or frequency.
Complete 3-5 sets of 5
minutes w/ a 5 min rest b/w
sets using 75-80% of FVC6.
Inhale and exhale maximally
at a comfortable frequency
focusing on expelling all air
on the exhale. The only
metrics on the device of
concern are balancing gas
exchange and depth of
inhales/ exhales, not speed.
Once an athlete can
comfortably complete this
they will do the same
workout with a RF of 10-20
breaths/ minute; and they can
progress this workout by
adding breaths per min while
maintaining depth of breath,
reps, sets, and rest periods. It
is recommended that this is
performed 1-2x/week, but not
before a heavy strength
training session.
A simple progression would
be to start with 10-15 minutes
of non stop breathing w/ a 20
breath per minute respiratory
frequency at 50% of FVC6.
I'd have the athlete do this
2-3x/ week, and every 4-6
sessions I'd increase the time
by 5 minutes. Once an athlete
can comfortably do 30
minutes at that respiratory
frequency, I drop them back
down to 10-15 minutes and
up the breath frequency by 5
per minute and then progress
forward by increasing time.
After continuously
progressing this workout until
the athlete can complete 40
breaths/ minute for an entire
30 minutes I would then
increase the bag size by .5-1L
and begin the process from
step one. If an athlete is not
trained enough for the initial
step 1 of this progression,
then I would start them with
1-5 minute intervals at 20
breaths/ min with 50% of
their vital capacity and build
up from there.
Use a spiro bag measuring
roughly 30% of FVC6.
On week 1 start with 20
breaths for 5 minutes to
establish a baseline, then
make a pyramid w/1 minute
steps going up by 5 breaths/
min until you cannot
complete a set. So, for
example....
5 Min @20 RF
1 Min @25 RF
1 Min @30 RF
1 Min @35 RF
1 Min @40 RF (Failure)
Then work down the pyramid
as you came
1 Min @35 RF
1 Min @30 RF
1 Min @25 RF
5 Min @20 RF
Once you can reach 40
breaths/ minute comfortably
and work back down without
an issue then you can start
with 5 minutes @25 RF, and
work in one minute steps upto
45RF and back down the
pyramid and so forth.
Reference Charts
Chapter 10: Training Interventions For Utilization Limited Athletes
73
Before discussing training interventions for utilization limited athletes it’s important to
acknowledge that the underlying causes of utilization limitations are quite broad, and as a result
we cannot have once catch all set of foundational components that need to be addressed for these
individuals. For example, a lack of mitochondrial density, a disruption to the normal muscle fiber
structure following injury, changes in intramuscular and intermuscular coordination, chronic
overtraining, and a left shift in the hemoglobin dissociation curve from hypocapnic breathing can
all impair skeletal muscle oxygen extraction. In order to reconcile this, I suggest we zoom in on
mitochondrial density as that will have a meaningful impact on both the magnitude of oxygen
extraction, as well as the rate. Additionally, that falls within the sphere of influence of coaches,
whereas some of the other contributing factors for utilization limitations are less easily assessed
and influenced without bringing other trained professionals into the fold.
What I find interesting about training utilization limited athletes is how tightly changes in
their physiology are linked to improvements in performance. Assuming a utilization limited
athlete is not overtrained or injured, the primary adaptations they’ll want to target in their
training are increased mitochondrial density, increased enzyme concentrations, improved
coordination and recruitment, and increased metabolic oxygen utilization. With a quick internet
search, you can look up any of these key terms and find a host of protocols that claim to improve
mitochondrial biogenesis. However, I’m always skeptical when I see cookie cutter protocols and
programs that claim to elicit a highly specific adaptation without any instruction for how to adapt
the program to the individual or any inbuilt autoregulatory components.
There are plenty of protocols that should elicit a given adaptation in theory. They may
even consistently improve performance. However, we don’t always have a reliable way of
knowing how and why they lead to performance improvements. As a coach, or athlete, you may
not even care why something works, as long as it does work, but there’s a good argument to be
made for why you should care. At some point you're bound to encounter an athlete who doesn't
respond to cookie-cutter training protocols. If you don’t understand what that individual's
underlying limitations are and how to target that specific limiter effectively you may be at a loss
for how to modify their training. In that scenario you can throw your hands in the air and tell
them they’re a non-responder, or you can select another protocol at random and throw darts at
the board with a blindfold on. Alternatively, you can use the process of inductive reasoning to
come up with an educated guess as to what they need, then follow that hypothesis to its natural
conclusion and put it to the test.
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A low cost way to better understand the effect of your training methods and how they
relate to increases in performance is through basic statistical methods. In figure sixteen we have
a tactical athlete’s rate of change of muscle oxygen saturation recorded with a NNOXX
biosensor, termed ΔSmO2, plotted against maximum power output on the Echo Bike over a
36-week training period. ΔSmO2 clues us into the balance between oxygen supply and demand
— the more negative ΔSmO2 becomes, the greater skeletal muscle oxygen extraction is relative
to skeletal muscle oxygen supply.
When I began coaching the athlete whose data we can observe above, we identified that
their maximal rate of oxygen extraction and utilization was a primary limiting factor for
increasing their VO2max. Additionally, through speed preservation testing we determined that
they needed to improve their maximum sprint speed (MSS) while maintaining their ability to
preserve a fixed % of MSS over a set distance. My hypothesis is that these energetic limitations
and sport specific limitations had a common cause. In testing we found that this individual's
maximum rate of oxygen extraction was 4.5% SmO2 per second and that their maximum sprint
speed on the echo bike was 1,315 watts. Over thirty six weeks of training we had them repeat the
exact same training protocol and we tracked the highest power output elicited in that session as
well as the most negative ΔSmO2 value. In figure sixteen you can see these data points plotted
against one another.
Over the thirty six week training period we saw a 31% increase in maximum oxygen
extraction and a 20% increase in maximum power output. But, the real kicker is that when we
calculated the correlation between their ΔSmO2 and maximum power output trends we saw an
inverse linear relationship between changes in oxygen extraction and changes in power output. In
other words, for every increase in oxygen extraction and utilization we saw a proportional
increase in maximum power output. Furthermore, when we calculated the correlation between
their training progress on a weekly basis and their increase in power output the correlation
coefficient was +0.84. Collectively, these data points give us a strong understanding of how the
protocol we used works, how it changes the individual’s underlying physiology, and how it
relates to increases in performance.
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In order to confirm that these findings
extrapolate to a larger population, I then
recruited 21 subjects to perform a six week
exercise trial where they performed the same
repeat desaturation training session weekly
and we tracked percent changes in maximum
power output and ΔSmO2. You can find the
data from that experiment in figure seventeen,
which shows a strong correlation between
changes in maximal oxygen extraction and
increase in power output such that the
individuals with the greater percent change in ΔSmO2 also had the greatest increase in maximal
power output.
In another instance I had an athlete who wanted to improve their performance on a
30-second Echo Bike for max calories. After assessing this athlete we determined that they need
to improve their maximal power output to get better at this test since they were holding a very
high percentage of their maximal sprint speed already. Additionally, we found this athlete was
limited by their rate of oxygen
utilization. Over a ten week period we
had this athlete complete one
developmental U2 training session as
well as a 30-second Echo Bike test. In
figure eighteen you'll find their five
most negative ΔSmO2 values captured
during their U2 training sessions
plotted against their performance on
the 30-second Echo Bike test. Over the
ten week training period they consistently hit more negative ΔSmO2 values, and they also
improve their score on the Echo Bike test nearly every week. When calculating the correlation
coefficient between ΔSmO2 and performance, I got a value of -0.97. This tells me that the
training intervention not only yielded the correct physiological outcome, which is an increase in
the rate of maximal oxygen extraction, but also that this physiologic change drove the desired
performance outcome. Now imagine that you apply these concepts to the bulk of your training
protocols and you have a streamlined system for identifying an individual's limiters — rather
than guessing what protocols to use when, you can create a surgical system for spotting and
training limitations.
Tier One Training Interventions
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In this subchapter I'm going to discuss the tier one energy system training interventions for
utilization limited athletes, which include U1 and U2 training respectively. Traditionally these
two training categories would be referred to as ‘anaerobic lactic endurance’ training and ‘alactic
power’ training, though it should be understood that these terms are misnomers given that
oxygen and lactate are both part of the energy transduction process at all times. U1 and U2
training can both be used to increase one’s magnitude and rate of oxygen utilization in the
skeletal muscle which we can juxtapose to the basic delivery training categories, D1 to D3, that
improve one’s rate of oxygen delivery. Consequently, U1 and U2 training are referred to as
deoxygenating training.
U1 training has traditionally been referred to as lactic endurance training in Crossfit,
anaerobic power endurance training in strength and conditioning circles, or purple training in
swimming. If you have ever done this type of training the purple designation will make intuitive
sense as that is the color you’d expect your face to be after completing a U1 training session. The
target adaptations for U1 training are improved tolerance to high levels of acidosis, increased
intramuscular and systemic buffering capacity, and an extension of the amount of time one can
operate with lowered muscle oxygen saturation levels. Examples of athletes who may benefit
from this type of training are elite Crossfit competitors preparing for a sanctional event, one
hundred to two hundred meter swimmers who need to be able to preserve a high percentage of
their max sprint speed for an extended duration, or elite eight hundred meter runners. My general
guidelines for performing U2 training are as follows:
1. U1 training is best completed in an interval format using forty second to one hundred
eight second long intervals and resting between three and twelve minutes between work
intervals. However, U1 training can also be performed in a continuous format with a
single work bout lasting between three and fifteen minutes. It should be noted that
athletes with poor delivery may not tolerate this style of work and will need longer than
average rest periods between sets whereas athletes who lack absolute power will get a
subpar stimulus from this style of training.
2. U1 training should be performed at a maximal or near maximal exertion level. This style
of training is exceptionally difficult and athletes will often develop a fear or distaste for
this style of training. For individuals recording biometric data we should expect to see
heart rate values between ~95-100% of an individual's maximum heart rate, moderate to
high blood lactate level, and muscle oxygen saturation levels that are rapidly declining or
stabilized between roughly 5 to twenty percent. For those without biometric data, U1
training should be done at ~95-100% effort and if asked an athlete should only be able to
speak in one to three word sentences before it disrupts their sense of composure.
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3. U1 training poses the greatest recovery demand compared to all of the other tier one
energy system training categories. As a result, it’s recommended that this style of training
is not performed more than once per week, and that it is not performed for more than
three to six consecutive weeks.
4. Cyclical modalities are most effective when performing U1 training sessions. However,
most global movements can elicit an appropriate training response assuming a near
maximal cycle speed can be maintained and power output stays relatively high. Regional
and local movements for U1 training due to the fact that they do not elicit a great enough
whole body energy demand.
Example U1 Sessions:
Row; open up with a hard
start at 85-90% of MSS, then
once SmO2 reaches a nadir
hold steady until you cannot
maintain that power output
without biomechanical or
cardiorespiratory
compensation. Rest until
SmO2 is at and/or above your
recovery baseline for 4-6
minutes, then repeat for a
total of three work sets.
200m Run at 95% effort
Rest 3:00
x4 Sets
(Rest 10:00)
x2 Series
For Time:
20 Unbroken Thruster
(95-115 lb)
-No more than :05 in transit15 Chest to Bar Pullups
AFAP
-No more than :05 in transit20 cal Echo Bike
(Rest 10:00-12:00)
x3 work sets
The most important things to keep in mind when prescribing U1 training sessions are as follows:
1. This style of training is exceptionally stressful to athletes, both mentally and physically.
As a result, it should be used sparingly in an athletes training program, if used at all. For
most athletes I would advise against performing more than one U1 training session per
week, and I would limit a progressive structure to 3-4 weeks in most cases.
2. Rest intervals should provide ample recovery so that an individual can maintain similar
power outputs across repeats. If training quality begins to deteriorate it’s recommended
that the rest duration is extended, or that the session is terminated early.
The final tier one energy system training category is U2, which is traditionally referred to
as ‘alactic power’ training. It should be noted that this term is a misnomer, because lactate is
certainly generated while performing this style of training. However, it tends to be consumed at a
relatively fast rate as well, which is why measured blood lactate concentrations will appear low
when performing this style of work. The target adaptations for U2 training are an increased rate
of oxygen utilization, increased recruitment of fast twitch muscle fibers, increased mitochondrial
density, and increased maximal power output. Examples of athletes who can benefit from this
style of training are Crossfit competitors who are enduring, but lack absolute power, two hundred
meter runners who need to improve their top end speed, or field speed athletes who have to cover
78
short distances in the fastest possible amount of time. As far as training guides go, U2 training is
best done within the following constraints:
1. Very short work bouts lasting between five to twenty seconds with long, complete, rest
periods between sets.
2. U2 training should be performed at a maximal intensity. While this style of training is
hard, the short time durations and extended rest periods make it quite tolerable for most
individuals. For those monitoring biometric data, muscle oxygen saturation levels should
reach personal minimum thresholds when performing this style of work. Heart rate is not
an applicable metric during this style of training, and while high levels of lactate are
produced during this style of work the complete rest periods allow for clearance rates to
exceed production. Thus, making blood lactate measurements an ineffective monitoring
technique for this style of training.
3. Most individuals need forty eight hours or more to recover from U2 training, though
some advanced athletes may require a longer period of time between training sessions.
4. U2 training is best done with specific cyclical modalities including running, sled pushing,
and cycling.
Example U2 Sessions:
10 second Echo Bike at 100% Every 4:00 for 16:00-20:00:
effort, Rest 2:00 x6-8 Sets
15 second Sled Pushup with a
light to moderate load at
100% effort (maintaining a
maximal turnover rate)
20m building to a maximal
sprint speed followed by
20-40m of sprinting at
maximal velocity. Rest 3-5
minutes between sets x4-8
total work sets on the day
based on your ability to
maintain maximal power
output.
The most important considerations when performing U2 training are two fold:
1. Most athletes will feel the urge to cut their rest intervals down during this style of
training. However, they should resist the urge to do so since this form of training requires
maximal intensity on every work set, without degradation from set to set.
2. Volume does not need to be high to get the desired training effect from U2 training.
Advanced athletes can often make improvements with no more than three to four sets per
week.
Tier Two Training Interventions
Imagine we take an elite cyclist and have her do a step test on a stationary bike with a
muscle oxygen saturation monitor affixed to her vastus lateralis or rectus femoris. We would see
79
that she has a well developed cardiovascular system, and subsequently a great ability to deliver
oxygen to her working muscles. Given her extensive training history on the bike it’s also likely
that she excels at utilizing oxygen in the working muscles while performing her sport. Now
imagine we take this same athlete and we have her perform a step test on a Skierg with a muscle
oxygen saturation monitor on her triceps and lat. It’s likely that she will still present with good
oxygen delivery to the working muscles, but i’d suspect that her oxygen utilization would be
impaired. The reason for this is that she lacks mitochondrial density in the extremity muscles of
the upper body. One way to improve this would be to have her perform repeat desaturation
training on a ski-erg. This method of training needs to be performed at a near maximal intensity
with an interval duration that is long enough for muscle oxygen saturation to reach a nadir. So far
as repetitions, we want this individual to keep going until she can no longer deoxygenate the
muscle down to the same nadir as previous sets or she cannot recover muscle oxygen saturation
back to the same baseline level. In the session examples below you’ll find a NIRS guided,
auto-regulated, and mixed repeat desaturation training session.
Example Repeat Desaturation Training:
As many rounds of.....
20 Second Row at 85-90%
max wattage
Rest 1 Minute b/w sets
*The session terminates when
SmO2 cannot be depleted to
the extent of previous sets,
you cannot reach a SmO2
recovery baseline during rest,
you can no longer hit the rx'd
wattage, you compensate
biomechanically, or effort
needed to sustain intensity
begins to exponentially
increase from set to set.
*This can also be completed
with a Skierg at 90-95% of
max watts or a 10 second
Echo Bike at 70-75% max
watts.
(Running time on 45:00
Clock)
As many rounds of.....
10 second Echo Bike at 75%
max watts
Rest 1 min b/w bouts
*terminate workout when you
begin to compensate
biomechanically (shifting or
changing movement pattern
to accommodate for fatigue),
breathing cannot get back
down to baseline while
rest/hyperventilation is
induced, you can no longer
elicit the Rx'd power output,
or quality of work
significantly drops off. For
remaining time in the 60 min
AB, wattbike, row, or walk at
a low intensity / cooldown
effort
As many rounds of.....
20 Second Skierg @90% max
watts
Rest 1 Minute
10 Thrusters AFAP (115lb)
Rest 1 Minute b/w sets
*The test terminates when
SmO2 cannot be depleted to
the extent of previous sets,
you can no longer hit the rx'd
wattage,or you begin to
compensate biomechanically
(shifting or changing
movement pattern to
accommodate for fatigue).
*This can also be completed
with a 20 second Skierg at
90-95% of max watts or a 20
second Row 85-90% of max
watts.
80
Before wrapping up this chapter on training utilization limited athletes I wanted to expose
a common misconception, which is that we only need to train an individual's limiter to increase
their performance. For example, only training to improve a utilization limited athlete’s rate of
oxygen utilization and ignoring all else. This is a mistake in my opinion. Just because you’re
limited by utilization in the vast majority of sport specific contexts does not mean that you
cannot be limited by your cardiopulmonary system, and oxygen supply, in other scenarios. You
do not fail in an event when your ‘limiter’ cannot cope with the imposed demand. You fail when
you’ve exhausted all forms of compensation. Improving your limiter gets you further before you
begin to rely on those compensation patterns, but you still need to improve those other systems,
for lack of a better term, as they will be pushed to their capacity eventually. While it’s important
to train known limitations and grab the ‘lowest hanging fruit’ that doesn’t mean that there is not
a time and place to climb a higher higher and grab some fruit from the top of the tree.
Reference Charts
81
Chapter 11: Movement Classification For Energy System Training
In chapters seven through nine I provided an overview of the training interventions and
tools I use for delivery, respiratory, and utilization limited athletes respectively. In this chapter
I'm going to hone in on exercise selection for energy system training. By the end of this chapter I
want you to understand when it is appropriate to use global, regional, and local exercise during
energy system training, how exercise selection and repetition count influence what adaptation is
conferred through energy system training, as well as how neural and metabolic strain influence
movement selection.
Global Movements
Global movements are a broad category of movements that use roughly sixty percent of
an athlete's total muscle mass or greater. Often coaches will refer to global movements as
compound, multi-joint, or functional movements. An example of a global movement used in
energy system training would be a thruster since the musculature in the hip flexors and hip
extensors, knee flexors, deltoids, and trunk are all going to be challenged as an athlete performs
this movement, taking a barbell through a large range of motion.
When performing global movements under high fatigue athletes are more likely to be
limited by central fatigue versus peripheral fatigue due to the fact that no single muscle group is
going to be overloaded. Additionally, since global movements use a large percentage of an
individual’s total muscle mass they will challenge an exerciser’s systemic cardiovascular control
mechanisms to a significant degree. However, some individuals may still present with local, or
peripheral, muscular limitations while performing these movements, so specific exercise
selection within this broad category will need to be assessed on a case by case basis. Other
examples of global movements are as follows:
1. Non-impact cyclical modalities like rowing, swimming, and skiing;
2. high-impact cyclical modalities like running; and
3. externally loaded movements like deadlifts and cleans.
Regional Movements
Regional movements are those that recruit regions of muscle mass, which equate to
roughly forty to sixty percent of an athlete’s total skeletal muscle mass. While performing
regional movements athletes may be either centrally or peripherally limited. Additionally, a
given regional movement may elicit a central, or systemic, limitation in one individual and a
local peripheral limitation in another. Prototypical examples of regional movements include
kipping pullups, or push presses. For both of these movements the loading and cycle rate can be
major determinants of whether an individual is limited by their cardiorespiratory system, or local
tissue limitations. Faster cycle rates will lend themselves to driving cardiorespiratory limitations
while slower cycle rates are more likely to elicit local muscular limitations. This is true both in a
movement like a push press, but also in cyclical modalities like cycling where rotations per
minute can be modulated independent of power output. Other examples of regional movement
include:
1. Non-impact cyclical modalities like road cycling, echo biking, or ski-erging;
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2. Externally loaded movements like push press, or belt squats; and
3. Basic conditioning and calisthenic movements like unloaded walking lunges, kettlebell
swings, box jumps, and kipping handstand pushups.
Local Movements
Local movements use forty percent of an athlete's total skeletal muscle mass or less.
When performing local movements athletes are primarily limited by peripheral, local muscle,
fatigue. Generally these types of movements will have little impact on an athlete's respiration, or
cardiovascular control. In the vast majority of circumstances local movements are not
appropriate for movement choices when performing energy system training unless an athlete's
sport requires them to train in this manner. Examples of local movements are as follows:
1. Nonimpact cyclical modalities like an arm ergometer;
2. Externally loaded movements like a strict press, bicep curl, or leg extension; and
3. Strict calisthenics movements like strict pull ups, strict handstand pushups, and pushups.
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Chapter 12: Combining Strength And Energy System Training
Concurrent Training is defined as the combination of resistance and endurance training
in a periodized program to maximize all aspects of physical performance. In simple terms this
can mean training multiple different types of training qualities within the same phase, or even the
same workout. Given this broad definition concurrent training can take on a lot of different
forms. For example, a soccer player who is spending time each day on the field, in the weight
room, and doing road work in order to improve their sport specific skills, gain muscle, and
improve their speed and endurance. Other examples could include a hybrid athlete who competes
in regional powerlifting competitions and local 5k running races as well as a Crossfit competitor
who needs to improve a vast array of physical qualities simultaneously for their sport.
The pros of concurrent training are that you can improve on more things at once without
as much compartmentalization. The cons are that while training different qualities
simultaneously they can compete with one another for adaptation currency. All types of training
produce specific responses in the body and fitness is a result of cellular changes that cause the
body to adapt in one way or another. These changes occur because of the activation or blocking
of specific genes and signaling pathways. One of the big arguments against concurrent training is
that the varied stimuli confuse the body as to how it should respond. This allegedly leads to
sub-par adaptations and is termed the interference effect.
Over the past ten years I've coached concurrent sport athletes across a number of
disciplines, including Crossfit athletes ranging from recreational competitors to individual and
team games competitors. Seeing what these individual athletes are able to accomplish, I once felt
that the proverbial nail had been put in the interference effects coffin. After all, if I can watch an
athlete snatch close to one hundred thirty kilograms and run a mile in less than five minutes then
it must not exist. However, that line of thinking was flawed. The best Crossfit athletes would be
mediocre high school runners and rowers at best, and their lifting numbers would hardly let them
pull rank at a regional powerlifting meet. Of course, being able to perform in both disciplines
simultaneously is a skill in and of itself, but my point is that we've yet to see anyone who is an
elite endurance runner and lifter.
So, perhaps the jury isn’t out on concurrent training. It’s clear that you can train all
qualities simultaneously and make excellent progress, but maybe the old saying about being a
jack of all trades and master of none isn’t so far off. After all, no one is going to win the Boston
marathon and USAPL nationals in the same training phase. While it does appear that there is a
degree of interference with concurrent training, perhaps it’s grossly overstated in the average
athlete who doesn't work at the limits of human performance. I think there is also a case to be
made that the mechanisms explaining it are incomplete, and that many of these effects can be
mitigated with good program designs. In this chapter I'll present some relevant heuristics for
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combining strength and endurance training which will help you sift through the nonsense and
apply your knowledge practically.
Best Practices For Concurrent Training
In order to understand how to write training programs for real world athletes I believe it
is important to understand what constitutes optimal training and what it looks like in practice.
Some basic guidelines that we try to follow when designing energy system training for athletes
are as follows:
1. Organize training from high to low skill - while this principle constitutes a ‘best practice’
there are exceptions to this rule when performing sport specific work. For example, a
biathlete may want to do hard interval work at or above race pace prior to skill work to
practice shooting under fatigue as that would occur in their sport. Similarly, a Crossfit
athlete may want to train the snatch at high percentages of their one rep max under
fatigue in order to prepare for a competition.
2. Order training from least fatiguing to most fatiguing - collectively, these first two points
ensure that athletes are able to perform higher skill movements and high power training
without the influence of fatigue from previous training pieces.
3. Do not mix high intensity, fatiguing, training inputs that drive the same physiological
adaptation - in truth, there is no reason you can't do this, but it's not an efficient way to
train. You can only adapt to so much of a given stimulus in a certain period of time, so
past a given volume threshold it's more efficient to space 'like' training inputs out to
maximize adaptation and manage fatigue.
4. Know when to break the rules - Of course, there are times when we'll want to break all of
these rules. If you're working with a CrossFit competitor you will need to train high skill
movements under fatigue, perform fatiguing training before non-fatiguing work, and hit
multiple high intensity workouts (with overlapping movement patterns) in a very short
period of time. As a result, we need to know when it is or isn't appropriate to break these
rules, why the rules need to be broken at times, who to break the rules with (and
conversely, who we should not break these rules with), and how to break the rules with
the least consequences for the athlete.
Now that we've laid out some of the ground work, we can start to discuss how to optimal
order training within a single session or day.
Ordering Training
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The order of training components can play a major role in what type of adaptation occurs.
For example, if you have an athlete perform U1 training where the goal is to drive blood lactate
levels up, and maintain tissue hypoxia for an extended period of time, and then ask them to
complete a B1 training set where the goal is to minimize lactate accumulation, and keep tissue
saturation levels stable, these conflicting training adaptations may yield a different result than
what was intended. From a conceptual standpoint we want to order our training in a way that
minimizes the impact of one training modality on the next. This means we want to organize the
sessions in the manner depicted in figure twenty.
This type of framework can be applied in a single training session, across a training day,
or across multiple days. For example, you may start a training session with some high neural
demand resistance training (featured below), followed by a high metabolic demand rowing
interval, and a low intensity cool down.
Sample Training Session:
Part I: High Neutral
Demand:
A. Hang Clean (1" above or
below knee); 1.1 every 2:00
for 8:00-12:00 (~8.5 RPE)
B. Clean Pull; 1.1 x3 sets, rest
2:00 b/w sets (100-105% load
from "A")
C. Back Squat; Max UB Reps
@88% 1RM, Rest to full
recovery x2-4 sets (# of sets
is determined by drop in reps
- more than 10% drop from 1
set to the next = shut it down)
D. Chest Supported BB Row;
6-8 x3, rest 2:00 (Pull hard,
then 1 sec pause in contracted
position, then control it down.
Part II: High Metabolic
Demand:
Part III: Low Intensity
Rower @375 watts until
10:00 AB @150-175 watts,
failure (you cannot hold the
then movement flow.
wattage, biomechanics start to
break down significantly,
RPE reaches >9.25/10); Rest
5:00 x2 Sets
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These should be powerful
reps, but no rapid changes of
direction)
Additionally, you may have an advanced athlete who starts their day with a high neural
demand resistance training session, performs a high metabolic sport specific interval session in
the afternoon, and finishes their training day with some low intensity movement work and
correctives. For a beginner to intermediate athlete you may spread these out and use a three day
rotation where they have a high neural demand day, a high metabolic demand day, and then an
active recovery session. There are many different combinations and possibilities you can use
depending on the athlete, their goal, and the sport they compete in.
Ensure Your Low Intensity Work Is Low Intensity
Hard training days should be hard are easy training days should be easy. You can call this
approach 80/20 training, polarized training, or even just a basic strategy for load management.
We've all heard this saying in one form or another. Unfortunately, however, few individuals do
this well. Seldom do athletes give up their active rest days without a fight and those who perform
low-intensity base training often use arbitrary heart rate zones to determine what low intensity is
for them without considering how much physiological stress they are imposing. Just because an
individual is working in the 120-140 beat per minute heart rate range and it subjectively feels
easy does not mean they’re doing low-intensity work, facilitating cardiovascular adaptations
associated with improved efficiency, or speeding up their recovery. In some contexts, what
individuals perceive to be their low intensity is one of their most significant stressors in their
training week.
Heavily muscled, powerful athletes often have trouble doing true low-intensity work. In
these cases, heart rate is not a reliable indicator of how much stress they impose on a given
activity. For example, in figure twenty-one, we have a NNOXX muscle oxygenation trend from a
sanctional level Crossfit athlete performing a 30-minute active recovery echo bike ride at a heart
rate of 110-120 beats per minute. Note the drop in muscle oxygen saturation mid way into the
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work bout followed by a maintenance of low muscle oxygen saturation. When muscle oxygen
saturation is low oxidative metabolism is compromised, which leads to an increased reliance on
glycolysis to replenish phosphocreatine, and subsequently ATP. This is bound to occur during
high-intensity training, but when this goes on for the majority of an athlete's low days, it means
that they are never genuinely polarizing their workouts. They have hard days where mental and
physical stress is high, then easy days where mental stress is low, but the physiological stress is
still meaningful. The aforementioned form of training that isn't hard enough to drive specific
adaptations and isn't easy enough to facilitate recovery and maintain health doesn't serve much
purpose. There are times and places where it can be used, but we shouldn't kid ourselves by
calling it active recovery or regeneration work. We need to accept that recovery work may look
very different for a two hundred pound CrossFit athlete than for a one hundred forty pound
distance runner. Everyone's physiology, movement coordination strategies, and responses to a
given type of training are unique. What might be a low-intensity training stimulus for one
individual drains another individual's adaptive reserves. Just as we individualize hard
developmental training, we need to individualize recovery sessions as well.
Progression
Progression in training is as important as having a well planned training day or week.
Without implementing a consistent increase in volume, intensity, as well as changes in density
and other variables, athletes will eventually stagnate and fitness will no longer improve. This is
especially true when working with high level competitive athletes. Fitness is a critical component
of sport and implementing planned progressions can ensure athlete’s are maximizing their fitness
at the correct times for optimal performance. ​There are a vast array of ways to progress an
athlete's training, but most of these progressions consist of some amalgamation of volume,
intensity, density, and complexity progressions. The combinations are limitless and they range
from very simple to extremely intricate. In this subsection I am going to discuss two of the most
common, and easiest to manage, points of control which are volume and intensity respectively.
The currency of training volume in most instances are repetitions, sets, series, and
duration of training. Volume progressions allow us to develop an athlete’s tolerance to training
stress in a controlled manner, which is why they are one of the most commonly used types of
progression. The simplest form of a volume progression is by simply increasing the amount of
work, in terms of interval duration, or number of reps, or number or series from week to week.
These progressions are best implemented in training categories which develop the endurance of
an energy system like D0-3, B4, and U1. Generally volume can be increased for relatively long
durations assuming that deload weeks are planned every 2-6 weeks or so to allow athlete’s a
chance to adapt or ‘catch up’ to the progression. It is recommended that you do not exceed the
maximum guidelines laid earlier in this chapter, with the exception of advanced or elite level
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athletes or those who compete in sports that require them to perform for that long like ultra
marathon runners, military selection candidates and so forth.
The second of the most commonly used types of progression is an intensity progression,
which is concerned with increasing the load, tension, pace, or velocity of training. An example of
this would be to have an athlete shift from B1 to B2 pace training leading into a competition or
to progress from running 20m sprints in 30 seconds to 28 seconds from one week to another.
Intensity progressions are efficacious in preparing athletes for the higher metabolic demands
associated with competition. These types of progressions are best implemented with the training
categories that improve the power of a given system like B2 or U2, then they can also be
effective with B1, U1, and blended energy system training as well. Intensity progressions do not
work well with the D0-3 training categories as their purpose is to build volume and endurance.
By progressing intensity in these training categories you are essentially stripping the athletes
muscles of oxygen and moving them into the next sequential training category. Generally
intensity is progressed for shorter periods of time than volume because developing the power of
an energy system can be quite taxing for athletes. Periods of three to four weeks of progression
followed by a deload are good starting points; and most athletes will hit a point of diminishing
returns between six to twelve weeks. Lastly, intensity progressions are preferred over volume
progressions at certain times of the year, like leading into a race or competition.
​
The last type of progression I will cover in this section is an alternating progression,
which is when volume and intensity are increased in an alternating weekly or fortnightly pattern.
These types of progressions are generally used to slow the rate of progression in the intensity
category for longer seasons. This can be very effective for high level athletes who have long
competitive phases throughout the year.
Program Design Heuristics
Finally, we'll finish off with some programing heuristics:
1. Respect the synergy between resistance training and energy system training: You can’t
just throw a Russian squat cycle together with Crossfit™ main site work, and a dash of
Jack Daniels running formula. You may get lucky, but most likely you won’t succeed
long term. Each of these programs were constructed with an optimal balance of stress and
recovery in mind; and as I previously mentioned everything is connected to everything
else. Strength training, energy system training, and movement training all fundamentally
impact the way our brains regulate adaptation, and in order to leverage this process we
need to respond to both how these types of training complement one another, and what is
the systemic impact they have on our bodies.
2. Don’t neglect the fundamentals: I get it, hard training is fun, but at the end of the day it’s
the least exciting aspect of a holistic training program that ultimately determines an
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athlete’s long term success. Are sleep, stress, food, and tissue quality in check ? Yes, then
have at it. If not, you need to spend less time worrying about the minutiae in a training
plan and more time taking care of the basics.
3. Balance intensity and recovery: Hard days are hard, and easy days are easy. You should
be able to tell the difference. The majority of workouts are small to moderate stressors,
which compound and cement adaptations over time, and we’ll layer in some ‘see god’
workouts on top. Too much of the latter, or a steady stream of equal volume/ intensity
(what I call the ‘grey zone’) day in and day out and we’ll inevitably hit a wall.
4. Build and maintain: Traditional block periodization structures are concerned with
building a given training quality (like an ‘aerobic base’) for a handful of weeks, then
switching the focus to something like speed in hopes that the athletes end up in a better
position than where they started. I believe this is a waste of time, and for Crossfitters
specifically I’m of the opinion that we should never drop one training quality off entirely
— instead I like to keep touches on everything at all times, but the relative contribution
of each training quality will be dictated by an athlete’s training priority at that moment.
5. Take the next logical step: Let's say we have a Crossfit athlete and this week I have him
do 6 sets of 10 Power Snatch, 10 Bar Facing Burpee, 200m Run; resting 1 minute
between sets. I know he can handle 10 sets of that the following week, but will the
magnitude of adaptation from that be greater than, say 8 ? Maybe, but not by a huge
margin. What matters is that the magnitude of stress increases from week to week —
whether or not we push it to the physical maximum isn’t as important in the vast majority
of scenarios, and in most cases it leaves the athlete less room to grow. Instead of going
for broke each and every week, it’s better to take the next logical step, collect all the low
hanging fruit, and then ramp things up when the need arises. In other words, don’t ‘go
there’ before you need to.
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Part III: Resistance Training
Chapter 13: Resistance Training Fundamentals
Traditionally, exercise physiologists and strength coaches alike believed there was a
dose-response relationship between the amount of reps in a set and the subsequent adaptation
accrued in the skeletal muscle. For example, it was believed that training in the 1-5 rep range
built strength, the 6-10 rep range was for functional hypertrophy, the 10-15 rep range was for
non-functional hypertrophy, and anything above fifteen reps increased muscular endurance.
However, the aforementioned dose-response relationship lacks supporting evidence. In fact, it
appears that training with very light loads can produce similar muscle gains as training with
much heavier loads. The only meaningful difference between the two loading conditions is the
number of reps an individual will be able to complete before volitional muscular failure.
Additionally, the current body of literature suggests that the intra-set repetition ranges aren’t of
the utmost importance for eliciting muscle hypertrophy as long as work sets are taken to
momentary muscular failure, or close to it.
Somewhere along the lines, most strength trainees have encountered the idea that there is
an optimal repetition range for eliciting muscle hypertrophy. In most instances the optimal rep
range is said to occur between eight and twelve repetitions. Why would a heavy load that an
exerciser can only perform three to five repetitions with create less of a stimulus for muscle
growth than a lighter load that they can perform eight to twelve repetitions with? Especially
when the heavier load puts more tension, which is the principal determinant of muscle growth,
on the muscle fibers. The truth is that neither lighter load, nor the heavier load, would not
produce greater hypertrophy when volume is equated. If strength training with less than eight
repetitions produces meaningful hypertrophy then how does the muscle adapt to work sets with
greater than twelve repetitions? Or twenty for that matter? Based on the current body of literature
it appears that works performed with as low as thirty percent of an exerciser’s one repetition
maximum will be equally effective as those using eighty percent of an exerciser’s one repetition
maximum as long as both sets are taken close to volitional failure. Does this mean that intensity
does not matter for muscle growth as long as sets are taken to momentary muscular failure, or
close to it? The short answer is no. Intensity does matter. There is a minimum and maximum
intensity threshold for optimizing muscle hypertrophy and while these thresholds vary between
individuals they are likely to occur around thirty and ninety percent of an exerciser's one
repetition maximum load respectively. However, I personally hedge my bets by using loads
between 40-85%. Assuming an individual performs all of their working sets within the
aforementioned intensity range the total number of sets, taken close to momentary muscle
failure, is the primary driver of muscle gain.
Since the number of repetitions per set is not of the utmost importance it leaves wiggle
room to personalize how an exerciser distributes their training volume across different intensity
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ranges. I personally would not advocate for performing all of your hypertrophy training at the
upper end of the effective intensity range, due to the increased risk of connective tissue and joint
injury, nor would I recommend only performing lower load training. My personal
recommendation is for exercisers to perform the bulk of their hypertrophy training volume
between 60-80% of their one repetition maximum and to distribute the remainder of their volume
between the lower and upper bounds of the effective intensity range. There is a both
physiological and psychological rationale for this recommendation. For example, if an exerciser
is doing heavy load training and is capable of performing four repetitions this week they would
need a 25% improvement in strength to complete five repetitions next week. While possible, one
cannot expect that type of weekly progress for an extended duration. Physiologically it’s not
necessary to add load or reps every week in order to build muscle, but many athletes struggle to
train hard day in and day out when they cannot observe acute progress. When performing light to
moderate load training there is a greater opportunity to have small wins in every workout, which
can improve an exerciser’s consistency. For example, if an athlete completes ten to twenty
repetitions in a work set they only need a 5-10% strength improvement to add another rep next
week. By blending light, moderate, and heavy load training an exercise can observe progress on
multiple different time scales, which helps create a positive feedback loop that ultimately
facilitates long term progress.
Coaches often neglect the fact that consistency is the key to physiological development
and adaptation over long time scales. I’d personally rather an individual do a training program
that isn’t optimal if they enjoy it and are able to stick with it week after week versus a perfectly
dialed-in program that they hate doing and have trouble committing to. Remember, progress is
about habit formation, consistent behaviors, and small changes compounding over time. The next
few sections of this chapter are dedicated to providing you with information about the current
body of evidence for what constitutes optimal training on average. However, it’s up to you to
integrate this information into your decision making framework and apply it to the individual.
My goal is not for you to take my words as blanket recommendations, but rather as suggestions
for how you can apply specific principles in practice.
The Mechanisms of Muscle Hypertrophy
In 2010 Dr. Brad Schoendeld published a paper, titled The mechanisms of Muscle
Hypertrophy and Their Application to Resistance Training 13, which presented a comprehensive
mechanistic model of muscle growth. In this paper Dr. Brad Schoendeld provided evidence for
what many traditionally believed, which is that muscle damage, mechanical tension, and
metabolic stress are the primary causative factors of skeletal muscle hypertrophy. The
13
Schoenfeld BJ (2010). The mechanisms of muscle hypertrophy and their application to resistance training. J Strength Cond Res.
10:2857-2872.
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importance of mechanical tension in promoting muscle growth is indisputable, but in recent
years the roles of metabolic stress and muscle damage in hypertrophy have been challenged.
Mechanotransduction is the process of turning a mechanical stimulus, like tension or
stretch on the muscle fibers, into a chemical signal. When a tension stimulus is applied to a
muscle fiber it begins the myogenic signaling process. Myo stems from the Greek word mŷs,
which means muscle, and genesis comes from the ancient Greek word gígnomai which is loosely
translated to “to be produced’. Using these root words we can derive that myogenic signaling
starts the process of skeletal muscle creation. The aforementioned myogenic signals include
IGF-1, IL-6, and other growth factors that are released in response to mechanical tension. The
next step includes mTOR signal integration which is where the mTOR enzyme integrates the
myogenic signals and initiates gene translation. Then muscle protein synthesis occurs, which is
the actual process of muscle growth where myo-fibular proteins are added to the muscle tissue,
and finally we have myonuclear addition. This process is depicted in figure twenty-three.
Muscle Damage is the tearing of muscle fibers and muscle cell membranes. Traditionally
it was believed that muscles grow in response to damage, which assumes that the growth process
involves a breaking down of muscle tissue and a subsequent phase of rebuilding. While muscle
damage does appear to be correlated with muscle growth, that does not imply causation. In all
actuality, it appears that muscle damage and muscle hypertrophy are both consequences of a
common cause, which is lifting weights and applying mechanical overload to a tissue. However,
this begs the question of why we can observe meaningful increases in muscle protein synthesis
after inducing muscle damage? After all, we have already established that increases in muscle
protein synthesis are the process of adding new myofibrillar proteins to a tissue, which should
translate to new muscle growth. It appears that these initial increases in muscle protein synthesis
above baseline after inducing muscle damage work to repair and remodel the muscle tissue, but
do little to contribute to muscle hypertrophy after the attenuation of damage. This is likely why
we can observe large increases in muscle protein synthesis after an individual performs downhill
running, but those increases in muscle protein synthesis don’t correspond to muscle growth.
Additionally, strength training protocols that do not promote muscle damage induce equal or
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greater levels of muscle hypertrophy than those that do promote muscle damage, which suggests
that in addition to muscle damage not being a prime contributor to muscle hypertrophy, it may be
counter productive as well. This also explains why individuals performing a well structured
hypertrophy training program see greater increases in muscle hypertrophy in the later weeks of
the program even though net muscle protein synthesis is greatest in the first few weeks of
training. In those instances the large spikes in muscle protein synthesis early into the training
program function to attenuate muscle damage from a novel stimulus, then as the program goes
on less muscle damage is induced and net protein synthesis is lower, but a greater fraction of
muscle protein synthesis is oriented towards increase muscle cross sectional area. This
relationship is depicted in figure twenty-four.
14
Metabolic stress is the accumulation of metabolic by-products in the muscle such as
lactate, inorganic phosphate, hydrogen ions, and hypoxia. Metabolic stress’ relationship to
muscle hypertrophy is more complicated than mechanical tension or muscle damage. This is
partly due to the fact that metabolic stress is extremely difficult to quantify. As a result, we’re
forced to rely more on the applied than mechanistic research. One interesting case study we can
look at to try and parse out the role of metabolic stress on muscle hypertrophy is the comparison
between HIIT training and standard resistance training protocols. On a set by set basis, HIIT
training induces greater metabolic stress than traditional resistance training methods, but when
volume is equated it actually appears to be less effective in its ability to promote muscle
hypertrophy. Additionally, it has been shown that longer rest periods are more effective than
shorter rest periods for enhancing muscle hypertrophy, even when volume is equated between the
two modalities. This suggests that if metabolic stress is an independent driver of hypertrophy, it
has less of a meaningful impact than mechanical tension since metabolic stress should be
elevated when performing shorter rest periods compared to longer rest periods.
In order to test the independent effects of metabolic stress we can also look at the effect
of blood flow restriction in the absence of an exercise stimulus. In a paper titled, Blood Flow
14
Figure 24 credit: Damas F, Libardi CA, Ugrinowitsch C (2017). The development of skeletal muscle hypertrophy through
resistance training: the role of muscle damage and muscle protein synthesis. Eur J Appl Physiol. 118: 485-500.
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Restriction Only Increases Myofibrillar Protein Synthesis With Exercise 15, by Jean Nyakayiru
and colleagues the investigators assessed the effect of blood flow restriction with and without
low-load resistance-type exercise on in vivo myofibrillar protein synthesis rates in young men.
Their findings suggest that blood flow restriction does not increase myofibrillar protein
synthesis, or stimulate muscle hypertrophy, under resting conditions despite inducing a
meaningful degree of metabolic stress. Additionally, in a separate investigation it has been
demonstrated that performing a set of dumbbell bicep curls to failure, then restricting blood flow
immediately after each set, does not lead to greater muscle hypertrophy than only performing a
set of bicep curls to failure, even though the former elicits greater metabolic stress. These
findings support the idea that metabolic stress is only anabolic in the presence of muscular
contractions and mechanical overload, which is why metabolic stress is often called a back door
pathway to muscle hypertrophy.
Balancing Mechanisms of Muscle Hypertrophy
As previously stated, mechanical tension is the primary driver of muscle hypertrophy, and
metabolic stress is likely to be a backdoor pathway to muscle hypertrophy. I’m going to revisit
this idea through the lens of integrative physiology, and refine metabolic stress as a negative rate
of change of muscle oxygenation, which indicates that oxygen utilization is outstripping oxygen
supply. When oxygen is utilized at a faster rate than it can be supplied to a working muscle there
will be an impairment in the sensitivity of
actin-myosin myofilaments to calcium ions, which
increases peripheral nervous system fatigue. The
increase in peripheral nervous system fatigue then
causes an increase in motor unit recruitment, which
will lead to an increase in mechanical tension. This
is in line with the observed oxygen conforming
response, which refers to the rapid adjustment of
muscle force production for the same motor neuron
activation in response to changes in muscle
oxygenation so that the cell's environment remains
stable. In other words, the skeletal muscles' inherent
response to changes in oxygenation is to adjust ATP
demand accordingly. Importantly, the oxygen
conforming response occurs in both directions: downregulation of force with decreased muscle
oxygenation and upregulation of force when muscle oxygenation is increased. This means that
muscle activation will rapidly rise and blood flow to a tissue is impaired and muscle oxygen
saturation reaches a nadir. This also explains why there are higher than expected increases in
motor unit recruitment and mechanical tension when lifting low loads to failure and why loads
ranging from roughly thirty to ninety percent of an individual's one rep max have an equal ability
15
Nyakayiru J, Fuchs CJ, Trommelen J, Smeets JSJ, Senden JM, Gijsen AP, Zorenc AH, VAN Loon LJC, Verdijk LB (2019). Blood
Flow Restriction Only Increases Myofibrillar Protein Synthesis with Exercise. Med Sci Sports Exerc. 51:1137-1145.
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to elicit muscle hypertrophy when volume is equated. Another interesting observation is the
relationship between loading and local muscle desaturation such that the heavier the load the
greater the rate and magnitude of muscle desaturation occurs. Since heavier loads, greater than
roughly seventy percent of an individual's one rep maximum, are sufficient to restrict both
arterial inflow and venous outflow this may explain why heavy lifting causes maximum motor
unit recruitment off the bat. So, in and of itself, local muscle desaturation and metabolic stress do
not appear to cause hypertrophy, but rather they lead to the generation of mechanical tension
which is the primary causative factor for muscle hypertrophy. This jives with the previous
observation that metabolic stress is only anabolic in the presence of muscular contractions and
mechanical overload to a muscle tissue. This relationship is depicted in figure twenty-five.
Basic Training Guidelines For Muscle Hypertrophy
If you accept that mechanical tension and local muscular fatigue are the two main drivers
of muscle hypertrophy, any choice of training intensity represents a tradeoff between those two
mechanisms. The heavier you go, the more tension you develop, but the less local muscular
fatigue and subsequently metabolic stress you develop before the point of fatigue and vice versa.
However, it seems that there needs to be some balance of both mechanisms to maximize growth.
From a practical standpoint the questions we need to be able to answer are as follows:
1. Intensity: how heavy is heavy enough, and where are the low and high end cutoffs?
2. Volume: how is it quantified and what is its role in hypertrophy?
3. Frequency: how is it derived from volume?
When thinking about the relationship between training volume and intensity I like to use
the following analogy. If you want to boil water on the stove you wouldn’t put the flame to the
lowest setting because the water would never reach a rolling boil no matter how much time you
lent it. Instead, you would set the flame to the appropriate intensity and then lend it the necessary
time it needs to heat the water until it begins to boil. For hypertrophy training the appropriate
intensity appears to be greater than thirty percent of an athletes one repetition maximum, and
based on the current body of literature it appears that a set performed with roughly that load
provides an equally meaningful stimulus for much growth as a work set performed with upwards
of ninety percent of an individual's one repetition maximum so long as both sets are taken within
a close proximity to failure. If an individual is training in the aforementioned effective loading
range and pushing their work sets close to failure then it appears that volume, defined as the total
number of work sets completed, is going to be the greatest point of leverage for inducing muscle
growth. The third training related factor that we can manipulate is frequency, which is derived
from the total volume per muscle group per week. As volume gets higher it appears that we need
to increase frequency to see continued gains, or prevent a backslide, which will be discussed in
greater depth in a later chapter.
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Chapter 14: A Decision Making Algorithm For Muscle Hypertrophy
Whether you’re coaching bodybuilders who need to grow specific muscle groups, a
weightlifter who needs to hypertrophy their quadriceps to improve their front squat, or general
fitness clients aiming to improve body composition, being able to create a comprehensive
hypertrophy training plan is a useful skill. After having read the previous chapters you should
understand the basics of training to increase muscle hypertrophy. However, there are cases where
exercisers present with lagging muscle groups that appear resistant to growth. For example, you
may encounter an individual who sleeps nine hours a night, is in a caloric surplus, and is making
good training progress with all major muscle groups except one specific lagging muscle.
Oftentimes individuals in this scenario will take the approach of increasing total weekly set
volume for their lagging muscle. While this can be an effective approach in some cases, it’s not
the only option, and oftentimes it is surely the wrong choice.
Figure twenty-six depicts a decision making algorithm for hypertrophying a lagging
muscle group. I’ve traded some nuance for ease of interpretation and applicability. However, my
hope is to use the remainder of this chapter to parse out the underlying principles that went into
creating this model so you can effectively troubleshoot issues with it as your guide.
Are You Recruiting The Target Muscle Effectively?
One of the surest signs that someone is not recruiting a target muscle effectively is that
they maintain a high muscle oxygenation level in that muscle even after pushing a work set to
momentary muscular failure. For example, figure twenty-seven shows two different athletes
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muscle oxygenation trends recorded with a NNOXX wearable on their biceps brachialis during a
set of hammer curls. Athlete ‘A’ desaturates their biceps brachialis down to ~15% muscle
oxygenation at the nadir, while Athlete ‘B’ has a muscle muscle oxygenation of ~45%. There are
a handful of factors that can influence an exercier’s ability to utilize oxygen effectively in a
target tissue including their pre-position, exercise selection, movement execution, metabolic
activity in the target tissue, and muscle recruitment.
Starting with coordination, we need to look at the position of the axial and appendicular
skeleton to see if there are any major postural faults. For example, if an individual is stuck in
thoracic flexion and shoulder internal rotation they’re not going to be in an advantageous
position to load the biceps. Before worrying about the nuances of exercise selection, volume, or
intensity they need to improve their position first. Then once they are able to get into the proper
pre-position, they can consider the specific movements they are using to train the target muscle.
Some movements lend themselves better to creating high levels of mechanical tension while
others lend themselves better to creating higher metabolic stress. Oftentimes individuals select
movements based on how much of a stretch they feel while performing it. However, that doesn’t
mean it’s actually an effective movement for loading the tissue. Additionally, it’s worth
considering whether the target muscle is being loaded in the shortened position, mid-range
position, or lengthened position. If all of your training is being done with movements that load
the muscle in the mid-range, which is a common occurrence, you may be missing out.
Now, assuming that an individual has optimized their pre-position and exercise selection,
the next factor I'd look into is exercise execution. Oftentimes simple changes in an exerciser’s
hand, wrist, or elbow position during a biceps curl can make a substantial difference, as can
specific tactile cues. For example, if an athlete has trouble feeling their biceps i’ll often make the
following recommendations: (1) Minimize movement at the shoulder joint and aim for full elbow
flexion and extension while keeping the elbows themselves in a fixed position through the full
range of motion, (2) Imagine trying to crush an imaginary pencil placed on the inside of the
elbow joint at the top of each rep. You should aim to touch your forearm to your bicep and if
you’re performing a supinated curl you can squeeze your pinky finger towards the shoulder of
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the same side, (3) Control the eccentric, then lightly contact the triceps at the bottom of the
eccentric.
Finally, if all else fails and the individual is doing everything right, but still cannot
desaturate the target muscle, I'll do a thermography screen to see if there are any underlying
tissue pathologies. The picture below depicts sample thermograms taken from an athlete
recovering from a left ACL injury and
a right achilles tendon injury. A
thermogram is a representation of heat
radiating from the body. Skin
temperature regulation is impacted by
blood flow, muscle recruitment
pattern, inflammation, and injury.
Despite the fact that our bodies are
thermally balanced, injuries can cause thermal asymmetries. As a result, infrared thermography
allows one to detect these thermal asymmetries, which represent regions of interest related to
tissue pathologies, faulty biomechanics, or changes in tissue perfusion. In figure twenty-eight
above you’ll see cases where an individual has a hypothermic asymmetry caused by decreased
metabolic activity in the tissue. In these scenarios individuals will often have atrophy in the
surrounding tissues, and will often note that they can’t get a pump in those muscles. In order to
hypertrophy these tissues normal function first needs to be restored.
Are You Training With Sufficient Intensity?
If you want to boil water on the stove, you would never put the flame on the lowest
setting. The water would never reach a rolling boil no matter how much time you gave it.
Instead, you would set the flame to the appropriate intensity and then lend it the proper time it
needs to make the water boil. The same concept applies to hypertrophy training. If you’re not
training with the requisite intensity, it doesn’t matter how much volume you’re accumulating
over time. You’re not going to make improvements.
The first component of intensity is loading. Based on the current body of research it looks
like a set performed with thirty percent of an individual's maximum voluntary contraction or one
repetition maximum provides the same stimulus for muscle growth as a set performed with
ninety percent, assuming both sets are taken to volitional failure. This has been demonstrated by
Jenkins and colleagues in their paper titled, Neuromuscular Adaptations After Two and Four
Weeks of 80% Versus 30% 1RM Resistance Training to Failure 16, as well as by Schoenfeld and
16
Jenkins ND, Housh TJ, Buckner SL, Bergstrom HC, Cochrane KC, Hill EC, Smith CM, Schmidt RJ, Johnson GO, Cramer JT
(2016). Neuromuscular Adaptations After 2 and 4 Weeks of 80% Versus 30% 1 Repetition Maximum Resistance Training to Failure.
J Strength Cond Res. 30: 2174-2185.
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colleagues in their paper titled, Effects of Low vs. High-Load Resistance Training on Muscle
Strength and Hypertrophy In Well-Trained Men 17.
If exerciser’s can elicit muscle hypertrophy with as little as thirty percent of their one
repetition maximum, can they do it with ten percent? Where is the low end cut off point? In a
study by Lasevicius and colleagues titled, Effects of Different Intensities of Resistance Training
With Equatted Volume Load on Muscle Strength and Hypertrophy 18, the investigators sought to
answer this question. Based on their findings we can infer that the low end cut off for muscle
hypertrophy occurs between twenty to thirty percent on an individual's one repetition maximum,
though I'd wager that it may be higher than thirty percent for select individuals who were
underrepresented in this study.
The crux for any athlete wishing to achieve a meaningful degree of muscle hypertrophy is
figuring out where their cut off points are so they can train with greater specificity. If the number
of hard work sets you can do for a given muscle group per week are limited, as they are for any
individual, then it’s crucial that all works sets be performed in an intensity range where an
individual is capable of desaturating a tissue, increasing motor unit recruitment, and eliciting
hypertrophy. Personally, I recommend exercisers err closer to ~40-85% of maximum voluntary
contraction for practical and logistic reasons, with the bulk of training being done within the
upper two-thirds of that loading range. The second component of intensity is proximity to failure.
I tend to advocate for leaving one to two repetitions in reserve on work sets for most individuals.
However, people often underestimate their proximity to failure, so it can be worth having lower
training age athletes extend their work sets until they reach momentary muscular failure every so
often, on exercises where it is safe to do so, as a means of calibrating their efforts.
Are You Training With Enough Volume?
An S-shaped curve, depicted in figure
twenty-nine, demonstrates the relationship between
total weekly training volume, defined as the number
of sets performed within an effective loading range
taken within close proximity to failure, and an
individual's rate of muscle growth. If an individual
performs too little effective training volume for a
given muscle group the rate of muscle growth will
be very slow. The lowest volume threshold needed
to produce a result is often termed the minimum
17
Schoenfeld BJ, Peterson MD, Ogborn D, Contreras B, Sonmez GT (2015). Effects of Low- vs. High-Load Resistance Training on
Muscle Strength and Hypertrophy in Well-Trained Men. J Strength Cond Res. 29: 2954-2963.
18
Lasevicius T, Ugrinowitsch C, Schoenfeld BJ, Roschel H, Tavares LD, De Souza EO, Laurentino G, Tricoli V (2018). Effects of
different intensities of resistance training with equated volume load on muscle strength and hypertrophy. Eur J Sport Sci.
18:772-780.
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effective volume (MEV). Then as volume increases, the rate of muscle hypertrophy will
increase, up until a point where additional volume yields diminishing returns. This threshold is
often referred to as maximum adaptive volume (MAV). Finally, there will be a point where even
more volume provides little additional gain and where crossing it becomes maladaptive. That
threshold is often referred to as the maximum recoverable volume (MRV). The goal is to
determine what range of work sets correspond to each of these thresholds for a given muscle
group. These ranges differ substantially from person to person and from muscle to muscle within
a given individual. A good starting point for beginners and early stage intermediates can be ten
sets per week per muscle group for a given individual. For late stage intermediates or advanced
athletes fifteen to twenty sets per muscle per week may be more appropriate. These ranges often
approximate MEV for many athletes and are unlikely to be within striking range of MRV, so they
are safe starting points. However, hard gainers' minimum effective volumes are often much
higher. If the primary goal is muscle growth, we’ll also typically want to work within volume
ranges on the right end of the s-curve closer to MAV.
Are You Managing Frequency Well?
Suppose an individual uses proper exercise selection, executes movements correctly, and
performs all of their training within an effective loading range. In that case, the total number of
work sets taken to near failure for a specific muscle group is likely the greatest determiner for
building muscle. However, as volumes get higher, it appears that we need to drive frequency up
to see gains or even prevent a backslide from occurring. Based on the current body of evidence,
it seems that the most productive sets an individual can do in a session for a given body part
range from eight to fourteen sets on average. The exact optimal volume in a session is likely a
product of the proximity to failure for each work set, the specifics of the training plan, the
muscle group being trained, and individual factors like recovery, genetics, work capacity,
physiological predisposition. For example, suppose you’re only doing ten sets of bicep training
per week. In that case, you’re probably fine doing all of your volume in a single session, though
splitting it up into two sessions may allow for higher training quality and subsequently greater
gains. But, if you’re performing twenty sets of biceps training per week, it is ill-advised to do all
of that in one session, and you’d probably fare better spreading that out over two to three
sessions.
It makes intuitive sense that you can only stimulate so much muscle growth, or any other
adaptation, within a single workout. Another reason why higher frequency may be desirable as
training volume, defined as total work sets per week for a given muscle group, is that there is a
limit to the amount of quality training you can do in one session. One of the more obvious
reasons for this is that neuromuscular fatigue will accumulate across a workout, which will
reduce muscle activation and, subsequently mechanical tension. Another reason is that we will
accumulate more muscle damage with each set performed. Past a given point, each additional
work set provides such little benefit that it is not worth the cost of being performed. If you keep
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pushing past that point, each set may not only provide little benefit but may actually be
counterproductive as it may result in a negative protein balance, due to muscle protein
breakdown, without stimulating more muscle growth or muscle protein synthesis. If this is done
frequently enough over time, you may end up in a net negative protein balance, leading to losses
in muscle mass.
The presence of a maximum productive training volume per workout would also explain
why some studies find benefits of higher training frequencies, but others do not. Most of the
studies that find benefits of higher training frequencies are in trained lifters with higher than
average weekly training volumes. Conversely, there are many studies where training frequency
does not seem to matter independent of training volume, and these studies are mainly done with
training volumes below ten sets per week for a given muscle group.
The key to maximizing volume over an extended duration is all about walking the razors
of ‘just enough’ before we start to see detriment, while simultaneously being able to drive
progressive overload as a proxy for ensuring we’re getting muscle growth. Additionally, training
volume should be optimized with training frequency in mind, not separately. Training volume
should also be considered on a per-workout basis, not just on a total weekly basis. Training your
chest two times per week with ten sets per session may have worse results than training three
times per week with six to seven sets per session or even four sessions per week with five sets
per session. That being said, when training with lower volumes, below twelve sets per week per
muscle group, manipulating frequency doesn’t appear to be nearly as important as when training
with fifteen to thirty sets per week for a given muscle group. The crux then becomes figuring out
which of the above options are optimal.
Troubleshooting
What happens if an individual answers yes to all of the questions in the decision-making
algorithm, depicted in figure twenty-six, but they are still not growing the target muscle? The
short answer is that they’re more than likely overlooking one of the components mentioned in
this chapter. Maybe their exercise execution isn’t as optimal as they think it is, they’re leaving
more reps in the tank each set than they think, they’re using too little or too much volume, or
they’re not dividing up their work sets throughout the week in a way that maximizes the quality
of their training. All of those are possibilities. There is also the possibility that they are making
improvements but just have unrealistic expectations of both the magnitude of change that will
occur on short time scales and the length of time it takes to make a perceptible change to a given
muscle.
If you find yourself in the aforementioned scenario my recommendation is to track
performance on an isolation movement for the target muscle group you’re training. If you’re
increasing total reps across multiple sets consistently over many weeks it’s more than likely a
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product of muscle gain. Alternatively, you can track your ten or fifteen rep max on an isolation
exercise, like a strict preacher curl, or a regional exercise, such as a leg press. Both of the
aforementioned choices are good litmus tests to gauge whether or not you’re making
measurement progress or not. If you are not making any measurable progress for a specific
muscle group, but are still progressing in the rest of your training, it's worth working back
through the decision making algorithm in figure twenty-seven to determine if you’re overlooking
any major variables. However, if your progress has stalled across the board my recommendation
is to deload for one to two weeks before resuming training and continuing to troubleshoot.
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Chapter 15: Auto-Regulation For Resistance Training
Imagine we performed an experiment where we took one hundred athletes and trained
them all in the exact same manner for one year. What do you predict would happen at the end of
the experiment when we checked in on their results? If the program was well constructed we’d
probably see a bell curve distribution with the majority of individuals getting good results and
then fifteen to twenty athletes getting either excellent results or doing very poorly. In the training
community, we tend to act as though everyone is capable of looking, performing, and adapting
the same. This is the premise on which every training plan sold in mass, and most training books,
are based. It’s the premise upon which Prepillin’s Table was derived, and which exercise
physiology studies are built upon when they try to isolate a single variable and neglect the fact
that the participants in the study aren’t homogenized. The truth is that we would all differ even if
we trained the same, ate the same, and lived in the exact same environment. These differences
are the result of the differences among our pasts, “differences that assert themselves from just
beneath the surface like some sea monster faintly visible in the dim light of our collective minds”
as Robb Dunn eloquently stated in his book The Wild Life Of Our Bodies.
The models depicted in the strength and conditioning literature are based on statistical
averages and not on an individual’s body, which is why the standard textbook protocols work for
some and not others. A common fault among coaches is that they try to make athletes fit their
rigid models and prescribe these protocols that should in theory elicit a given adaptation. While
this may work for those whose physiologies are congruent with their protocols, it will yield
subpar results for others. Those that don’t fit this profile may simply assume they don’t have the
genetics to elicit a given adaptation, like muscular hypertrophy, for example, when in reality they
just need to take a different path to get there. After all, we cannot fight mother nature. Instead we
need to maximize an athlete’s ability and augment what they already possess. This relates to a
concept in research called response heterogeneity, which can be defined as important individual
differences in the physiological response to the same intervention that cannot be attributed to
random within-subject variability. A great example of this was observed in a study conducted by
Felipe Damas and colleagues titled, Individual Muscle Hypertrophy and Strength Responses to
High vs. Low Resistance Training Frequencies 19. In this study the researchers had a population
of participants train one leg with high frequency (5x/week) and the other leg with low frequency
(2x/week). The researchers measured the participants muscle cross sectional area and one
repetition maxes before and after an eight week training periods, and the results were as follows:
for muscle hypertrophy, six individuals (31.6% of the sample) responded better from high
frequency training, seven individuals (36.8% of the sample) responded better from low
frequency training, and the other six individuals (31.6% of the sample) showed no difference in
the hypertrophic responses between training frequencies.
19
Damas F, Barcelos C, Nóbrega SR, Ugrinowitsch C, Lixandrão ME, Santos LMED, Conceição MS, Vechin FC, Libardi CA (2019).
Individual Muscle Hypertrophy and Strength Responses to High vs. Low Resistance Training Frequencies. J Strength Cond Res. 33:
897-901.
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The purpose of the aforementioned study wasn’t to say that high or low frequency
training was superior, but to show that different people respond to training differently. This might
be why you see some people proclaiming that something like HIIT training, which necessitates a
lower frequency, is superior while others will support high frequency training with just as much
fervor. In reality, both camps may be ‘right’ in that whatever they are doing might be ‘optimal’
for them, but that doesn’t mean that everyone will respond in the same way to that method.
While this study was able to sort out individual variation, this isn’t an easy task when designing a
study. As a result it’s extremely difficult to actually filter out the effects of response
heterogeneity. This is why I generally don’t advocate basing training solely off of studies.
Studies rarely, if ever, tell us what to do. Instead, they dimly light a path for us and it’s up to the
practitioner to decide how to proceed and navigate the path. While the ‘bros’ often make the
mistake of thinking what works for them will work for others I often see evidence based coaches
make a similar mistake. That is, that they think what works for the average in a study will work
for the individual or that a single study qualifies as ‘evidence’ of something. This is also why
tracking your own training response over time is so important. If you’ve struggled to achieve a
certain training outcome, while simultaneously doing everything else correctly, you’re more than
likely using training methodologies that are ill suited for your individual physiology. I know this
has certainly been the case for myself and many of my clients who have come to me after stalling
out or hitting major plateaus in their training. Oftentimes figuring out how to make
non-responders adapt means letting go of constraints and what constitutes optimal training from
a textbook perspective.
The majority of people are clustered around the mean, or within a few standard
deviations of it. However, in one area or another they may be misrepresented by the mean. The
only way to know this is to collect reliable observations and data points over time, as well as to
experiment with training volumes, intensities, or methods that deviate from the norm.
Textbook training recommendations and constraints are useful for helping novice and
early stage intermediate athletes organize their training. However, following constraints can
eventually become a limiting factor that prevents an individual from progressing to the advanced
phase. One way to circumvent this trap is to apply auto-regulation to your training. There are
many ways to autoregulate training, some of which are included in figure thirty. The chart in
figure thirty is intended to demonstrate common ways of auto-regulating training based on
subjective perception and biomarker readings. If you plan to experiment with these methods my
recommendation is to pick one exercise per week to autoregulate, such as a back squat, and
continue using the same protocol for four to six consecutive weeks. By doing so you can gain an
understanding of what normal rates of progress look like for yourself, as well as how your body
adapts to this type of stimulus.
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Part IV: Models Of Performance
Chapter 16: Critical Power And Critical Metabolic Rate
For something so familiar that everyone has experienced it, fatigue is paradoxically
challenging to define. This is partly due to the limits of language and the fact that different fields
of science define fatigue differently. But, it’s also due to the complexity of all of the underlying
processes that lead to fatigue. For much of the time that fatigue science has been a field, the
catastrophic model of fatigue was used to describe what occurs when an athlete reaches the
absolute limit of their physical performance. Proponents of this model assert that the body either
runs out of key nutrients or is ‘poisoned’ due to metabolite accumulation in the working skeletal
muscles. However, as early as the dawn of the twentieth century, some individuals challenged
these assumptions, one such example being Angelo Mosso, who stated, “At first sight [fatigue]
might appear an imperfection of our body, is on the contrary one of its most marvelous
perfections. The fatigue increases more rapidly than the amount of work done saves us from the
injury which lesser sensibility would involve for the organism”. If we take a look through the
lens provided by Angelo Mosso we can begin to see fatigue as an immensely complex derivative
of a number of functions, behaviors, and psychological processes. As a result, exercise
limitations involve a wide range of systems working together in harmony to maintain
homeostasis.
While these descriptive views of fatigue and exercise limitations can be useful, they don’t
improve practitioners’ ability to predict or manage fatigue in athletes. As a result, the link
between fatigue and performance has always been elusive. However, in recent years compelling
evidence has indicated that the relationship between fatigue and performance is enshrined in the
concept of critical power. At its core, Critical power represents the highest power-output that can
be sustained indefinitely, and the total amount of work that can be performed above this critical
power is referred to as W’. Traditionally W’, pronounced as “W Prime”, has been described as
an anaerobic work capacity’, yet there is a lot of compelling evidence that suggests that W’ is
sensitive to oxygen delivery. When we view Critical Power and W’ through the lens of oxygen
delivery and utilization, which are two of the major components of exercise capacity, we can
gain a new perspective that allows us to better model and predict time to fatigue in athletes.
What Is Critical Power And How Is It Calculated?
Critical power is mathematically defined as the power-asymptote of the hyperbolic
relationship between power output and time to exhaustion. In essence, critical power describes
the duration that an individual can sustain a fixed power output in the severe exercise intensity
domain, and physiologically critical power represents the boundary between steady-state and
non-steady-state exercise. As a result, critical power may provide a more meaningful fitness
index over better known measurements such as heart rate, VO2max or functional threshold
power. The hyperbolic equation which describes the relationship between power output and
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exercise tolerance within the severe exercise intensity domain is as follows: Time to Exhaustion
= W’ / (Power - Critical Power).
This equation creates a two-parameter model where critical power represents the
asymptote for power, and W’ represents the finite amount of work that can be done above
critical power, as depicted in figure
thirty-one. Taken together, these two
parameters can be used to predict how long
an individual can exercise at any intensity
above their critical power output.
Interestingly, the critical power model
appears to apply across kingdoms, phylums,
and classes of animal life as well as different
forms of exercise, and individual muscle
groups for a given individual. These
observations suggest a highly conserved and organized physiological process, and perhaps a
unifying principle of bioenergetics.
There are currently two validated methods for determining critical power and the fixed
amount of work that can be done above critical power, termed W’. Traditionally critical power
and W’ were calculated after having an individual perform three to seven all-out work bouts
where they hold a fixed power-output until failure. These test results are then plotted on a chart
where the X-axis and Y-axis variables respectively represent time to failure and power for each
trial. Critical power is then determined as the slope of the work-time relationship, whereas W’ is
determined from the y-intercept. More recently, though, investigators have introduced a 3-minute
all-out exercise test, known as the 3MT, that has enabled the determination of critical power and
W’ from a single exercise bout. The idea behind the 3-minute all-out test is that when a subject
exerts themselves fully and expends W’ wholly, their finishing power output equals their critical
power. This idea can be summarized and expressed with the following equations: (1) Power =
W’ / Time to Exhaustion + Critical Power and (2) Critical Power = Power - W’ / Time to
Exhaustion.
Using the aforementioned testing methods, critical power was originally defined as the
external power output that could be sustained indefinitely. However, it should be understood that
this definition is largely theoretical since no bout of exercise can be sustained forever regardless
of the intensity. As a result, we can better understand critical power as the highest power output
that can be sustained for a very long period of time without fatigue. In contrast to the historical
definition, critical power is now considered to represent the greatest metabolic rate that results in
wholly oxidative energy provision, where wholly-oxidative considers the active organism as a
whole. This means that energy supply through substrate-level phosphorylation reaches a
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steady-state and that there is no progressive accumulation of blood lactate or progressive
breakdown of intramuscular phosphocreatine. Given that muscle oxygenation, as measured with
the NNOXX biosensor, approximates phosphocreatine kinetics measured with magnetic
resonance spectroscopy, we can conclude that a relationship between critical power and oxygen
kinetics exists. As a result, the balance of oxygen supply and demand, which are two of the
major determinants of exercise performance, can be used as a means of understanding critical
power and W’.
What Is The Relationship Between Critical Power And Oxygen Delivery?
As previously stated, critical power is the maximal power output at which a metabolic
steady state characterized by stable intracellular levels of ATP, phosphocreatine, hydrogen ions,
inorganic phosphate, and blood lactate are reached. When exercising above critical power, an
exerciser begins to deplete W’, which is characterized by a finite amount of work that can be
done above critical power. W’ was initially described as an anaerobic work capacity but has
subsequently been shown to be associated with the depletion of intramuscular energy stores and
is sensitive to alterations in oxygen delivery. When exercising at a fixed power output that is
above critical power there will be a progressive increase in VO2, intracellular inorganic
phosphates, and blood lactate until exhaustion occurs. At that point VO2 will also reach a
maximum value, termed VO2max.
VO2max refers to the maximum rate of oxygen consumption measured during intense
exercise, and it represents the maximum integrated capacity of the pulmonary, cardiovascular,
and muscle system to uptake, transport, and utilize oxygen. VO2max can be measured in
absolute liters of oxygen consumed per minute (L/min) or relative to weight in milliliters of
oxygen per kilogram of body mass per minute (mL/Kg/min). VO2max is a physiological
characteristic bounded by the parametric limits of the Fick Equation, which states that VO2 = Q̇
× [(a-v)O2], where Q stands for cardiac output, which can be calculated as stroke volume
multiplied by heart rate and (a-v)O2 diff represents the arteriovenous oxygen difference.
According to the Fick equation, every change in VO2max is matched by a concomitant
change in maximal cardiac output or arteriovenous difference. If VO2 reaches a maximum value
when work done above critical power is performed, and as W’ is depleted, it would indicate that
there may be a causal relationship between critical power and oxygen delivery and extraction. If
this were the case, then there should be evidence that increasing an individual's VO2max will
come with a concomitant upward shift in critical power. According to Archibald Hill, Long, and
Lupton, “In running the oxygen requirement increases continuously as the speed increases,
attaining enormous values at the highest speeds; the actual oxygen intake; however, reaches a
maximum beyond which no effort can drive it. The oxygen intake may attain its maximum and
remain constant merely because it cannot go any higher owing to the limitation of the circulatory
and respiratory system”. Since then, there has been additional evidence supporting the belief that
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the pulmonary system can be a limiting factor in maximal effort exercise. For example, in elite
athletes with very high maximal cardiac outputs, the decreased transit time of red blood cells in
the pulmonary capillaries can lead to a pulmonary diffusion limitation. This was demonstrated in
1965 when the former mile world record holder Peter Snell performed a maximal treadmill step
test, where he finished with a SpO2 level of 80%. Additionally, this finding was later
independently confirmed by Jerome Dempsey and Scott Powers when they showed that arterial
oxygen desaturation occurs in some highly trained endurance athletes and when these subjects
breathe hyperoxic gas mixtures, their hemoglobin saturation and VO2max increase.
In 2010 Anni Vanhatalo, and colleagues, found that the power-duration curve asymptote
was shifted upwards when exercise was performed while breathing hyperoxic air, as
demonstrated in their paper titled, Influence of hyperoxia on muscle metabolic responses and the
power-duration relationship during severe-intensity exercise in humans: a 31P magnetic
resonance spectroscopy study. On the other hand, Jeanne Dekerle and colleagues demonstrated
that the power-duration curve asymptote was shifted downwards when exercise was performed
while breathing hypoxic air, as explained in their paper titled, Influence of moderate hypoxia on
tolerance to high-intensity exercise 20. These experiments involved the within‐subject
manipulation of arterial oxygen content by having study participants breath hypoxic and
hyperoxic gas, which alters oxygen delivery to the exercising muscle. By doing so they
demonstrated that critical power was increased with hyperoxia and decreased with hypoxia. This
lends support for the relationship between critical power and oxygen transport given that oxygen
transport to the skeletal muscle is a product of both cardiac output and arterial oxygen saturation,
both of which can be limiting factors for VO2max. Jeanne Dekerle, and colleagues, have already
shown that reductions in oxygen transport, through breathing hypoxic air, result in a downward
shift of the power-duration asymptote. However, in order to further substantiate the relationship
between oxygen transport and critical power, there should be evidence that reductions in blood
flow will cause a similar downward shift in critical power as well.
During occlusion exercise, where blood flow is restricted, the Fick equation states that
VO2max is proportional to oxygen extraction. Given the speculative relationship between
oxygen delivery and critical power, Monod & Scherrer published a speculative paper titled,
Capacity for static work in a synergistic muscular group in man 21, where they postulated that
that blood flow occlusion during exercise would reduce critical power to zero watts without
altering the curvature constant W’. This was later empirically tested by Ryan Broxterman and
colleagues, in an investigation titled, Influence of blood flow occlusion on muscle oxygenation
characteristics and the parameters of the power-duration relationship 22, where they assessed the
20
Dekerle J, Mucci P, Carter H (2012). Influence of moderate hypoxia on tolerance to high-intensity exercise. Eur J Appl Physiol.
112: 327-35.
21
Monod H, Scherrer J (1957). Capacity for static work in a synergistic muscular group in man. C R Seances Soc Biol Fil.
115:1358-1362.
22
Broxterman RM, Ade CJ, Craig JC, Wilcox SL, Schlup SJ, Barstow TJ (2015). Influence of blood flow occlusion on muscle
oxygenation characteristics and the parameters of the power-duration relationship. J Appl Physiol. 118: 880-889.
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influence of blood flow occlusion on critical power, W’, and muscle oxygen kinetics. In this
case, it was found that the reduction in oxygen delivery with blood flow occlusion decreased
critical power to zero watts and led to an increased W’ compared with the control group. These
findings support the aerobic nature of critical power and demonstrate that the amount of work
that can be done above critical power can vary across conditions. Moreover, the amount of work
that can be done above critical power appears to be a consequence of the depletion of
intramuscular energy stores and the accumulation of fatigue-inducing metabolites, limiting
exercise tolerance and determining W’. Based on these findings, it appears that reductions in
blood flow, and subsequently, oxygen delivery, lower critical power, resulting in the utilization of
W’ and fatigue at lower relative intensities. Additionally, the larger body of evidence suggests
that any alteration in oxygen delivery, whether through blood flow changes or inspired oxygen
concentration changes, will directly affect critical power and W’ depletion.
The Impact Of Oxygen Delivery On W’ and It’s Reconstitution
The curvilinear relationship between power output and the time for which it can be
sustained is a fundamental and well-known feature of high-intensity exercise performance.
Simply put, the harder you work the sooner you’ll have to stop. This relationship levels off at a
critical power that separates power outputs that can be sustained with stable values of, for
example, muscle phosphocreatine, blood lactate, and pulmonary oxygen uptake, from power
outputs where these variables change continuously with time until their respective minimum and
maximum values are reached and exercise intolerance occurs. The amount of work that can be
done during exercise above critical power is known as the W’. The W’ is constant but may be
utilized at different rates depending on the exercise power output's proximity to critical power.
As a result, the W’ represents a fixed amount of work that can be performed above critical power
before exhaustion ensues. The mechanistic basis of the W’ are complex and remain ambiguous.
The W’ was originally described as an anaerobic work capacity, but it is now understood to be
sensitive to manipulating in oxygen delivery and extraction via blood flow occlusion and
alterations in the muscle contraction duty cycle. Additionally, it appears that the amount of work
that can be performed above critical power does not appear to be a determinant of W’, but rather
a consequence of the depletion of intramuscular energy stores like phosphocreatine and
glycogen, and oxygen, as well as the accumulation of fatigue-inducing metabolites like inorganic
phosphate and hydrogen ions, which limit exercise tolerance and determine the W’.
We can conceptualize W’ as a fuel tank where fuel is expended when power output
exceeds critical power and it is refilled when power output is below critical power. However, if
W’s reconstitution during relaxation phases between bouts of work done above critical is
insufficient, a net depletion of W’ will occur and when W’ is fully depleted task failure ensues.
This depletion of W’ may be causally linked to insufficient re-oxygenation of the muscle during
the periods of relaxation. While W’ will be used in its entirety for exercise intensities above
critical power, the proportion of W’ that contributes directly to external work is not constant
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across all power outputs. For example, at rest under occlusion W’ will be used it it’s entirety to
support factors distinct from external work like resting cellular processes and ion handling,
which is demonstrated by resting blood flow occlusion leading to myoglobin desaturation,
increases in adenosine diphosphate, and decreased phosphocreatine. As power output increases, a
greater proportion of W’ would be utilized for external work, though it appears that some of the
energy derived from the utilization of W’ still contributes to factors that are distinct from
external work. Additionally, W’ is reduced following resting blood flow occlusion, which
impedes oxygen delivery. Based on the aforementioned evidence, we can infer that W’ is tightly
correlated with oxygen delivery and availability such that a very low muscle oxygenation
saturation is an indication of depleted W’. Based on empirical evidence that appears to be the
case. Not only is muscle oxygen a predictor of proximity to momentary muscle failure, but
maximum and minimum values of deoxyhemoglobin and oxyhemoglobin, respectively, are
strongly correlated with a loss of force production.
The Impact Of Hypoxia On VO2max, Critical Power, and W’
During exercise the circulatory system is challenged to improve oxygen delivery to the
working tissues. Both convective and diffusive factors regulate oxygen delivery. Convective
oxygen transport refers to the bulk movement of oxygen in the blood and depends on active,
energy-consuming processes that generate flow in the tracheobronchial tree and circulation.
Diffusive oxygen transport refers to the passive movement of oxygen down its concentration
gradient across tissue barriers, including the alveolar-capillary membrane and the extracellular
matrix between the tissue capillaries and individual cells mitochondria. During exercise in
hypoxia and at exhaustion, the circulatory system is challenged to facilitate oxygen delivery to
the working tissues, which ultimately impacts performance and the development of fatigue.
As altitude increases, there is an expected and logical decrease in convective oxygen
transport. Specifically, there is a decreased peak oxygen uptake in the pulmonary system and
systemic circulation and a reduction in pulse oxygen saturation at the capillaries level. At and
above 3,800m, maximal heart rate is also decreased. Given that VO2max is determined through a
combination of central factors, like stroke volume and heart rate, as well as peripheral factors
like arterial oxygen saturation, it is logical that VO2max is meaningfully decreased at altitude
and in hypoxia. These convective oxygen delivery changes can also occur through modifications
in blood flow, and they can even be induced in a healthy human exercising heavily at sea level.
As exercise increases up to a heavy exertion level or close to a maximal power output, there is a
progressive decrease in muscle oxygen saturation to a minimal point or plateau, which gives rise
to exhaustion. In hypoxic conditions, this plateau or bottoming out in oxygenated hemoglobin
concentration is considered an indication of maximal skeletal muscle oxygen extraction as a
product of reduced oxygen availability. These oxygenation and hemodynamics changes can be
observed non-invasively with near-infrared spectroscopy in live time.
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Consistent with the data on hypoxia's dose-response effect on VO2max, there is a
curvilinear decrease in critical power under hypoxia conditions. It is important to note that VO2
at critical power is below VO2max, and that critical power is associated with the highest exercise
intensity where a VO2 steady state occurs. The VO2 steady state indicated the highest intensity
where a ‘metabolic stability’ can be achieved, where metabolic stability is characterized by
minimal disturbances to intramuscular phosphocreatine stores among other factors. There is
evidence supporting the idea that phosphocreatine is not only reconstituted via oxidative means
but dependent on oxygen availability. In hypoxia, convective oxygen transport to the working
muscles occurs, and the VO2 primary component decelerates. Since the VO2 primary component
is considered an epiphenomenon of metabolic stability and has been shown to correlate with
critical power, then an oxygen supply and delivery limitation on VO2 kinetics may impair
metabolic stability and thus explain why critical power is reduced in hypoxia.
Since critical power is lower under conditions of hypoxia, then it holds that a given
absolute intensity will cause a faster depletion of W’ under these conditions. According to the
critical power model, faster depletion of W’ will cause a reduction in time to exhaustion at a
given fixed power output above critical power. This would be associated with an exacerbated
rate of fatigue development in hypoxia, which has been demonstrated by Lee Romer and
colleagues in an investigation titled, Effect of acute severe hypoxia on peripheral fatigue and
endurance capacity in healthy humans. Hence, rather than conceptualizing hypoxia per se as the
mechanism which exacerbates fatigue, it is the effect of hypoxia on decreasing critical power that
leads to a more rapid onset of fatigue coinciding with the depletion of W’ at a given fixed
absolute power output. However, there is also evidence that W’ will be reduced at altitude and
that changes in W’ are related to changes in critical power relative to VO2max, which suggests
that W’ isn’t simply an aerobic energy store as was once believed. Additionally, the effect of
hypoxia on W’ appears to display a threshold characteristic since there is no significant change
in W’ at a lower altitude, but past 4,250m meaningful reductions were observed. Giambattista
Valli and colleagues have suggested that the decrease in W’ at altitude is consistent with reduced
muscle-venous oxygen storage in a paper titled, Exercise intolerance at high altitude: critical
power and W'. This seems plausible given the decreased peak oxygen uptake that occurs at
altitude, which results in lower arterial oxygen saturation and as well as lower muscle oxygen
saturation. Both of these have been shown to cause a direct decrease in VO2max and critical
power. This suggests that oxygen uptake and transport can be rate-limiting factors that determine
critical power and W’.
Pacing With Critical Power
The critical power model describes the relationship between sustainable power output
and severe intensity exercise above the ‘critical power’. In this model W’ is progressively
depleted during exercise whenever power output exceeds critical power and it is reconstituted
whenever power output falls below critical power. Additionally, if W’ is depleted to zero, then
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time to exhaustion also reaches zero, and task failure occurs. If we know an athlete's critical
power output, as well as their W’, we can use this information to inform their tactics in a race.
Most endurance athletes will know if they are a pace pusher or a kicker. A pace pusher
can force a field of runners to run at a fast speed out of the gate knowing that their own max
steady-state speed is higher than their competitors. This athlete knows their best shot at winning
is to slowly burn out their competitors by forcing them to run above their respective critical
power outputs, or critical speeds. The kicker wants to play a different game though. They fare
best when they can lull everyone into complacency early on. A kicker knows that their own max
steady state pace may not be the fastest in the field of athletes, but that their advantage lies in
their ability to force a blistering pace in the back quarter of a race and outkick everyone else to
the finish line.
Anyone who has ever competed in cross country or the middle to long distance track and
field events knows which of the two aforementioned camps they fall into, but seldom are athletes
aware of the science behind why racing tactics are individualized based on their physiology.
However, this can be explained through the lens of critical power and W’.
Let's say we have two athletes, Bob and Jim. Bob has a critical power of 400 watts and a
W' of 10,000 KJ. In this case, 400 watts is the cutoff where if Bob works at a higher output, he
depletes W', and if he works at a lower output, he restores W'. Our second athlete, Jim, has a
critical power of 350 watts, and a W' of 15,000 Kj. Bob is the pace pusher. If he forces a pace of
375 watts out of the gate, he will trick Jim into depleting his W' early on without depleting his
own W'. Once Jim depletes his W' he's done for. The only way for him to reconstitute his W’ will
be to drop below 350 watts of power, and if he were to do that Bob would be long gone by the
time Jim’s W’ was recharged. However, if Jim can lull Bob into complacency early into the race,
his W' will be enough that he can blast off towards the end of the race, and Bob will not have
enough W' to match Jim's speed over a fixed short distance.
In order for the critical power model to accurately demonstrate fatigue and performance
predictions though, a few basic assumptions need to be made. First, sufficient apriori testing data
is required for accuracy. Second, W’ reconstitution rates are individualized and can vary
depending on an individual’s fitness level at any given point in time as well as the modality they
are using. Third, Time to exhaustion pre-tests need to match the racing conditions and finally,
continual inputs are required to get relevant critical power and W’ estimates as fitness changes
over time.
Critical Metabolic Rate
In Perrey and Ferrari’s systematic review, titled Muscle Oximetry in Sports Science, they
state that tissue oximeters provide information on the balance between oxygen supply and
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oxygen demand in skeletal muscle and that regional oxygen saturation represents a tissue reserve
capacity following oxygen extraction. In essence, the concept can be summed up with the
following equation: SmO2%= ((Oxygenated hemoglobin + myoglobin) / (total hemoglobin +
myoglobin)) x 100.
If we combine this the aforementioned concepts relating to regional oxygen saturation
and modeling time to exhaustion with critical power, we can can hypothesize that the following
statement will hold true: Time to exhaustion = SmO2% / ΔSmO2, where SmO2% represents a
live muscle oxygen saturation reading and ΔSmO2 is the rate of change of muscle oxygen
saturation. However, because this statement assumes that task failure will occur at 0% SmO2, it
must be modified based on an individual's minimum achieved muscle oxygen saturation based
on prior date. As a result, a more accurate equation describing the relationship between oxygen
kinetics and task failure is as follows: Time to exhaustion = (SmO2min - SmO2max) / ΔSmO2.
There is evidence showing that the aforementioned equation accurately predicts time to
exhaustion during static exercise. Interestingly, this formula also holds accurate during dynamic
exercise with occlusion, because like static exercise SmO2min is relatively fixed. However,
during dynamic exercise without occlusion SmO2min is too variable for this to be accurate. As a
result, more accurate means are needed to predictive model dynamic exercise without occlusion.
Whereas critical power represents the higher power-output that can be sustained
indefinitely, critical metabolic rate represents the highest rate of steady state oxygen supply and
demand. In essence both critical power and critical metabolic rate can modulate intensity
independent of one another. Demonstrating this concept is a case study from an elite post
collegiate rower I coached through his 2019 competitive season. Over three separate days this
athlete completed time to exhaustion trials on an erg where they held 350, 375, and 400 watts
until failure. For each test I recorded his average power output, time to task failure, and his rate
of change of muscle oxygen saturation, termed ΔSmO2. Based on his average power output and
time to task failure data points I calculated his critical power to be 322 watts. I also calculated his
critical energetic rate using his ΔSmO2 and time to task failure data points. The hyperbolic
equation which describes the relationship between the balance of oxygen supply and oxygen
utilization and exercise tolerance within the severe exercise intensity domain is as follows: Time
to Exhaustion = M’ / (ΔSmO2 - Critical Energetic Rate).
Using this formula I calculated this athlete's critical energetic rate to be -0.05% SmO2 per
second, which represents the rate of change of muscle oxygen saturation that can be sustained
indefinitely before oxygen utilization outstrips oxygen supply. One week after completing the
three aforementioned tests I had this athlete do one final trial where they were asked to hold 365
watts on the erg until task failure ensued. Based on this individual's critical power and critical
energetic rate curves I predicted they would fail in twenty two minutes and thirty eight seconds
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with a ΔSmO2 of -0.29 %/second. In actuality they sustained this power output for twenty two
minutes and forty six seconds with a ΔSmO2 of -0.28 %/second. This demonstrates the fact that
both critical power and critical metabolic rate can predict time to exhaustion independent of one
another. However, critical metabolic rate makes up for many of critical power’s shortcomings.
For example, critical metabolic rate predicts exercise intensity and an athlete's current proximity
to task failure in constant fixed power output, constant mixed power output, and intermittent
activities. Additionally, critical energetic rate removes the need for individualized W’ recharge
rates and it lessens the testing burden required to create accurate predictions compared to critical
power. Finally, the critical metabolic rate demonstrates a clear intensity duration relationship.
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Chapter 17: Fitness-Fatigue Dynamics
In the book Antifragile, Nassim Taleb tells the story of a king who, in a fit of rage,
declares that his son must be punished for a misdeed and that the punishment will consist of
having a boulder dropped on his head, which would without a doubt kill him on impact. As the
day of the punishment grew closer, the king began to regret his decision, yet he was also
reluctant to withdraw his decree of punishment fearing that his subjects would see him as being
weak. As a result, his advisors developed an ingenious solution to his dilemma. Rather than
dropping one large boulder on his son's head, he would break the boulder into a thousand pieces
and drop them onto his son's head one by one. The same total would be dropped on his son, but
rather than it having a fatal outcome it would really just lead to mild discomfort.
This story, in all its silliness, demonstrates a key feature of the biological response to
stress. Specifically, it's non-linearity. We all understand this intuitively. If I were to deadlift 500
lbs for a single rep, it would impose much more stress than deadlifting 100 lbs five times, despite
the fact that the net load is the same in both cases. Similarly, running for 10 minutes at an RPE of
5 arbitrary units is much less stressful than running for 5 minutes at an RPE of 10 arbitrary units,
even though the net amount of stress is 50 arbitrary units in both instances. As a result, it's not
only important how much work we do, and at what intensity, but also how that work is
distributed. Most methods of quantifying training loads under-represent the amount of stress
imposed by short very high intensity work bouts compared to longer, more voluminous,
workouts done at more moderate intensities. One way to get around this issue, and quantify
volume in a more rigorous way, is to use more complex models. One such example is the
impulse response model. While not always practical to apply, the impulse response model gives a
very accurate representation of an athlete's fitness, fatigue, and ability to perform at any given
point in time. This chapter is merely intended to introduce you to the concept of
impulse-response and give you some of the background information as well as some simple tools
to help you apply it if you so chose to do so.
Fitness Fatigue Dynamics
For those who have been training for a few years, it’s well known that early into one's
training career performance improves quickly, then it later improves more slowly, and finally
progress tends to screech to a halt. One reason for this is that early into a training career we can
make substantial improvements with relatively little work, but over time the amount of work
needed to yield further performance improvements has such a high fatigue cost, that any true
‘developmental’ load is bound to carry enough weight of fatigue that we won’t see an immediate
performance improvement. We can understand this concept through the lens of fitness fatigue
dynamics. With any imposed training load there will be a near immediate increase in fitness, as
well as a near immediate increase in acute fatigue.
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In 1984 Eric Banister gave a speech at the Olympic Scientific Congress where he defined
performance as fitness minus fatigue, which was later amended with performance being
multiplied with an exponential decay function that accounts for fatigue. In this model
performance can increase or decrease modestly or substantially over both short and long time
intervals. Using arbitrary units, let's say that after performing a rigorous training session an
athlete gains five AU’s of fitness, with a cost of negative ten AU’s of fatigue. The sum of these
two variables is negative five, which represents performance at the first measured time point
along the fitness-fatigue curve. Despite the fact that this individual did in fact get fitter from
performing a challenging training session, the weight of fatigue is greater than the influence of
fitness, and as a result performance drops acutely. This makes intuitive sense. If you train very
hard today, your performance will likely suffer tomorrow. However, fatigue is reduced at a faster
rate than fitness, which is why we see an increase in performance after an appropriate period of
rest. The term fitness-fatigue dynamics refers to the push and pull relationship between these two
variables, which ultimately dictates the level of performance than an athlete can express at any
given point in time. Before getting into the nuances of how the impulse-response model can be
used to understand fitness-fatigue dynamics, it’s worth noting that this model does not aim to
interrogate the underlying physiology of how these processes occur. In this way, the
impulse-response model differs from descriptive theories of how adaptation occurs as well as the
underlying physiological changes that lead to increases in performance.
In the history of adaptation research, one of the earliest proposed ideas was the concept of
overload by Julius Wolff who linked the loading of bones to their adaptation and remodeling in
the late 1800’s. His hypothesis was later extended to other organs and the term overload was
expanded to include forms of loading that are not mechanical in nature. While Wolff’s general
principle of overload and adaptation was correct, it didn’t explain the underlying mechanisms by
which these changes occurred. It wasn’t until a separate theory, called supercompensation theory,
was proposed that anyone provided a potential mechanistic explanation for adaptation.
Supercompensation theory is rooted in the general adaptation syndrome concept proposed by
Hans Selye in the mid 1900’s. The supercompensation hypothesis is defined by a decline in an
often undefined Y-axis variable during exercise and its recovery after exercise. According to this
hypothesis, the recovery does not only reach pre-exercise levels, but it overshoots it. Despite the
fact that this hypothesis is widely accepted among exercise scientists and coaches it is riddled
with flaws and there is little mechanistic evidence to suggest that it is true. In recent years the
scientific justification for this hypothesis has largely evaporated, yet it continues to be cited in
training books and coaching manuals in a near ubiquitous fashion. I believe this is largely a case
of path dependency.
As early as the 1960’s and 1970’s emerging scientific evidence began to chip away at
Hans Selye’s theories. According to Dr. John Kiely, “Classic Selye inspired theory was straining
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to accommodate evidence demonstrating that neither homeostasis nor the stress response was
static, but varied dynamically under the influence of life history and oscillating biological
rhythms.” Then, as the twentieth century entered its final quarter, the explanatory limitations of
Selye’s model were increasingly exposed. Most notably, the portrayal of stress as a predictable
biologically mediated phenomenon was undermined by the demonstrable effects of non-physical
factors on the physiological stress response and an emergence of increasingly convincing
evidence that the stress responses were not generalized and non-specific, but rather highly
individualized and context specific.
You may be wondering if this really disproves the notion that supercompensation exists.
Can the stress response not be highly individualized, yet still follow the supercompensation time
course? This is a question that I had wondered about myself, and there is a wealth of information
repudiating supercompensation theory. The supercompensation theory implies that recovery
periods are essentially for adaptation. However, this need not be the case. For example, the heart
adapts to exercise despite continuous contraction and skeletal muscles can adapt and hypertrophy
in response to chronic electrical stimulation applies continuously over weeks as well. Despite
being propagated for decades, there is little evidence that the supercompensation time course is
essential for adaptation. In contrast, there are hundreds of scientific references supporting an
alternative hypothesis that signal transduction pathways mediate all adaptations to exercise.
According to the signal transduction theory, specific sensor proteins detect exercise-regulated
signals which are then computed by transduction pathways or networks. These early signals
regulate downstream events including gene transcription, gene translation, protein synthesis, and
protein breakdown. The results are tissues, organs, organ systems, and organisms that have
adapted to exercise.
Impulse-Response Modeling
The impulse-response model quantitatively relates an individual's performance potential
at a specific time point to the cumulative effects of prior training loads and it succinctly describes
an individual's exercise dose-response relationship and handles the complicating factors of
nonlinear time dependence and individuality in a single framework. Eric Banister and colleagues
recognized the difficulty in translating the results of training studies into practice and in their
original paper titled, Modeling Human Performance In Running , they state that, “quantitative
data relating performance to different programs of training has been obtained by several
investigators but it is still difficult to predict the results of a particular training program.” To
address this need Eric Bannister conceived the impulse-response model for training planning
organization and optimization. Although its use to date has primarily been confined to laboratory
studies, the model has attracted renewed interest among elite athletes. In examining a
hypothesized time course that followed from training, Chris Calvert and colleagues proposed that
performance kinetics behave like a first order system. A system whose behavior varies over time
is typically modeled using ordinary differential equations.
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The impulse response model provides a window into the dynamics of adaptation to
physical training where we have positive training effects (PTE) and negative training effects
(NTE). The PTE and NTE profiles qualitatively correlate with measurable physiological
parameters related to fitness and fatigue respectively. For example, the kinetics of iron status
biomarkers in female runner generally follow that of the NTEs, as do biomarkers of muscle cell
damage such as elevated serum enzyme activities including creatine kinase, lactate
dehydrogenase, and aspartate aminotransferase.
Figure thirty-two shows a recursive form of the impulse-response equation. A recursive
formula is a formula that defines each term of a sequence using preceding terms. As such,
recursive formulas must always state the initial term, or terms, of the sequence. In order, the
terms used in this equation are as follows: P(t) and P(0) represent performance at a specified, and
defined, point in time and the initial performance level respectively; Ka is the weighing factor for
PTE’s, or positive training effects; τa is the time constant and decay factor for PTE’s; Kf is the
weighted factor for NTE’s or negative training effects (fatigue); τf is the time constant and decay
factor for NTE’s; and WS is the ‘work score’ or daily training does.
Under all circumstances the weight of Ka is less than the weight of Kf and the time
constant τa is greater than the time constant τf. This means that when initial conditions are
present there is a positive and negative training effect from a given training stimulus, but
performance decreases because the weight of negative training effects supersedes the weight of
positive training effects. However, during continued periods of training the net effect of PTEs
supersedes the net effect of NTEs because τa is greater than τf, which means that training
induced fatigue fades at a faster rate than training induced adaptation. Finally, during deload or
taper periods performance rapidly increases because Ka and Kf both decrease meaningfully, but
PTEs degrade much faster than NTEs, which results in a transient expression of peak
performance.
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Part V: Integrated Biomechanics
Chapter 18: Variations Of Human Movement
Human movement is a combination of both mobility and stability, as well as the brain’s
ability to plan and execute movement. Mobility, or passive range of motion, can be equated to
our movement potential and it is influenced by the extensibility of our muscle, the flexibility of
our connective tissues, and the kinematics of our joints. Mobility is regulated by the central
nervous system, which is why someone out under general anesthesia will immediately gain more
range of motion. Stability on the other hand refers to how well we an individual can control
themself dynamically, statically, and passively, through the ranges of motion they currently
possess. Finally, we have the brain’s ability to plan and execute movement, which can best be
explained through dynamical systems theory, which asserts that human movement is an intricate
network of co-dependant systems including the respiratory, circulatory, nervous,
skeletomuscular, and perceptual systems. Proponents of dynamical systems theory advocate that
humans do not come pre-programed with the ability to perform certain movements, but rather
that movement emerges through a process of self-organization in response to environmental and
task specific cues. It follows that no two environments will ever be exactly the same and
therefore no two individuals will execute a given movement in the exact same manner either.
When the human nervous system is tasked with planning the execution of a novel skill,
like learning to kick a soccer ball, there is no kick program available to tap into at any
movement. Instead, novices search for and display many different movement strategies while
learning to perform a novel task. As that individual practices the new skill, specific components
of their movement pattern become stable, consistent, and repeatable, which is referred to as an
attractor state. However, this specific skill composed of attractor states also contains variable
components called fluctuators, which allow it to be flexible enough to accommodate the varying
demands placed on an individual like taking the newly acquired skill of kicking a soccer ball on
flat ground and then learning to kick the ball at different angles on an uneven playing field.
​
Variations of Human Movement
​
Most modern gym movements are simple and take place in a single plane of motion such
as vertical pressing and pulling, horizontal pressing and pulling, squatting and hinging. These six
patterns and their various derivations compose the vast majority of training programs. I am not
inferring that there is not a great value in specialization, but we also need to acknowledge the
fact that human movement is infinitely complex and by clinging to the reductionist ways of our
specialty we ignore the big picture. Movement allows all systems to be freely expressed, but by
training solely in the bilateral sagittal plane, we rob ourselves of what it means to be human.
Equally as important as the aforementioned patterns are those that involve hanging, tumbling,
inverting, lunging, twists, throwing, and so forth. As stated by Ido Portal, “It does not matter how
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much you can load in alignment - if you cannot absorb shock outside of those positions you are
weak,” and as we know, going out of alignment at one point or another is a certainty, not a
probability. As such, there is value in training tri-planar and multi-planar movements in various
combinations. Rather than training these movements for load, reps, or time as you would for
sport-specific movements, it is best to create flow in your movement practice when the goal is to
improve variability. Flow is characterized by a chaotic and improvised practice where one is
constantly changing joint angles, sequencing, entries and exits, and the movements contained in
a given session. Additionally, it is key that one’s practice is deliberate in this effort and that the
focus is on quality of movement, and exploration, versus trying to get a set amount of work done
in a given period.
When trying to develop flow in a movement practice many people are hindered because
they perceive there is a right or wrong way to move. There are more safe or less safe ways to
move, more stable and less stable ways to move, more economical and less economical ways to
move, and so forth, but the truth is there is no one right way to move. We all create some form of
compensation to generate motion and no one is perfect. Even if there were a perfect standard of
movement no one would be able to meet it. In order to better understand movement, most people
pick skills they want to cultivate. Then they learn the muscles involved, how to breathe in that
pattern, how to brace, how to relax, and so forth. As this process unfolds, people aren't always
conscious of it, and as a result, they often can't transfer these skills to other movements quickly.
But, by zooming out, or taking a step back, they can see the big picture and individual skills
become easier to learn. For example, if someone wants to get better at handstand push ups where
do they start and how do they identify limitations or create progressions? One way to tackle this
issue is to work through the skill in a stepwise fashion focusing first on movement freedom, then
strength, endurance, and variability.
Movement freedom encompasses the ability to access the relevant ranges of motion to
perform a movement safely and without significant mechanical compensations. For example,
having sufficient range of motion in the wrists and shoulders to be able to support oneself in the
inverted position during a handstand pushup. Movement strength is the ability to support oneself
through the entire functional range of motion for a given movement without any mechanical aids
or supports. For example, having the core and shoulder strength to support oneself while inverted
during a handstand pushup, or having the strength to stand up with a given load after controlling
oneself through the eccentric phase on a front squat. Movement endurance is the ability to
withstand repeated stressors in a given movement pattern. For example, having the ability to
tolerate a meaningful amount of handstand pushup volume in training week after week without
an increased risk of shoulder, wrist, elbow, or neck injuries. Movement variability is the ability
to react to changing movement demands and stabilize. For example, having the ability to create
effective compensatory movement patterns under fatigue, without injuring oneself, or having the
ability to transfer a given skill to a context other than that which has been previously practiced.
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Each of the four aforementioned characteristics can function as a lens through which you can
view movement in order to identify areas for growth, and will be expanded on in the preceding
chapters.
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Chapter 19: Tensegrity And Regional Interdependence
Traditional anatomical education focuses on the structural and mechanical understanding
of individualized human structures, such as muscles, ligaments, nerves, and organs. While
anatomy textbooks list that we have roughly six-hundred muscles, it is more accurate to say that
we have one muscle and six-hundred pockets of fascial webbing. Fascia is a densely woven
system in the body, resembling a spider’s web, that covers every muscle, bone, nerve, and organ.
It should be noted that these fascial coverings are not separate entities. They are part of one
continuous structure that wraps us from head to toe without interruption. In this way, you can see
that each part of the body is connected to every other part by the fascia, like a gigantic spider’s
web. However, this limited description of fascia only encapsulates its function from a
morphological tissue and structure perspective. In 2007 at the International Fascia Research
Congress, Robert Schleip and Thomas Findley proposed a much more nuanced definition of
fascia stated as, “Fascia is the soft tissue component of the connective tissue system that
permeates the human body, forming a whole-body continuous three-dimensional matrix of
structural support. It interpenetrates and surrounds all organs, muscles, bones, and nerve fibers,
creating a unique environment for body system functioning. The scope of this definition and
interest in fascia extends to all fibrous connective tissues including aponeurosis, ligaments,
tendons, retinaculum, joint capsules, organ and vessel tunes, and so forth”.
​
Tensegrity and Tissue Properties
The human body is a massive network length-tension relationship. Whatever muscles
may be doing individually, they also operate across integrated body-wide continuities within
their fascial webbing, which forms a connective tissue fabric that warps to the shape of the body.
Thus, all tissues are interconnected and all force transmission or strain will be felt by all tissues
to some degree. In this way, the human body acts like a tensegrity structure. The word tensegrity
is a portmanteau of the words tension and integrity. By definition, tensegrity is the characteristic
property of a stable three-dimensional structure consisting of members under tension that are
contiguous and members under compression that are not.
Buildings do not act like tensegrity structures. For example, if a tree comes crashing
down on one side of the house it will damage the roof and the structural components under that
spot may collapse, but the rest of the building will remain in perfect condition as if nothing
happened. The building collapsed where force was directly applied and where the strain was
most significant. This is intuitive and easy to understand. If you smash the downstairs window of
a house with a baseball you wouldn’t expect the upstairs toilet to shatter. However, that is not the
case with a tensegrity structure like the human body. A tensegrity structure breaks at its weakest
point regardless of where a force is applied. Therefore, as humans and tensegrity structures a
stressor applied to our foot or shoulder may manifest as pain in the lower back or vice versa. The
human pelvis, which consists of three bones fused together, is a great example of the principle of
tensegrity. Without muscles, ligaments, and fascia the pelvis would float somewhere around our
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midsection. Luckily, this isn’t the case. The pelvis is like a house of cards, and what keeps a
house of cards from collapsing to one side or another is an equal amount of tension imparted in
each direction. On the front of the pelvis we have the hip flexors and on the back we have
hamstrings. If the hamstrings lack tension the pelvis will tilt forward and give the hip flexors
leverage. Additionally, if one or both sides of the pelvis carry too much tension then an
individual will be more prone to injury, which will manifest where the tensegrity structure is
weakest.
If you want a practical demonstration of how our bodies act like tensegrity structures you
can attempt a forward fold, marking how far down you were able to touch. Then spend one
minute rolling a lacrosse ball under your bare feet before retesting your forward fold. There is a
high probability that your ability to reach further increases. The reason for this is that the sole of
the foot and hamstring are connected via the superficial back fascial line and as a result the
rolling of the foot provided neurological stimulation that caused a decrease in tension both in the
foot as well as through other areas in the superficial back line such as the hamstring. This is a
case where a local intervention has a regional effect on tension, which is only possible because
the relative tension in any given area of the body is influenced by the tension in other
interconnected regions.
If we choose to use this model as our way to view the structure and adaptation of
bio-organisms, then we can start to consider how stress being applied to the human body can lead
to targeted and specific adaptations depending on what type of stress is applied and where it is
applied. Different forms of mechanical stress are classified in a multitude of ways including
torsion, tension, shear, ease, compression, stretch, bending and friction. Each of these different
mechanical stresses lead to a different form of mechanotransduction, which is the process
through which cells sense and respond to mechanical stimuli by converting them into
biochemical signals, which elicit specific cellular responses. This process of turning mechanical
stressors into chemical activity is capable of changing gene expression and our inflammatory
response. For example, if you perform a set of moderate load bicep curls to failure you will
stimulate the mechanoreceptors in your bicep, which will lead to a cascade of biochemical
responses that will help shape the way you adapt to that mechanical stimulus.
Fascia and Fascial Lines
Regardless of what muscles do individually, they also affect tissues throughout the entire
body through fascial based interconnections. These interconnections are called facial lines and
are seen by tracing the body’s connective tissue structures during dissection. Fascial lines help
create stability, movement, elasticity, compensatory postures. While all tissues in the body are
linked to the fascial network, the fascial lines can be distinguished and viewed as distinct
entities.
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The superficial back line connects the entire posterior side of the body running from
underneath the feet to the top of the skull and it helps keep the body in an upright posture.
Because of the structure and function of this fascial line it’s not uncommon that athletes lacking
intrinsic foot strength and flexibility present with lower back pain. When viewed through a
traditional lens this type of back pain’s origin is often mysterious as it cannot be attributed to a
standard local tissue related diagnosis, however when looking through the lens of the fascial
​theory alternative explanations can be gleaned. The superficial front line, which connects the
entire anterior side of the body running from the top of the feet to the sides of the skull, is in
juxtaposition with the superficial back line when the body is upright and the hips are extended,
The lateral line begins on both sides of the body on the center of the foot and frames the body by
extending along the outside of the leg and thigh, passing over the torso in a zigzag pattern and
attaching near the ears. The function of the lateral line is to stabilize the torso relative to the legs,
to help with coordinating full body movements, and to control forces transmitted from the
superficial front and back lines.
The spiral line creates a loop around the body in two circles, running opposite one
another right and left. Starting at the skull, these lines cross the upper back and run under the
arms until they go around the chest crossing each other at the naval and then running to the sides
of the hips and forming an ‘X’ before trailing down the outside of the thighs, running under the
feet, and finally running back up the thighs and converging at the spinal erectors. The spiral line
stabilizes the body in all planes of motion and is especially useful for regulating the position of
the knee during the gait cycle by connecting the foot and pelvis. Because of the position of the
spiral line individuals with excessive hip flexor tone or strength, compared to pec tone or
strength, often present with lower back pain.
The arm lines are the most complex of those previously mentioned since they run through
the shoulder joint in four different planes and along the arm on multiple sides including two deep
lines on the front and back of the arms respectively. With the structure and function of these lines
in mind, we can consider how this influences exercise selection. For example, if we want to train
our biceps through all of the functional ranges of the muscle we cannot only rely on standard
single plane pronated and neutral grip curl variations. We may also want to incorporate other
functions of the bicep into our training repertoire including bracing the arm in a locked out
position, creating shoulder flexion, and working rotationally along the plane that the muscle
fibers are laid out.
The functional lines cross both the front and back side of the body, creating a large ‘X’ on
both sides. Additionally, a third function line runs from the shoulder to the inside of the knee on
the same side. The functional lines are not very active during static standing posters, do aid in
stabilizing the body and generating power in movements where we push off the ground to create
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force from the opposite side of the body. For example, winding up to throw a punch by pushing
off the ground and rotating the hips.
Finally, the deep lines form a three-dimensional shape rather than a line, taking up more
space than any other fascial line and running through the legs, around and the torso, through the
chest cavity, and around the neck. The deep line contains many stabilizing muscle fibers and can
be contraindicated in many injuries if dysfunction is present.
​
By working in sync with one another the different facial lines aid in the generation of
balanced, fluid, and integrated movement. This runs counter to the traditional view of muscle
function where muscles work only at their point of origin and either contract or resist. When we
consider fascia’s ability to transmit force the picture becomes much more nuanced. In the past,
fascia has been viewed as a passive structure that gives the muscle extra support and serves as a
second skin barrier. However, it actually serves an integral role in the human body. Contrary to
popular belief, fascia is not a passive tissue and it has the ability to contract and has its own
sensory network. On a pound by pound basis, fascial can have upwards of eight times the tensile
strength of muscle tissue. It is my speculation that the contractile abilities of fascia are
responsible for many of the superhuman feats of strength seen by acrobats, climbers, gymnastics,
and elite weightlifters who can squat upwards of four times their bodyweight.
Pound for pound gymnasts and acrobats are some of the strongest athletes and if you
gave them a barbell it is likely they would outperform many high level strength athletes. Yet,
gymnasts and acrobats rarely train with weights. I believe much of that strength comes from the
fascial system, which is developed as a result of their training with complex and full body
integrated movements under loading. These movements which often involve twisting, contorting,
and rotating under load are the perfect stimulus for creating adaptations in the fascia and
exercising it’s contractile abilities. However, most people simply cannot perform these
movements let alone do so under load due to the fact that their fascia is bound up as a result of
repetitive training in a single plane of motion, and repetitive postures. In order to depict the
negative effects these inputs have on fascia I like to use the following tee-shirt analogy. If you
pull up on the right corner of your tee-shirt the whole shirt will move along with it, not just that
corner. Then when you let go of that corner the shirt will snap back to its original spot and there
will be no wrinkles in it. But, if you pull on that corner and hold it there for hours, or days, when
you release it, it will not snap back and there will be wrinkles. This is akin to what happens to
our fascia when we perform repetitive training in a single plane for years on end. A good
example of this is shoulder or pec minor pain that comes from repeated bench press training.
Through a traditional lens one might say that an athlete can just do some external rotation work
or rear delt work to offset the bench pressing or balance out the motions, but in practice this
seldom works. Comparably, an athlete will always be able to overload the pecs more than their
antagonists and, as a result, viewing the body through this narrow structural balance perspective
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is not the answer. It’s not uncommon for athletes to also try to take the approach of doing
horizontal rowing to offset horizontal pressing, but this is equally misguided as the pecs and lats
both function as internal rotators of the humerus which further compounds the issue. It is only
through the lens of holism that we can begin to move in the right direction by viewing the body
as a single integrated unit. This means addressing restrictions in the fascia, breaking the pattern
of repetitive motion, and training with complex movement patterns that integrate the body as a
single unit.
Regional Interdependence
Earlier in this chapter I stated that many musculoskeletal issues, like back pain, are often
non-attributable to standard tissue related diagnosis and as a consequence of that we need to
focus on the interrelationships between muscles and their functions to understand those types of
issues. This is directly related to the concept of regional interdependence, which asserts that
seemingly unrelated musculoskeletal impairments in remote anatomical or body regions may be
associated with or can contribute to one another. Additionally, contemporary research on
regional interdependence has shown that varying body systems can also be affected by one
another. What this means is that the body needs to be observed in its entirety if we are to truly
understand it. This runs in opposition to the traditional medical model where each component is
assessed in isolation. Vladimir Janda, the late 1960’s Physical Therapist, was ahead of his time in
understanding this concept when he stated, “The motor system functions as an entity. It is a
principally wrong approach to try to understand impairments of different parts of the motor
system separately without understanding the function of the motor system as a whole”. When we
embrace this concept wholeheartedly, we can begin to see human movement from a holistic
standpoint.
One way to view regional interdependence is through the interrelationship
between mobile and stable segments of the body. If any joint that has it's primary movement in
one plane of motion is considered a stable joint, and consider those that don't have just one
primary range of motion a mobile joint, you can observe that the human body works in a pattern
of alternating stable segments connected by mobile segments. For example, if we work from the
ground up we can observe a pattern of alternating mobile and stable joint segments, as
demonstrated in figure thirty-three.
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By looking through the lens of regional interdependence and alternating mobility and
stability you can see how dysfunction in this pattern will occur through predictable patterns of
compensation. For example, Crossfit athletes often present with low back pain, shortened hip
flexors, and a lack of thoracic spine mobility. This lack of mobility and range of motion in the
hips and thoracic spine, which should be mobile segments, causes a compensation pattern. As a
result, the lumbar spine, which should be a stable segment, sacrifices that stability in order to
obtain more range of motion. As a result, they often end up with low back pain that is
non-attributable to the standard tissue based diagnosis and in turn it often goes solved. This same
concept can be applied to other areas of the body as well. For example, one might lose thoracic
mobility and get neck and shoulder pain as a result of that or one may lose wrist mobility and get
elbow pain as a consequence. Thus, examination of joints that are both proximal and distal to
joints that are afflicted with pain is a crucial concept of regional interdependence.
Thus far I have discussed the concept of regional interdependence as it relates to pain and
rehabilitation. Specifically, how a lack of mobility or stability in a joint can impact the function,
and cause pain, in the joints proximal or distal to it. However, this concept also has implications
to, and applications for, sports performance. Whereas the mobility of a joint can impact those
surrounding it, the strength and endurance of the musculature surrounding a joint can impact the
function of muscles upstream from it. In 2018 Dr. Maximilian Sanno and his colleagues at the
German Sport University of Cologne conducted a study titled, Positive Work Contribution Shifts
from Distal to Proximal Joints During a Prolonged Run. The investigators found that as
extended duration runs, at a slightly slower pace than 10,000m race efforts, are performed,
runners progressively do less and less work with their ankles and progressively do more work
with their knees and hips. What this shows is that as distal joints and muscles fatigue more
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proximal ones compensate to take the brunt of loading, raising the question of whether or not the
runners could improve their performance simply by strengthening their ankles and improving
fatigue resistance in the surrounding muscle groups. According to the investigators in this study,
that does in fact appear to be the case. As a result, I would make the argument that athletes
involved in work capacity sports that require high levels of strength and endurance train the
fatigue resistance of muscles that are both proximal and distal to the primary muscles used in
their sport. For a Crossfit athlete this can mean strengthening the feet, ankles, elbows, and wrists,
all of which are often overlooked in training programs. Another application of this concept is
what I refer to as landmark movement routines which can be performed as stand alone training
sessions or tacked onto the back of a stimulative training session. Landmark movement routines
consist of foot, ankle, diaphragm, thoracic spine, neck, and shoulder training. Addressing these
common problem areas will often remediate upstream and downstream issues as well, making
landmark movement routines a low investment insurance policy for athletes in a variety of
sports. That said, if someone prevents with a specific pathology or movement dysfunction then
that should be addressed with a targeted intervention. However, for those who move well and
aren’t currently experiencing any pain or dysfunction you'll find a landmark movement routines
are often enough to stave off injuries and improve resilience.
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Chapter 20: Gait, Posture, And Locomotion
Leonardo Da Vinci once remarked that in addition to being a work of art, the human body
is a marvel of engineering. Da Vinci’s statement is particularly true when it comes to the
anatomical structures necessary to allow for bipedality since walking on two legs presents an
engineering conundrum. During the gait cycle, our lower extremities must be supple enough to
absorb shock and accommodate for changes in terrain as well as become rigid enough to tolerate
the forces of acceleration during propulsion off the ground. This is in contrast to quadrupeds,
who have the luxury of being able to absorb shock with their forelimbs while their hind limbs are
used for support and acceleration like a pouncing house cat for example. The human body can
accomplish these contradictory functions through a series of complex articular interactions that
allow the same anatomical structure to behave differently during the early and later phases of
gait. In this way, gait is not owned by the feet as many would assume. Instead, it is owned by the
processes of perception of all our senses. Because of this, and the fact that our bodies are a
network of length-tension relationships, gait and posture are the epitomes of repetitive
compensation patterns.
In addition to the engineering quandary posed by bipedality, an even more significant
problem lies in the fact that the human body is not symmetrical. The neurological, respiratory,
circulatory, muscular and vision systems are not the same on the left side of the body as they are
on the right. They have different responsibilities, functions, positions, and demands placed on
them. These systemic asymmetries are a fantastic design, and in fact the human body is balanced
through these systemic imbalances. For example, the torso is balanced with the liver on the right
side and the heart on the left, and extremity dominance is balanced through a reciprocal function,
meaning that the left arm moves with the right leg and vice versa.
When these normal imbalances are not regulated by reciprocal function during walking,
breathing, or other activities a pattern emerges which creates structural instabilities and often
manifest with musculoskeletal pain or weakness. By assessing an individual's posture and gait
we can gain insight into unilateral discrepancies, discrepancies between active and passive
ranges of motion, potential aberrant joints, as well as global compensation patterns.
What is Posture?
The dictionary definition of posture is “the position in which someone holds their body
when standing or sitting”. For something so simple and mundaneI find it paradoxical how
complex posture can be when we seek to understand the underlying factors that influence it.
Posture is a reflection of the ‘position’ of many systems that are regulated, determined, and
created through limited functional patterns which reflect our ability and inability to breath,
rotate, and rest symmetrically. The term ‘limited functional pattern’, refers to a movement that is
restricted in directions, planes, or normal boundaries of functional range as a result of
improvement of joint and muscle resting positions. An individual's function is therefore limited
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because of soft tissue and osseous restrictions that prevent them from using muscles and joints in
their normal range.
Adaptation and compensation for these limitations require neuromotor encoding and
hyperactivity of muscles that are placed in improper positions that exceed normal physiological
length or in positions that make them a mover or counter-mover in planes and directions that are
not observed when one is in a neutral or more symmetrical state of rest. This compensatory
activity and hyperactivity usually become dyssynchronous in the accessory muscles of
respiration and at the appendicular flexors and axial extensors, thus limiting functional rotation at
the trunk and through the lumbopelvic-femoral and cranial-mandibular-cervical complex”. This
means that these limited functional patterns which result from an improper joint position, soft
tissue restrictions, muscle weakness, and maladaptive biomechanics determine the compensation
patterns we employ, which give rise to our default posture and mode of locomotion.
​
What Constitutes Perfect Posture?
​
"Sit up straight:, "stop slouching", "stand up tall". These are all statements that aim to
instill a sense of perfect posture as defined by the society at large. The reality is that we cannot
truly, or objectively, determine what perfect posture entails but there are common positions that
should be expressed to both increase longevity and alleviate movement dysfunctions. These
include a neutral pelvis, neutral head position, not rounding the upper back, keeping the ribs
pressed down, and keeping the abs braced. A lack, or excess, of any of these positions, can lead
to issues such as thoracic kyphosis and hyperlordosis.
Thoracic kyphosis is a forward rounding of the back. While some rounding is normal, the
term ‘postural kyphosis’ is used to reference an exaggerated rounding of the upper back . This
impairment results from short, and weak, hamstrings, and often serratus anterior, combined with
overactive pecs and lats. In many cases, the sternocleidomastoid muscle will present as
overactive as well, which leads to the forward head posture that often occurs in those with
postural kyphosis. Therefore, when treating kyphosis, our goal is to inhibit the lats while
simultaneously lengthening the hamstrings and serratus anterior. Oftentimes those with postural
kyphosis present with a posterior pelvic tilt as well, which occurs via an extension of the lower
back. A posterior pelvic tilt occurs when the front of the pelvis rises, and the back of the pelvis
drops. This typically occurs in those who spend a lot of time sitting, which ‘shortens’ their hip
flexors. The hip flexors connect the femur to the hips and lower back, and while standing,
shortened hip flexors will cause the hip to tilt forward and the curvature of the lower back to
increase.
Lordosis refers to the normal inward curvature of the lumbar and cervical spine regions,
and an excessive inward curvature is known as hyperlordosis. A significant feature of
hyperlordosis is a forward pelvic tilt, also known as an anterior pelvic tilt, which results in the
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pelvis resting on top of the thighs. The primary cause of hyperlordosis and anterior pelvic tilting
is a combination or immobile hip flexors, a tight lower back, as well as weak glutes, hamstrings,
and abs.
In our modern climate, where we spend much of our days sitting, hunched over typing on
computers, and with our heads craned downward looking at phones, we often lose the vital
capacity to stand erect without encountering the aforementioned issues. Those covered in this
chapter are some of the most commonly encountered, and pervasive, postural faults and
understanding how to spot and treat them is a big step in developing a system to understand
human movement. Once you learn to identify these issues, you can also begin to observe the
compensation patterns that unfold around them.
When discussing posture it's important to distinguish between acute and chronic. While I
believe chronic thoracic kyphosis, or lordosis, are issues that should be addressed I do not think
these positions are inherently bad. For example, in some circumstances an athlete may leverage
their ability to get into lordotic posture in order to gain a mechanical advantage while sprinting
or deadlifting. Additionally, a kyphotic posture may confer a benefit during a sandbag carry as it
allows for more functional length in the arms due to the forward rounding of the shoulders which
makes it easier to grab the bag. The issue with these postural faults is not that we have the ability
to get into those positions or that we can leverage them in specific scenarios, but instead when
they become our normal resting postures or when we cannot get out of those positions. This
distinction between acute and chronic is critical as many positions which appear to be
maladaptive for general health and wellbeing, or as normal resting postures, can be leveraged to
a positive effect during sport as long as the athlete is able to find neutral or a safe baseline
position after the task is complete.
Postural Patterns
While the concept of a postural pattern is a bit reductionist in scope, it is mighty in that it
allows a practitioner or coach to take in, chunk, and convey large amounts of information
quickly, which can help them decide how to move forward with a movement training program.
The patterns describe an individual's musculoskeletal position, and overactive and underactive
joints and muscles. Some of the most common compensation patterns people fall into are the
Left Anterior Interior Chain (AIC) pattern, Right Brachial Chain (BC) pattern, and Posterior
Exterior Chain (PEC) pattern, which come from the Postural Restoration Institute. Before
discussing the specifics related to each of these patterns, it's necessary to recognize that they all
manifest from the inherent asymmetry between the left and right side of the body. While this
asymmetry should be balanced through a complex system of imbalances, problems arise when
disturbances in this system occur.
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A typical example of the inherent asymmetry of the human body is the diaphragm which
has a larger attachment on the right side and is more stable there as a result. Our diaphragm is a
primary spinal stabilizer and is the primary muscle of respiration. With the average adult having
an average daily respiration rate of twelve to twenty-five breaths per minute this means we use
the diaphragm 18,000-36,000 times a day, and as a result, if it's not working correctly it can have
a deleterious effect on our posture and ability to withstand loading. An example of this would be
the left side of the diaphragm flattening out which in turn causes the left abdominals to become
less active and the ribs on the left side to flare outwards. As a result of this, our trunk will also
bend slightly toward the right, and our left side of the pelvis will rotate forward, which is a
crucial feature of the left AIC pattern. When the left side of the pelvis is rotated forward in this
position, we stand more on our right leg than our left. As a result, the pelvis will shift more load
onto the right foot than the left foot and the load will resign on the outside of the right foot and
instep of the left foot, which often causes lower back, knee, and hip pain. A classic example of
the left AIC pattern is The Statue of David.
When someone is in the left AIC pattern, and the pelvis rotates to the right side of the
body, he or she will often compensate by counter-rotating their trunk to the left as a means of
keeping their body oriented straight ahead. The primary muscles that keep the body in this
leftward upper body counter rotation are the muscles that comprise the right brachial chain. In
this scenario, a one-sided lower body problem gives rise to a one-sided upper body counter
compensation, thus leading to the formation of the right BC pattern. When the body shifts into
the right BC pattern the ribs flare on the left side while the trunk rotates to the right. This
orientation of the ribs often causes the right scapula to sit lower and farther from the spine than
the left scapula, which makes it inherently unstable. Because the scapula is the base of the
shoulder joint, this pattern often locks down the right shoulder, which can manifest in ways
ranging from general pain to rotator cuff injuries, impingements, or slap tears.
The final compensation pattern I will discuss is the Posterior Exterior Chain pattern. This
pattern often emerges when someone has been stuck in the left AIC pattern for an extended
period of time, and as a result, they create a secondary compensation to allow for functionality
without pain. The PEC pattern is essentially a bilateral AIC pattern meaning both sides of the
pelvis have rotated forward. This causes a dramatic arch in the lower back. In return, the thoracic
spine will come into extension, the abdominals turn off, and subsequently the ribs flare out on
both sides. When this occurs, the head and shoulders move forward to aid in reaching or pressing
activities, which can result in shoulder and neck pathologies, persistent headaches, and often low
back and knee pain.
​
Gait and Locomotion
As previously mentioned, walking is a compensatory strategy. In order to assess faults
and compensations in gait, it is essential to understand the intricacies of a proper gait cycle. The
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gait cycle is broken into two primary phases, the stance phase and swing phase, which can both
be broken down into various sub-phases. When analyzing the gait cycle, one foot is taken as the
‘reference foot,’ and all motions are studied relative to it. The Stance phase is the portion of the
gait cycle in which the foot remains in contact with the ground. This phase constitutes roughly
60% of the gait cycle and can be further broken down into the five following movements:
1. Initial contact - during the initial contact the heel is the first bone of the lead foot to touch
the ground.
2. Loading response - in the loading response phase we transfer our weight onto the
reference foot, shifting to a flat-footed position, which allows us to absorb shock and
begin forward motion.
3. Mid stance - during the mistance we align our center of mass with the reference foot.
4. Terminal stance - during this phase of gait the lead, or reference, foot begins to rise while
the toe is still in contact with the ground.
5. Toe off - during toe off the reference foot rises and swings in the air, which begins the
swing phase of the gait cycle.
The swing phase is the part of the gait cycle where the reference foot is not in contact
with the ground and it swings through the air. This phase constitutes roughly 40% of the gait
cycle and is composed of three parts which include the initial swing, mid swing, and terminal
swing. These represent the different orientations of the reference limb as it moves through space.
While there are countless potential gait-related dysfunctions, some of the most common are as
follows:
6. Contralateral hips and shoulders moving out of sync.
7. Unilateral discrepancies between hands, shoulders, hips, and feet.
8. Knees extending when they should be flexing.
9. Overpronation of the feet.
10. Leaning to one side over the other.
11. Rotational orientation of hands and feet.
In gait literature, there is quite a bit of debate as it relates to working through gait-related
dysfunction, or retraining gait. Few studies compare holistic impacts of conducting gait
retraining versus not conducting gait retraining. However, there seems to be good evidence
supporting the fact that gait retraining can halt or slow the progression of some pathologies and
even reverse them in some cases. The clinical application of gait retraining is beyond the scope
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of this book or my depth of knowledge on the topic, but I can speak to the level of its application
in sport. The most applicable example being running as there is a large body of evidence linking
mechanics with injury, which justifies altering those mechanics. While more work is needed to
understand the optimal way to retrain gait patterns in runners, simple cues that correct the cause
of the faulty pattern are often a powerful enough tool to begin catalyzing change. Figure
thirty-four lists the most commonly observed faults in runner’s gait patterns, their potential
causes, and cues or solutions that can be used in the gait retraining process.
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Chapter 21: Pain, A Complex Emotion
Language is important for many reasons. Some uses of language are practical, like
instructing an athlete during a training session or communicating the nuances of their program to
them. Other times language is helpful in conveying heartfelt needs, communicating emotions, or
resolving issues. Language is so ubiquitous and comes in handy in such a wide array of
circumstances that it would be foolhardy to denigrate it as being unimportant. Still, it seems that
language is not up to the task of capturing the fullness of reality, or conveying the intricacies of
complex emotions like pain. For something so familiar that everyone has experienced at one
point or another, pain is paradoxically difficult to define. In the literature pain is described as a
complex emotion with the teleological function of preventing us from harming ourselves. Said
differently, pain is a public service announcement about a credible threat to our safety. In the
case of pain induced by a burn the message is simple. Fire is dangerous! Do not touch it again!
Pain is also emotionally traumatic, which ensures that we remain permanently keen to avoid
whatever caused it initially. However, the biology of pain is never really straight forward, even
when it appears to be. Take chronic pain, phantom limb pain, or pain with no apparent cause, for
example. What information is encoded in that? Perhaps pain is not only a message from injured
tissues to be accepted at face value, but rather that it is a complex experience that is thoroughly
tuned by our brains. In this chapter I'll delve into the science of pain and how pain may be
influenced by neurological, psychological, and physiological factors.
Plasticity, Pain, & Perception
​
Neuroplasticity is the capacity of the brain to adapt and remodel itself as a result of an
individual's interactions with their environment. Plasticity can have positive or negative
outcomes. We can leverage the ability of our brains to adapt in order to develop new skills or
ingrain a positive habit. We can also undergo changes referred to as negative plasticity, which
can produce post traumatic stress disorder, chronic pain disorders, phantom pain, and other
conditions where our neural communication pathways become more efficient at creating negative
responses. For example, athletes can develop chronic pain related ailments due to negative
plasticity. In these instances the pathways in their brains that generate pain signals become more
developed and more efficient at generating the pain response in the future. For example, an
individual with a herniated disk may experience ongoing pain for years as a result of the pain
pathways becoming very efficient at generating pain. Additionally, pain receiving fibers can
increase in number and brain out to further increase pain perception. Over time these new
pathways heighten the pain response even though the initial injury may no longer be present. In
these cases the individual experiencing pain is undergoing a low-grade form of post traumatic
stress which is caused by an overactivation of the sympathetic nervous system. They have been
trained to experience and perceive pain when no actual threat is present.
​
Perception is the brain’s best guess about what is happening in the outside world.
Perception is an inference. There are cases where a specific sight, sound, smell, or specific
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bodily sensation can elicit a physiological response, like pain or even an immune response.
Additionally, specific environmental cues can cause the onset of pain or bring traumatic
memories back to the surface. Most of the time we aren’t even consciously aware of the impact
that these sights, sounds, smells, or environments have on us. This raises an interesting question.
Is the pain we experience in these instances real if nothing has changed physically that would
indicate physical damage? In many instances we can perceive pain when it is not real, in that
there is no structural abnormality causing it. Brain regions like the amygdala and hippocampus
work together to protect us from danger, perceived or real, when certain sensations, that you may
or may not be aware of, reach a critical threshold. When this occurs a threat response is
triggered, which may lead to the sensation of pain from a past injury in the present. These painful
memories are real, but they need not be accepted at face value as that can alter our perception
and create a feedforward loop that perpetuates the pain response. When we tell ourselves a story
about our bodies and repeat it over and over we use thought to regulate our physical sensations
instead of awareness. The more we focus on an injury and the more resources we allocate to
thinking about it the more the brain continues to perceive it as a threat due to the process of
potentiation. Potentiation is a process by which synaptic connections between neurons become
stronger with frequent activation and it is thought to be a way which the brain changes in
response to experience, and thus may be a mechanism underlying learning and memory.
You cannot think your way out of a physical problem. At some point you need to be
present in your body, which can be challenging when you have been in pain or reacting to
external stimuli for a long time. To turn down the volume on the pain response, when no
structural abnormalities are present, you need to create space between your perceptions and
reality and recognize what is occurring in real time. You need to ask yourself whether your
thoughts and bodily sensations are accurate representations of where you are at right now.
Additionally, you need to examine how your body is reacting to your current environmental cues
and understand how your subjective experience is our brain's best guess at how to protect you
from a perceived threat. If your left knee is aching for no apparent reason, then move your right
knee and notice the subtleties of the movement. Is there something fundamentally different
between the issue free side and the side that hurts? Oftentimes when we experience a sudden
ache or pain we become more attune to bodily sensations like crepitus and we attribute the pain
to these phenomena. When we expand our focus we may realize that the sensation of crepitus
occurs elsewhere where pain is absent. This outward expansion of our attention allows us to not
become hyper focused on a specific bodily region and it can help free us from the compulsion of
tightening up, rapidly breathing, or obsessing about a minor ache or pain, which often
perpetuates the problem. By doing something different like changing your environment, altering
your movement, exploring new movements and feeling new sensations you become less
interoceptive. This allows you to adjust your perception and turn down the noise on the brain's
threat detection system when no true threat is present. This relates to the allegory of the stone
cutter which tells the tale of a man who relentlessly strikes a massive stone day in and day out.
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After four days and one thousand strikes of the stroke cutters hammer a young man
approaches the stone cutter remarking that the stone shows no evidence of damage. All of the
stone cutters' efforts were for naught. Finally, one day, the stone cutter deals the final flow
completely shattering the stone. Was the the one thousand and oneth strike that shattered the
stone, or was it the culmination of all of the stone cutters efforts and determination any evidence
of triumph up to that point? The answer should be clear that it was the culmination of repeated
strikes that shattered the stone. This allegory also applies to the process of getting out of pain,
whether that pain is caused by a movement dysfunction, tissue trauma, or it is a chronic pain
based issue. The systems that respond to and generate pain are idiosyncratic and as the pain
response continually occurs it becomes more difficult to produce other outputs as the brain
becomes increasingly proficient at creating protective signals. The longer this cycle repeats itself
the longer it will take to get out of pain. Additionally, recovery is not a linear process and we can
go long stretches without any discernible difference in the level of pain we experience day to
day. This does not mean that progress is not being made, but as with the allegory of the stone
cutter, our labor may not bear fruit until the job is complete.
The process of delayed results often leads athletes to select more aggressive treatment
methodologies in hopes that their work will manifest an immediate change or decrease their
subjective sensation of pain sooner. This is not the correct solution and it can potentially undue
days worth of work by re-potentiating the pain response. Instead graded exposure based
approaches borrowed from cognitive behavioral therapy should be used. Graded exposure can
best be analogized as slowly filling up a cup without it overflowing. In this case the cup
represents our threshold pain response and the water in the cup is our sense of threat. If we fill
the cup too quickly we’re at risk of it overflowing, thus triggering a protective pain response.
Instead the goal is to slowly increase exposure to threats at a rate where a pain response is not
elicited such that an individual can return to normal activity overtime without experiencing pain.
The pain science literature suggests that these types of interventions can form lasting changes to
the brain through positive plasticity so long as the volume, frequency, and duration of
interventions are not perceived as stressful to the individual undergoing treatment.
Pain and Motor Control
Pain alters motor control in an unpredictable manner that cannot be perfectly modeled.
This is counter to the traditional, reductionist, models of pain and motor control that were based
on joint inhibition. Joint inhibition is when a damaged, or painful, joint inhibits the muscles
surrounding it from functioning at peak capacity. This is a form of reflexive inhibition. An
example of this process would be a decrease in muscle fiber recruitment and force production of
the biceps muscles as a result of an elbow injury. However, more recent research suggests that
pain’s impact on muscle activation is not so clear cut. In fact, there are some circumstances in
which it can have the opposite effect of joint inhibition and increase muscle activation instead of
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decreasing it. Although pain’s role in muscle function and motor control is still not fully
understood, there have been major breakthroughs in recent years. The latest research indicates
that despite pain's impact on motor control being somewhat unpredictable, it is most likely
related to the specific task being performed. This means that the brain will increase or decrease
muscle activation in the presence of pain in response to the task being performed. This has many
implications, but one of the most far reaching is that individuals in pain are utilizing motor
patterns that are compensatory in nature.
In 2011 Paul Hodges and Kylie Tucker proposed a new theory of pain and motor control
which describes the process the motor control system undergoes to provide short term protection
for an afflicted bodily area. The consequence of the natural protective change in motor control is
altered muscle activation and movement. This helps explain why changes in muscle function can
be so unpredictable because they depend on, and are informed by, the specific problem at hand.
As a result, increases or decreases in muscle activation can both serve a protective function in the
context of a specific injury. These subtle changes in movement at a micro level can culminate
into clinically observable dysfunctions at a macro level, which can also be identified with
technologies like NIRS or surface electro electromyography.
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Chapter 22: Breathing And Autonomics
Mindfulness meditation and breathing based practices are keystones in many eastern
cultures. These practices have the ability to integrate and connect us physically, neurologically,
and emotionally. It is said that breath equals behavior, and behavior is the culmination of the way
we move, how we perceive our environment, our self awareness, and our ability to adapt to our
surroundings and cope with environmental stressors. For a practice that is so highly valued and
common in eastern cultures, its existence is wholly lacking in the west. This does not mean we
need to adapt an esoteric or spiritual approach to mindfulness, but it is worth considering the
value that a deliberate mindfulness practice can have in a holistic training or rehabilitation
program. Deliberate practice is the key word. Quality is much more important than quantity,
especially so when dealing with mindfulness practices, movement practices, and rehabilitation.
The human body has an incredible ability to adapt to poor movement patterns as well as
optimal ones. If the demands we impose on ourselves are causing us to default to weak and
unstable positions, then the body will adapt to those subpar positions. The purpose of this chapter
is to identify the relationship between breathing, the nervous system, movement capacity, and the
integration of breathing based practices as a means of working towards addressing movement
dysfunction and improving athletic performance.
Respiration, the Diaphragm, and the Nervous System
​
The autonomic nervous system is a key regulator of physiological functions including the
control of respiration, cardiac regulation, vasomotor activity, and reflexivity. This system acts
unconsciously and is the primary control mechanism for the ‘fight, flight, or freeze’ and ‘rest and
digest’’ responses. The diaphragm is the autonomic nervous system’s connection to the rest of
the body. In this way the diaphragm and respiration influence myriad bodily functions. The
diaphragm also attaches directly to the lumbar spine and contracts before extremity limb
movement, making it a major core stabilizer. During inhalation the diaphragm contracts and
descends into the abdomen while out interval organs are pushed forward and downward against
the abdominal musculature. When this happens intra-abdominal pressure and systemic tension
increase, perpetuating a sympathetic nervous system response via excitation. This causes heart
rate to increase with inhalation and decrease during exhalation with the latter increasing
parasympathetic tone through inhibition. Following exhalation there is a slight pause before the
next breath cycle, which allows the diaphragm to relax and ascend as well as helping to build up
carbon dioxide tolerance which aids in control of the respiratory drive. Lastly, the abdominals
serve as an anchor for the diaphragm and the obliques, as well as the transverse abdominis which
controls both the ribs and the diaphragm’s position during respiration. During inhalation the ribs
expand and externally rotate and during exhalation the ribs return and internally rotate. This
motion of the ribs lengthens and decompresses the thoracic column.
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​
Breath manipulation in a general sense is about autonomic nervous system control and
breathing is neurologically linked to the stress response. In times of stress our heart rate and
cardiac output increase, cortisol frees up glucose for immediate energy, oru muscles tense, and
we begin to hyperventilate which causes hemoglobin’s oxygen dissociation curve to shift to the
right and it also hyper-inflates our lungs to rigidify the spine as a means of increasing stability.
These behaviors and actions are highly beneficial in the presence of danger but are maladaptive
when they become chronic. In other words, when we are not in danger, but are breathing like we
are. Shallow breathing patterns that create hyper-inflated states put us into extension and keep us
in a sympathetic dominant state. When the sympathetic nervous system is overly active our
prefrontal cortex is inhibited which reduces motor variability and leads to rigidity. This decrease
in prefrontal cortex activation and increase in rigidity squanders our ability to learn new motor
tasks and relieve chronic pain symptoms. In order to decrease rigidity and increase function we
can use breathing based practices.
​ reathing Based Practices
B
​
The impacts of breathing practices on our health and wellbeing are numerous. In addition
to calming the nervous system, controlled breathing practices, done with proper mechanics,
improve oxygen delivery, self-awareness, movement variability, and can be used to alter the tone
of the autonomic nervous system.
While our breathing patterns can be altered to facilitate the sympathetic nervous system
and perpetuate a threat response, the primary value of breath training is to calm the nervous
system via slow, deep, breathing with an emphasis on full exhalations. This helps to increase
nociceptive tolerance and decrease systemic tension. In other words, turning down the alarm on
the stress response. The best place to start for beginners who would like to incorporate a new
breathing based practice is with simple breath awareness. A basic beginner protocol is as
follows:
1. Lay supine on on your back with your knees bent, or sit upright in a yoga
position;
2. Breath in slowly and gently through your nose with your tongue against the roof
of your mouth;
3. Once you have completed your relaxed inhale, exhale slowly letting the last bit
out air out with a slightly forced exhale;
4. Pause at the end of the exhale until you feel the first subtle urge to breathe again.
5. During this time you should be observing your breathing frequency without trying
to change it. You should note how this changes over time.
As you become more accustomed to diaphragmatic breathing you can begin to use
rhythm as an indicator of control and make note of how different breathing patterns impact your
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mood, level of pain, and sensitivity to stress. You can and should begin to explore new status and
dynamic positions as well. As Gray Cook has said, “If you cannot breathe in a movement you do
not own that movement.” It’s also worth reflecting on some of the common breathing faults that
athletes may have as well as how to fix these faults so they can ‘own their movements’, so to
speak. First and foremost, the position of the thoracic spine and ribcage govern the function of
the diaphragm muscle. If an athlete’s positions are compromised, then their ability to breathe
with optimal mechanics and volumes will be compromised as well. We want to ensure that an
athlete has sufficient, but not excessive, thoracic flexion and extension, that their scapula sits
properly on their ribcage, and that their ribs are not flared. These factors compromise the
foundation of proper breathing and once they are addressed we can start to think about the
mechanics of breathing.
One of the major mechanical faults that athletes often have is an overreliance on inhaling
through the mouth, versus breathing through both the nose and the mouth combined. This can be
due to nasal congestion or a deviation in the nasal septum, but in most instances the solution can
be found in simple cueing. For example, you can first have an athlete focus on pressing their
tongue to the roof of their mouth while simultaneously breathing through their nose, which will
preserve the maxillary arch and keep their neck muscles relaxed. Once an athlete gets
comfortable breathing through their nose in a relaxed posture or during low intensity training you
can begin working with them to breathe through their nose and mouth simultaneously with the
tongue in a neutral or depressed position. This allows for greater gas exchange during high
intensity work bouts, which is an advantage as they try to extend their work durations. After
addressing an athlete's positions and inhalatory mechanics the third most common fault is a lack
of complete exhalation, which manifests itself as hyperinflation and an overextended posture
where an individual is incapable of finding a neutral position. In some cases fixing this issue is as
simple as drawing an individual's conscious awareness to it and cueing them to focus on slow
smooth exhales through the mouth until all air is expelled from the lunges. It’s important to
emphasize that the exhales should be smooth, and not forced, to avoid clamping down on the
rectus abdominis muscles or straight the neck.
The role of breathing based practices in an athletes training, and how much they should
dedicate to these practices, can vary widely. For those who are currently in pain or suffering from
chronic injuries it can be helpful to dedicate entire training sessions to breath work, manual
therapy, and corrective exercises.
For those who are just looking to augment their current training routine simply
integrating breath work within warmups can be great focused reminders. The addition of breath
work to warmups allows for time, not under load, to help athletes feel the dynamics of the rib
cage during inhalation and exhalation. This also sets athletes up to be more receptive to coaching
cues during the subsequent training session. For individuals who are having trouble bridging the
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gap between breathing with optimal mechanics during warmups and prehab exercises and doing
so during dynamic exercises i’ll often use loaded carries and holds, then low load dynamic
exercises, and over time we’ll increase the cardiorespiratory demand in accordance with an
individual's ability to adapt.
Respiration and Holism
In the previous subsection of this chapter I mentioned that an athlete who does not fully
exhale during the respiratory cycle often ends up in a hyperinflation posture, which results in
them defaulting to an overextended position. In this subsection I will expand on that concept by
taking a whole organism approach and demonstrating how a subtle breathing fault can perpetuate
issues throughout the body. These issues may manifest in a particular bodily region, but are often
non-attributable to localized tissues and are difficult to remediate without addressing the root
causes. For example, when an athlete is stuck in an overextended posture as a result of
hyperinflation the diaphragm cannot fully expand during respiration, as as a result the superficial
neck muscles and sternocleidomastoid will pull the distal head of the clavicle upwards to create
vertical space for the diaphragm to expand. The upward pull on the distal head of the clavicles
can often create the appearance of the clavicle forming an ‘V’ shape when viewed from the front.
Over long stretches of time the chronic tension placed on the superficial neck muscles can result
in compensatory hypertrophy and which places the accessory inspiratory muscles under
increased stress. This excess tension can also lead to shoulder and pec minor pathologies as well.
When the superficial neck muscles are constantly shortened they will become overused
and as a result the jaw will clench down, creating tension through the superficial front line that
runs from the sides of the skull down to the tops of the feet. The excess tension in the superficial
front line manifests where the chain is weakest, as with any other tensegrity structure. In many
cases this means excessive tightness, decreased force output, and pain in the adductors. Often
these athletes who present with adductor pain aim to treat this issue with standard local tissue
based therapies, only to come up short time and time again. It isn’t until they address the root
causes of excessive superficial neck muscle tension and breath dysfunction that can rid
themselves of this issue. To demonstrate the impact of superficial neck muscle tension on
adductor length you can try the following drill. Start by laying on your back without bending
your knees and then try to raise your leg to the side into a split position. Next, spend two minutes
applying gentle pressure and massaging the jaw muscles, superficial neck muscles, and the area
where the neck meets the earlobes. Finally, you should retest for mobility.
Chances are that after performing the above exercise your adductor range of motion will
have increased. The purpose of including this subsection is to depict how everything in the
human body is interconnected and how a minor breathing fault can manifest as tension in
various, seemingly unrelated, bodily regions. Athletes experiencing tension and pain in these
regions will often try to treat the affected tissue without success because they are addressing a
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symptom and not the root cause. When they learn to view the body as an integrated unit they can
make connections and see how things like adductor tightness, jaw tension, and shoulder pain are
not only connected to one another, but can also stem from something as simple as not fully
exhaling during respiration. Additionally, they can see how these seemingly unrelated issues can
cascade out and have rippling effects throughout the body. For example, let's take the individual
with a hyperinflated postures whose thoracic spine is locked into extension. They have turned the
thoracic spine which should be a mobile joint segment in a stable joint segment. In order to
create more degrees of freedom for motion this individual may sacrifice lumbar spine stability
for mobility, and as a result they may experience chronic lower back pain that does not respond
to standard tissue related therapies. This can lead athletes to become frustrated over time and it
isn’t until they begin viewing movement through a holistic lens like a detective that they find the
root cause of their issues, allowing them to achieve long lasting relief.
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Chapter 23: Muscle Tension
Have you ever stretched a muscle for days on end with little impact on the perceived
tightness of that tissue? Maybe you tried foam rolling it, performed banded distraction work, or
dug into it with a massage tool, but the tissue is as stiff as ever. If you are not seeing changes in
mobility with the work you’re doing you need to take a step back, reassess, and view the body as
a system of systems. The key is to find an accepting relationship with tension that allows you to
engage and be more aware. If you aimlessly stretch, smash, and roll tissues it is unlikely that
you’ll find the long term developmental progress that you’re seeking.
Muscle tension, and subsequently mobility, is highly regulated by the central nervous
system. Despite the negative connotation that the word tension carries in the high performance
community it is not something to be feared. Humans live and die by tension. Without sufficient
muscle tension we lack the ability to create intramuscular compression and regulate our blood
pressure during activity and the ability to tolerate and meaningful external load placed on us.
Additionally, our bodies are held together by a network of length tension relationships and
without these relationships we would lose the ability to generate movement, let alone keep
ourselves upright. Tension simply refers to the degree of tautness in the muscles at any given
point. Our muscles are never entirely relaxed, even where we are at rest. The amount of muscle
tension our tissues maintain at rest can be altered and it plays a role in determining our active and
passive ranges of motion, both of which are relevant for performance. If resting muscle tension is
too low then muscles cannot contract as rapidly or produce as much work. On the other hand, if
tension is too high then muscles are less efficient at contracting and producing force, and their
active range of motion may be impaired as well.
​
Our bodies maintain our muscle tension based on both active and passive components
and the nervous system actively adjusted tension based on feedback it receives from the muscle
itself. Specific portions of the muscle such as the muscle spindle cells monitor the degree of
stretch in the muscle and relay that information back to the central nervous system. If the muscle
is stretched too much, or too little, the brain responds by altering the length of the tissue and
resetting its tension. Additionally, muscle tension can be manipulated through physical training
and movement based therapies. This can be a natural, unintended, outcome of our training or it
can be something that is strategically altered as a means of optimizing force production and
efficiency.
Stretch Physiology ​
The stretch reflex is set by the central nervous system based on our previous experiences
and our muscles capability of functioning within a given range. If we spend much of our time in
a certain position, or posture, our body will adapt in order to maximize efficiency within those
active ranges. In order to change our default setting, so to speak, we need to disrupt the system.
The central nervous system is resistant to significant changes, and it will guard against
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disruptions and perturbations. If you try to take a joint past it’s normal active range your body
will react by pulling you back into your normal range. This process is mediated through the
stretch reflex. If we want to increase an athlete's active range of motion we first need to improve
their ability to control themselves in all of their currently accessible ranges, then we can begin
teaching their nervous system to control progressively larger ranges as well as preparing tissues
to function in these newly acquired ranges. The simplest way to accomplish this is through a
combination of stretching and isometric loading. For example, taking a given joint to, or near, it’s
end range of motion and then applying an isometric muscle control above eighty percent of the
maximum voluntary contraction force. This will override the stretch reflex and allow one to gain
access to newly acquired ranges or motion. Isometrics are the safest and most effective way to
bypass the stretch reflex and are highly effective for activation motor units. Additionally, this
process can be expedited through the use of breathing drills that help to change mobility and
move athletes into new ranges of motion in a safe manner. Mind you, athletes will not maintain
all of their newly acquired ranges of motion, but they will retain some of it. In this way the
process of increasing active range of motion is akin to taking three steps forward and two steps
backward. It's a continuous battle to gain new ranges and capture them through deliberate
movement practices, breathing patterns, and habits.
Identifying tension
​
Manipulating tension in a strategic manner requires that you be able to identify it. This
means identifying which tissues and bodily regions are too tense, too lax, or lacking stability and
control relative to the demands that someone wishes to put on their body. A simple, albeit
subjective, way to identify tension is through our ability to rebound off the ground and produce
force. If you are able to rebound off the ground and produce force easily, compared to your
baseline, then your muscle tension is higher than normal. If you find yourself unable to jump as
high as usual, feeling like your stride lacks your normal springiness, or your ability to generate
force is compromised then your muscle tension is lower than normal. However, the latter
assumes that losses of power that you’re experiencing are due to lower muscle tension, and not
generalized fatigue and sluggishness. Decreases in muscle tension are localized and impact
regions of tissues, while sluggishness from fatigue causes a global malaise that impacts the entire
body. Determining whether the issue is localized to the primary muscle groups in question, or
felt across the body, is the key to differentiating low localized tension and systemic fatigue.
A more objective way to gauge tension in a muscle is through palpation. While at rest
you can push into the belly of a major muscle, noting how much give it has to your action. The
more force that is required to press into the muscle, the greater the tension. Conversely, if you
can easily push into a muscle with little resistance then tension is low. You can also use a
reactive strength index test to estimate the effects of muscle tension as well. An individual’s
reactive strength index can be calculated with the following formula where time to takeoff
includes both the eccentric and concentric phases of the stretch shortening cycle: RSI = jump
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height / time to take off. The higher an athlete's jump height and the lower their ground contact
time, the higher the reactive strength index score. Too much, or too little, tension in the system
will dampen an athlete's reactive strength, so this information should be tracked and compared to
their mean jump height over time.An effective way of gauging muscle tension is to use a
combination of the aforementioned subjective and objective techniques. It’s important to
understand that high resting muscle tension can be indicative of both mechanical tension and
neurological tension, which need to be handled differently. Mechanical tension is often caused by
tissue fibrosis whereas neurological tension is caused by an increase in neural drive. If a tissue is
taut and gives resistance to pressure while it is static then the manifested tension is likely to be
neurological. If the tissue has a lot of give while static, but is restricted while passively taken
through ranges of motion then mechanical tension is the likely culprit. Mechanical tension can be
moderated through manual therapy techniques that aim to remove fibrosis and neurological
tension can be addressed through treatments that focus on resetting the nervous system. Lastly,
even though the terms tension and trigger points are used interchangeably by some, there is a
distinction between two. The true definition of a trigger point is a hyperirritable region in the
fascia surrounding skeletal muscle with pain referral when it is compressed. Trigger points are
associated with palpable nodules in taut bands of muscle fibers and can be caused by both a
hyper excited neurological area or a mechanical lesion.
​
Manipulating Muscle Tension
All muscle fibers have an optimal length for force production, which is known as the
length-tension relationship. The optimal length-tension relationship varies considerably in the
context of the desired performance outcome. If muscle tension is too low or too high, you will
not be able to generate force optimally or efficiently for the task at hand. Our nervous system
ultimately regulates how muscle tension is managed, but our muscle spindle cells provide the
inputs that the nervous system needs to do so. There is an optimal level of muscle length and
tension for a given activity and our muscle spindle cells will optimize tension to maximize
efficiency for that activity. For example, if an athlete performs a high volume of threshold run
training their muscle spindle cells will optimize tension for that activity which includes very high
volumes of low force muscle contractions. By virtue of optimizing tension for that task, tension
will not be optimized for strength and power based activities that require very high levels of
tension, and a small number of maximal force contractions. Knowing this, one of the
mechanisms by which some individuals seem to lose strength when performing high volume of
energy system training is a simple mismanagement of muscle tension and not an interference
effect from concurrent training as many would believe. In order to counteract this effect you can
use varying training inputs to conserve or manipulate tension across a training day or a training
week. Figure thirty-five depicts the impacts of different training variables on muscle tension.
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One way that the information in figure thirty-five can be used is to help optimize a
runner's peak and taper leading into a competition. In many instances athletes will cut back their
training intensity too much leading into a competition, and they’ll show up feeling flat as a
consequence. This is a case where an athlete comes into their competition with too low muscle
tension, which could have been avoided with the strategic use of high intensity training in the
days leading into the race. For energy system dominant sports, a good rule of thumb is to make
more substantial adjustments to tension a week out from competition and then make
progressively smaller changes on a day to day basis leading up to the event to ensure an athlete
has the right ‘feel’ for their event. Another example of this chart can be used with mixed sport
athletes who are required to strength training and perform energy system training throughout the
week. As previously mentioned, many of the negative effects on maximal strength and power
that are associated with aerobic training are due to a mismanagement of muscle tension across a
training week. In order to mitigate these effects and make simultaneous improvements in
strength and aerobic capacity you can phase tension management protocols across a session. If
an athlete is performing threshold style training today and I know they are planning on lifting
heavy tomorrow I may have them finish their workout with a few sprints or plyometric drills to
ramp tension up. Similarly, if an athlete is performing speed and power training today and they
plan to do delivery training the next day I may have them wrap today’s session up with ground
based movement work, low intensity spin biking, and progressive muscular relaxation drills to
lower systemic tension in anticipation of the next day's training.
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Chapter 24: Load Management
Measuring acute to chronic workloads has become a ubiquitous practice within
professional sports over the past few years. But, I really question the efficacy of these practices.
Of course, anything that teams can use to manage training loads is better than nothing, but that’s
less of an argument for the acute to chronic workload ratio (ACWR) concept and really just
points to the fact that we should make logical decisions with how we handle training volume on
a week to week basis.
For those unfamiliar with the ACWR concept, the idea is that coaches can predict injury
risk by calculating the ratio between acute training loads, typically over a five to seven day
period, and chronic training loads over a three to four week period. The theory is that if acute
training loads are too high in relation to chronic workloads, the athlete is at an increased risk of
injury. I have no qualms with either of these assertions, broadly speaking. Of course, if you
double your training volume from one week to the next, it’s likely to open you up to an increased
risk of injury, but the devil really is in the details. Most coaches measure workloads by
multiplying session RPE (rating of perceived exertion) and session duration, which creates a
daily workload score in arbitrary units. This fails to acknowledge the influence of different types
of training, for example, resistance training versus energy system training, and it also assumes
that a given external workload will always create the same internal stress — having used
technologies like NIRS for years now, I can comfortably say that is not the case.
Many people reading this will say, “Who cares if the methodology is flawed? If coaches
are using acute to chronic workload ratios and it’s helping them make informed decisions about
training loads, that’s a net positive.” I understand this argument, and it’s a good one. I’ve
consulted with professional sports teams and military special operations training groups for years
now and I’m comfortable saying that anything that increases dialogue around training loads and
their impact is a win in and of itself. A few years back, it wasn’t uncommon for me to see MLB
coaches that have no clue what their pitcher’s pitch counts were, volleyball teams that didn’t
even think about jump counts, and CrossFit athletes that had no volume control whatsoever. To
that effect, implementing ACWRs has been a game-changer in many cases. That being said,
‘better than nothing’ is far from optimal.
To make informed decisions about an athlete's training loads, we not only need to have
accurate measurements of their external training loads, but we also need to consider internal
training loads — that is, the physiologic impact of training. Some strength and conditioning
coaches in professional sports will acknowledge the limitations of ACWRs and use it as a tool to
have discussions about training loads with the team's head coach or other support staff. However,
the idea of measuring something for the sake of increasing the potential for conversation is a
little silly. Additionally, anytime we measure something, we assign some inherent level of value
to it. When we assign value to a measurement, it’s hard to dismiss it outright. Even if you know
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ACWRs are not ideal, it’s hard not to get a little panicked when you see a player’s number jump
from 1.6 (right in the sweet spot) to 2.2 (into the danger zone).
Challenging these load management ideas doesn’t mean we say they are meaningless.
Instead, I propose a more nuanced approach to player load management where we account for
both external and internal loads, which allows for much more nuanced data collection, analysis,
and insights. While there are a number of load monitoring tools I see value in, like NIRS, the
same principles govern how all of them inform an athlete centric training system.
First, an athlete does a workout, then the athlete's performance in the session and
response to the session inform both future training sessions as well as the ‘load monitoring
algorithm’. Next the load monitoring algorithm looks at the athletes response, total training
volume, training intensity, and training distribution and tells us if the training load appears to be
too much, too little, or ‘good’. Then, the load monitoring algorithm helps steer future training
decisions. Should the coach increase volume or is there a specific muscle group or region that
needs less loading? Finally, the coach adjusts training to help steer the athletes response and
progression, and then the cycle repeats itself. In this process load monitoring doesn’t always give
comprehensive answers — instead, it allows coaches to ask better questions and helps them
make informed decisions.
In terms of the types of load management we can do, I break them into offensive and
defensive strategies. The offensive strategies include methods for auto-regulating intra-session
volume and intensity, as well as training frequency. The defensive strategies include injury
prevention strategies used to detect regions of interest (ROIs) and modify the training plan,
treatment modification strategies, as well as return to play protocols.
Load Management Heuristics
As previously mentioned, there is an offensive and defensive side of load management.
On the defensive side we have injury prevention tactics, treatment modification techniques, and
return to play protocols. Unjust prevention can include questionnaires, movement screens, as
well as tools such as surface electromyography, muscle oximeters, and infrared thermography to
detect regions of interest and adapt training plans accordingly. Treatment modification
techniques include monitoring the effectiveness of current treatment modalities and adjustment
treatments relative to that incoming information. Return to play protocols entail quantifying how
much compensation is occurring in live time as a means of determining the optimal training load
to increase fitness while simultaneously mitigating injury risk and speeding up an exerciser’s
return time after injury.
The offensive load management techniques include within session tactics to auto-regulate
training volume, intensity, and density in order to elicit a specific training response as well as
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between session tactics to determine an exerciser’s readiness such that they can manipulate
training frequency to get as many effective training exposures in through the week with the
lowest possible fatigue cost. The defensive and offensive load management techniques are both
depicted in figure thirty-six.
Injury Prevention And Treatment Modification With Infrared Thermography
A thermogram is a representation of heat radiating from the body. Skin temperature
regulation is impacted by blood flow, muscle recruitment pattern, inflammation, and injury.
Despite the fact that our bodies are thermally balanced, injuries can cause thermal asymmetries.
As a result, infrared thermography allows one to detect these thermal asymmetries which
represent regions of interest (ROIs). ROIs show potential injury risk from workload
mismanagement, biomechanical inefficiencies, tissue pathologies, or other sources or thermal
asymmetry.
An injury is often related to variations in regional blood flow, and these changes in blood
flow can affect skin temperature which increases in the case of inflammation or decreases in the
case of tissues with poor perfusion, degeneration or reduced muscular activity. Evaluating
thermal profiles of athletes pre-season and intra-season can be extremely useful as functional
thermal asymmetries are highly correlated with risk of soft tissue and overload injury. Infrared
thermography can help identify ROI’s that need specific attention for injury prevention,
treatment modification, and return to play scenarios. When looking at left to right symmetry we
can classify injuries based on the degree of thermal asymmetry, which correspond to the varying
alarm phases. For example, a 0.0-0.3 °C difference between sides is normal variation; 0.3-0.6°C
is the first sign of a potential ROI; 0.6-0.9°C is when injury prevention strategies should start
being employed; 0.9-1.2°C is when an athlete is actively undergoing treatment and significant
modifications need to be made to their training; 1.2-1.5°C means injury is likely to occur if it
hasn’t already; and 1.5°C or greater is an indication of severe injury.
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Alarm phase one is the first sign of a potential region of interest, which we can use to flag
an issue or let a coach know it’s something to keep an eye on. Alarm phase two is when we start
to employ injury prevention strategies. Alarm phase three is when an athlete is actively
undergoing treatment and significant modifications need to be made to their training. Alarm
phase four indicates that injury is likely to occur and alarm phase five indicates that an injury is
likely to have already occurred. As a result, it is possible to use infrared thermography as another
form of pre-training or post-training screen, which can help steer the training process. On the left
hand side of figure thirty-seven we have an athlete who is three years post operation after a left
ACL rupture and repair. This athlete has reported periodic pain around the patella and often
presents with a temperature variation of greater than one degree celsius from right to left side. In
this instance the previously injured leg presents with a hypothermic asymmetry. This
hypothermic tissue region indicated lowered metabolic activity and perfusion in the tissues
surrounding the knee joint, which can be corroborated with NIRS. On the right hand side of
figure thirty-seven we have a twenty two year old distance runner training roughly sixty miles
per week who was diagnosed with mid-portion achilles tendinopathy. The temperature difference
on the right achilles was roughly 1.4 degrees celsius lower on the left leg, which indicates a
decrease in metabolic activity with the loss of a normal muscle fiber structure.
There are also cases where infrared thermography can be used for treatment modification
as well, which is demonstrated in figure thirty-nine. This is a case where an athlete was
diagnosed with what was believed to be achilles tendonitis on their right achilles, and was not
responding to the treatment for that. Using infrared thermography they were able to identify that
the afflicted area was actually hypothermic. Because tendonitis is an inflammatory issue, which
is associated with increased heat, this would indicate that they are actually suffering from a
tendinopathy, which is associated with decreased skin temperature as a result of lower metabolic
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activity. As a result, they can modify their treatment plan as a consequence of this data.
Optimizing Return to Play With The NNOXX Wearable
Active nitric oxide is associated with a wide range of physiological processes including
smooth muscle relaxation, vasodilation, inflammatory responses, and the inhibition of platelet
adhesion and relaxation. Additionally, active nitric oxide controls the release of oxygen from red
blood cells into tissues and acts as a signaling molecule that plays a vital role in dilating blood
vessels. Until recently, no one has been able to measure active nitric oxide levels in tissues
non-invasively. However, NNOXX has developed a novel measure of nitric oxide bioactivity and
muscle blood flow called personal nitric oxide, or PNO for short.
Personal nitric oxide is a dynamic measurement of active nitric oxide release from the red
blood cells during exercise, thus making PNO a measurement of the primary determinant of
blood flow to working muscles. Additionally, PNO can be used to assess limb asymmetries in
active nitric oxide release, which when combined with other NNOXX biomarker measurements
can be used to flag increased injury risk in live time.
Figure thirty-nine shows an NHL Forwad’s personal nitric oxide levels during three
consecutive exercise bouts labeled A, B, and C. The aforementioned NHL player struggled with
recurring right knee injuries and premature fatigue in the right leg while skating. Using
NNOXX’s platform, the athlete’s active nitric oxide release in their right leg was found to be
impaired compared to their left leg. Additionally, the asymmetry in active nitric oxide release is
exacerbated with each additional work set. By identifying the aforementioned trends in live time,
the NNOXX platform can inform coaches about an athlete’s ability to handle loading before or
during a training session. Additionally, the NNOXX platform can make recommendations for
how an individual should modify their exercise to increase their fitness while simultaneously
mitigating their risk of injury.
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Part VI: Athlete-Centric Coaching
Chapter 25: Exercise Adaptation
Adaptability is the property of a system to increase its capacity as a result of stress,
shocks, or perturbations. In other words, adaptability is the ability of a system to strengthen
under disorder. The process of training is rooted in the adaptable nature of human beings. We
impose a stressor, big or small, and through our adaptive capacity we become stronger, faster, or
more enduring, as a consequence. The process is often referred to as supercompensation in the
training literature, however it is not so cut and dry. Complex biological systems, like the human
body, are filled with nonlinear responses and mechanisms evolved to maintain homeostasis,
which is the tendency of our bodies to seek and maintain balance. Additionally, physiological
adaptation comes with a cost and in order to create change we must pay a price.
The goal of training is to achieve a given output, or physiological response, with a
minimum cost of adaptation to the individual. In order to do so it is critical that we take a holistic
view, and study methods for controlling the training process based on known mechanisms of
adaptation. Additionally, we must respect the synergistic effect of different energy system
training methods, resistance training methods, movement work, stress management, sleep,
nutrition, and all other inputs. In order to fully understand the topic of physiological adaptation,
as it applies to training, I think it is first important to understand the history of this topic. Which
can be best explained through the phenomenon of path dependence.
​
At any point in time a large percentage of scholars in a given field all hold the same basic
assumptions, whether or not they are true. Call it dogma, or simply the echoes of the past
continuing to resonate. As time goes on, and a new generation of scientists come into age, the
dogma of yesteryear tends to fade away. Thus, allowing the field to progress as a whole. But,
what happens when the field fails to progress; and when it cannot move forward despite all
evidence pointing to a new direction ? This is directly related to the concept of path dependence,
which explains how the set of decisions one faces for any given circumstance is limited by the
decisions made in the past, even though past circumstances may no longer be relevant. The
classic example of path dependence is the QWERTY keyboard we are all accustomed to. The
QWERTY keyboard was designed to reduce typing speed in order to prevent mechanical
jamming on typewriters. By separating the most often used keys on the keyboard, and creating a
very inefficient key configuration, the QWERTY keyboard eliminates jamming on mechanical
typewriters. Although new technological innovations ensure that jamming on keys on a keyboard
is no longer an issue, we still live with the legacy of a solution to a nonexistent problem. As
such, the phenomenon of path dependency provides a window through which we can reflect
upon the influence that historical precepts hold over future innovations. In this way, ideas
perpetuated by path dependence serve as a conceptual ceiling constraining the evolution of more
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creative and effective paradigms. This is never more apparent than when looking at the way
training induced adaptations are viewed.
Supercompensation Hypothesis vs. Signal Transduction Theory
Physiological adaptations are changes that occur within individuals in response to
external factors like exercise or environmental factors such as altitude. In the history of
adaptation research, one of the earliest proposed ideas was the concept of overload by Julius
Wolff who linked the loading of bones to their adaptation in the late 1800's. His hypothesis was
later extended to other organs and the term overload was expanded to include forms of loading
that weren’t mechanical in nature.
While Wolff’s general principle was correct, in that it is true that exercise is required for
exercise-induced adaptations, it didn’t explain the underlying mechanisms by which that
occurred. It wasn’t until a different theory, called the super-compensation hypothesis, depicted in
figure forty, was proposed that anyone provided a potential mechanistic explanation for
adaptation. Supercompensation hypothesis is rooted in the general adaptation syndrome concept
proposed by Hans Seyle and it is defined by a decline of an often undefined Y-axis variable
during exercise and its recovery after exercise. According to this hypothesis, the recovery does
not just reach pre-exercise levels, but it overshoots it. Despite the fact that this hypothesis is
widely accepted, it has many flaws and there are no clear mechanistic explanations for it. In
recent years the scientific justifications for this hypothesis have largely eroded, despite the fact
that it is still so widely cited. I believe this is largely a case of path dependence. Already, In the
60's and 70's emerging science started to erode Seyle's theories.
According to John Kiely, "Classic Selye-inspired theory was straining to accommodate
evidence demonstrating that neither homeostasis nor the stress response was static, but varied
dynamically under the influence of life history and oscillating biological rhythms.” Then as the
twentieth century entered its final quarter, the explanatory limitations of Hans Selye’s paradigm
were increasingly exposed. Most notably, the portrayal of stress as a predictable biologically
mediated phenomenon was undermined by the demonstrable effects of non-physical factors on
physiological stress responses and increasingly convincing evidence that stress responses were
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not generalized and non-specific, but highly individualized and context-specific You may be
wondering if this really disproves the notion that super-compensation is an underlying principle
of adaptation. Can stress responses not be highly individualized, yet still follow the
supercompensation time course? That is a question I had wondered myself and there is actually
quite a bit of evidence against supercompensation theory.The super-compensation hypothesis
implies that recovery periods are essential for adaptation. This isn’t actually the case. For
example, the heart adapts to exercise despite continuous contraction and skeletal muscles can
adapt to chronic electrical stimulation applied continuously over weeks as well.Despite being
propagated for decades, there is little actual evidence that the supercompensation time course is
essential for adaptation. In contrast, there are hundreds of scientific references supporting an
alternative hypothesis that signal transduction pathways mediate all adaptations to exercise.
According to the signal transduction theory specific sensor proteins detect
exercise-related signals which are then computed by transduction pathways or networks. These
early signals regulate downstream events including
gene transcription, translation, or protein synthesis
and protein breakdown. The result is tissues, organs,
organ systems, or organisms that have adapted to
exercise. Figure forty-one depicts the signal
transduction process that leads to muscle hypertrophy
in response to resistance training. First a mechanical
stimulus is applied to the muscle fibers, which
activates myogenic signaling and in turn initiates the
process of adding myofibrillar proteins to muscle
tissue. Next the myogenic signals such as insulin-like
growth factor-1, mechano-growth factor, and
interleukin-6 are released. After that the mTOR enzyme, also known as the mammalian target of
rapamycin, integrates the mitogenic signals which begins the process of gene translation. Finally,
muscle protein synthesis begins. Ultimately, all forms of exercise training work by activating
different genetic, epigenetic, and metabolomic expression circuits shape relevant physical,
cognitive, and behavioral traits. For example, it’s well understood that certain forms of
endurance training lead to blood vessel formation. However, this is only the case if the vascular
endothelial growth factor gene is increased above basal levels in response to training. In the
future wearable devices will be able to continuously track the aforementioned expression circuits
and provide instantaneous feedback, which will help athletes enhance their performance in a
previously unprecedented way.
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Chapter 26: The Limiter-Bridge-Performance Model
The more training literature you read the more you’ll notice specific training schema and
theories being rehashed and recycled by different training camps. For example, it's not
uncommon for training books to include a section on the supercompensation model of
adaptations, which is used as a justification for the progressive training structures and
periodization plans explained later on. Supercompensation theory, which is based on classic
stress physiology literature, has been used to rationalize specific periodization models since its
genesis. However, the field of stress physiology has shifted dramatically in the last thirty years
and despite its evolution outdated theories of yesteryear are still firmly rooted in training culture
at large. All training plans are created with the goal of driving adaptation, but the aforementioned
plans are only as found as the theories they are based upon. Training models built around
supercompensation theory are flawed in that they do not account for how the human body truly
adapts to training. Additionally, the aforementioned models lack dynamic flexibility because
they do not consider the wide ranging inter-individual variability in training responses. As a
result, I created the limiter bridge performance model.
The limiter bridge performance model of training is designed to improve physiological
limiters, raise the ceiling for future performance, as well as to drive functional and structural
adaptations simultaneously.
Functional adaptations are the transient adaptations to an overabundance of stress that
result in temporary increases in physical capacity. Functional adaptations occur over short time
scales and are effectively adaptive survival mechanisms. These adaptive mechanisms can be
taken advantage of in training in order to elicit a specific physiological response. For example, a
coach may create a workout where an athlete needs to cope with every increasing amount of
metabolic by-products week to week. As a result, their athletes' weekly improvement will be
driven by a need to survive the aforementioned short term, transient, stressor. Once this stressor
is removed and the need to tolerate increased metabolic by-products subsides the athlete will
return to their baseline state. This is why athletes often see rapid gains in fitness after beginning
an overly aggressive training program but quickly revert to their baseline level of fitness
following their inevitable burnout or injury. In these scenarios the athletes see quick
improvements due to functional adaptations despite the fact that they have not developed
structural adaptations to support their increased training loads long term. However, if a stressor is
applied at an optimal dose with a high enough frequency, and for a long enough duration, it will
become an environmental stressor that elicits structural adaptations over time. Structural
adaptations are changes to the muscles, bone, heart, lungs, and mitochondria that allow our
bodies to cope with the demands of training long term. Additionally, structural adaptations are
the base which functional adaptations are layered on top of. As such, we are always going
through overlapping processes of functional and structural adaptation.
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In the next subsection I'm going to present a more comprehensive model for phasing
training called the Limiter-Bridge-Performance (LBP) model, which is based on the principles
of athlete centric coaching and dynamic programming. Prior to creating the LBP model my
approach to training involved analyzing the performance demands in a given work capacity
based work and then reducing those demands down so they can be isolated and trained. In this
system training was based on internals targeting discrete training zones intended to elicit specific
adaptations. The problem is that neither sport-specific training and physiological adaptations do
not fit nicely into discrete categorizations. While the aforementioned approach was effective for
increasing an athlete’s potential it seldom maximized performance and as a result athletes were
left underprepared for competition. On the flip side, many training programs emphasize
sport-specific training at the expense of developing limiters, which leaves athletes poorly
conditioned despite being technically and tactically prepared. The LBP model aims to prevent
both of the aforementioned scenarios by touching on all training qualities at all times with
different degrees of emphasis based on an individual's priority at any given time point.
The Limiter-Bridge-Performance Model
As the name implies, the Limiter-Bridge-Performance model is broken down into three
different types of training, each emphasizing different aspects of performance. Limiter training
intends to drive biological adaptations that are specific to improving an athlete's rate limiting
factor for maximal oxygen consumption. Additionally, limiter training is used to raise the ceiling
for future performance as well as to pave the pay for future adaptations, versus maximizing
performance in the short term. Examples of limiter training include tier two energy system
training protocols such as hard start intervals, gradual desaturation intervals, and repeat
desaturation training.
Bridge training is used to seamlessly transition from limiter to performance training, or as
the name implies to bridge the gap between developing an athlete’s limiter and maximizing their
sport-specific fitness. As a result, bridge training puts less of an emphasis on driving specific
physiological adaptations and more of a focus on preparing the body for performance training,
which is an often overlooked step. Example bridge training protocols include broken intervals,
and fast twitch fatigue resistance intervals.
The final phase in the LBP model is the performance phase, which is used to develop the
specific physiological and psychological qualities that are needed to maximize sports
performance. The key to performance training is taking a multi-faceted approach where training
mimics the demands of competition in all regards. For example, the environment that training is
performed in, the feelings of psychological stimulation or threat associated with competition, as
well as the volume, intensity, and density of exercise. Performance training sessions are the most
stressful among the various types of workouts included in the LBP model. Example performance
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training sessions include time trials, competition simulations, scrimmages, and small sided
games.
Despite the limiter-bridge-performance model including a phased training approach, it is
not a periodization model. Rather, it is a method of phasing training protocols over time to elicit
specific adaptations. However, the LBP model can be combined with a dynamic programming
approach in order to create a comprehensive athlete centric training system.
Dynamic programming is an approach to training where workouts are not pre planned
well in advance. Instead, programming is informed by prior sessions. In other words, the
workout plan depends on the athlete's feedback and status and fluidly adapts to changing
conditions. In an ideal scenario this can even be done on a daily basis.
Combining the principles of dynamic programming with the LBP model allows one to
avoid many of the common pitfalls associated with traditional periodization schemes. For
example, a common flaw when periodization training is to create too much polarization between
training phases. For example, a traditional block periodization model for an endurance athlete
may start with an accumulation phase consisting of a high volume of easy aerobic training
followed by an intensification phase consisting of sport specific training and special endurance
work, and then it will finish with a realization phase where the focus is integrative preparedness
and event specific tactics. While this approach has been shown to work in the past, I do not
believe it is optimal as it does not coincide with how our bodies build, maintain, and regulate
adaptation. For example, block periodization structures are concerned with building a given
training quality, like an aerobic base for a handful of weeks, then switching the focus to other
qualities such as speed in hopes that the athlete will end up in a better position then when they
started. I believe a better approach is to never drop off any given training quality entirely —
instead I advocate for training all qualities at all times and adjusting the relative contribution of
each training quality based on an individual’s highest priority at the moment. Despite the LBP
model being split into phases I do not recommend only prioritizing limiter training in the limiter
phase, bridge training in the bridge phase, and so forth. Instead I recommend that limiter training
is the highest priority in a limiter phase and that the remaining training time is spent on bridge
and performance training, or maintaining other adaptations. The same concept holds true for the
bridge and performance phases as well. Additionally, I advocate for programming in short one to
two week training cycles with micro adjustments made between each cycle based on the athlete’s
feedback. This arrangement allows for dynamic adjustments and makes it easier to build and
maintain adaptations versus a block periodisation approach. From one mini cycle to the next few
changes are made to the training program, but over multiple months clear distinctions before
identifiable. I liken this approach to the arc the iphone has taken over the past fifteen years. From
the first to second generation iphone, or the ninth to tenth, little has changed. But, when you
compare the first and tenth generation iphone there is a massive difference. However, the
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aforementioned changes occurred so gradually as to not be noticeable. Training should work in a
similar way. In an athlete centric training paradigm the next mini cycle depends on the response
to the prior one, which means that few changes are warranted if the athlete is actively
progressing.
Athlete Centric Coaching Made Simple
Monitoring internal and external workloads over time simplifies the athlete centric
coaching process and removes the need for guesswork when designing training programs. In the
image above you’ll find muscle oxygenation measurements from a tactical athlete performing the
exact same workout on two different days separated by three weeks. The workout they
performed included eight sets of a four hundred meter run in seventy-six to seventy-eight
seconds per set with thirty seconds between sets.
In the interim period between the first and second time this athlete performed the workout
they prioritized workouts that enhanced their respiratory muscle endurance and cardiac output
with the eventual goal of improving their two mile run performance. The aforementioned key
performance indicators were chosen because this athlete needs to improve their cardiovascular
control. During race pace efforts this individual diverts a high percentage of their cardiac output
to their respiratory muscles to support continuous and prolonged hyperventilation. For them the
easiest way to improve cardiovascular control is to increase the strength and capacity of the
respiratory muscles so they do not require as much oxygen while running at race pace.
Additionally, they can increase cardiac output which will allow them to shunt more blood to the
respiratory muscles so when they do inevitably fatigue extremity muscle blood flow will not be
compromised to as meaningful a degree.
In addition to displaying muscle oxygenation in the image above, you’ll also find the
aforementioned athlete’s rate of change of muscle oxygenation, termed ΔSmO2. Whereas SmO2
reflects the amount of oxygen in a muscle at a given point, ΔSmO2 reflects the balance of
oxygen supply and demand in said muscle. The more negative the ΔSmO2 value gets the greater
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the rate oxygen utilization is outstripping oxygen supply, and vice versa. Of particular note is
that from week one to week four my athlete is not desaturating the working muscle as much
during the 400m repeats — this is reflected by the fact that the SmO2 trend from week four (in
green) is higher than the trend in week one (in purple). Additionally, their ΔSmO2 from week
one is -0.4 (%/s) versus -0.1 (%/s) in week four, indicating that this athlete’s ability to supply
oxygen to the working muscles has improved relative to their muscle oxidative capacity. When
we consider the fact that this athlete maintained their speed across the two sessions we can
contextualize this physiologic data and come to the conclusion that they have improved their
efficiency and running economy.
In the absence of performance data we can’t make sense of muscle oxygenation
measurements, but when we contextualize this physiologic data with measurements of power,
speed, or endurance we can start to get a more complete picture of how an athlete is adapting to
training over time. This is a major benefit of the NNOXX wearable because it captures internal
biomarker measurements as well as external measurements of speed and power output.
Furthermore, it can help us decide what the next step is for making additional performance
improvements. Had we decided to prioritize improving this athlete's oxygen extraction after
week one, we would have quickly hit a wall since the margin for improvement was so small
considering that they were already deoxygenating the working muscles down to 3-5% SmO2.
However, after the second workout there are more paths to improvement, and we can aim for
some combination of improving oxygen supply and demand.
By combining physiologic measurements and performance metrics we can take the
guesswork out of the coaching equation and simplify lofty concepts such as athlete centric
coaching and dynamic periodization. Rather than projecting our plans out weeks in advance we
can turn each training session into an assessment, allowing for tighter feedback loops and more
strategic decision making.
Are You Really Assessing Performance Improvements?
Having an evaluation process that determines if an athlete has improved in key
performance indicators is critical for understanding how successful an individual’s training is
over time as well as how different protocols impact a given individual's physiology and fitness.
As coaches, sports scientists, and trainers we’re always working in an applied setting — as a
result we’re tasked with making decisions that will have the greatest impact on a specific athlete
with a unique performance fingerprint. It’s not enough to say that 8/10 athletes in your program
are improving in some specific quality — we need everyone to improve and that warrants having
a somewhat sophisticated assessment process.
For starters, analyzing athlete data requires understanding what the test is measuring, and
if it’s a valid test for what you’re trying to measure in the first place. Assuming the test is capable
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of measuring what you want it to we then need it to have a minimal amount of noise and error.
Tests that are too noisy make it exceptionally difficult to know if improvements (or lack thereof)
are due to true improvements in fitness, measurement error, or just biological variation. For
example, let’s say that you wanted to improve your athlete’s VO2max (which represents the
maximum integrated capacity of the pulmonary, cardiovascular, and muscular system to uptake,
transport, and utilize oxygen respectively), but you lack a metabolic analyzer to measure expired
gas concentrations. In this hypothetical scenario you come across a research paper saying that
improvements in 2,000m row time trial performance are valid predictors of VO2max
improvements. Even if that were true, there is a lot of noise in this test. For example, racing
tactics, a willingness to suffer, and day to day variability in performance can all have a
significant impact on trial performance, which can lead a coach to believe that their athletes
VO2max improved by a much greater margin than it really did, or that they didn’t make
improvements to their VO2max when they did in fact.
It’s also important to acknowledge and accept the role of random chance, or dumb luck,
in performance. As a result, recognizing that all athletes exhibit some level of regression to the
mean helps us contextualize their performance on a given day. Additionally, because of the
inevitable regression to the mean, an athlete is most likely to not improve on a performance test
after having a major breakthrough. It’s easy to mistake a regression towards the mean as a failure
to increase sports specific fitness, which highlights the importance of looking at longer term data
trends. For example, in the image below we have an athlete's snatch 1-RM recorded from a
weekly mock meet plotted against time in weeks. Note that in weeks 1-3 they lift loads ranging
from 103-104.5kg. In week 4 they have a breakthrough, hitting 108kg, then over the next 6
weeks they fail to beat 108kg. Does that mean that this individual increased their sport specific
strength for 4 weeks, then failed to make additional progress? The short answer is no. If we look
at their loads for weeks 5-8 for example we see that their 1-RM ranges from 104.75kg to 106 kg,
and in week 7-10 their 1-RM ranges from 105.75kg to 106.75kg. Despite the fact that this
individual does not best 108kg in weeks 5-10, the 3 week rolling average of their 1-RM increases
significantly, as does their normalized snatch 1-RM. Similarly, if a baseball player starts the
season going 7 for 10 we wouldn't assume that they have a 0.700 batting average — we
intuitively know that they will regress towards their own mean, settling to something more
normal given their true abilities.
Given all of the points mentioned above I’m inclined to take the results of any given
performance test with a grain of salt. As a result, I seldom make decisions about how to
restructure an athletes training plan based on a single test or competition. I’m also skeptical of
the traditional test-retest method of program design. Instead, I like to look at long term
performance trends as well as biomarker data to make informed decisions about the direction of
an athletes program
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