Molecular Exercise Physiology
Endurance training
Presentation 2
Henning Wackerhage
Learning outcomes
At the end of this presentation you should be able to:
• Explain how a maximal oxygen uptake test and lactate
threshold test are carried out and how the data are
interpreted.
• Describe the major cardiovascular and muscular adaptations
to endurance training.
• List the major forms of endurance training.
Adaptation to endurance training
Part 1
How to test for endurance capacity?
What makes a good endurance athlete?
Endurance athletes need to have a large heart (athlete’s heart
syndrome) and a high maximal cardiac output (COmax) to pump
oxygenated blood to their working muscles. The blood should have a
high haematocrit (i.e oxygen transport capacity). Their exercising
muscles need to have a high percentage of slow fibres (also known
as type I fibres) surrounded by many capillaries. Trained muscle
fibres contain more mitochondria, enzymes for fat metabolism
and have a higher glycogen concentration when rested than
untrained muscle fibres. In addition, good endurance athletes need a
high economy (i.e. energy for given work) for the sport they engage
in.
How can we test the performance of an endurance athlete? There are
two major tests:
1) Determination of maximal oxygen uptake;
2) Determination of the lactate “threshold”.
Determination of maximal oxygen uptake
Subjects perform a graded exercise test (i.e. the work is increased
stepwise). Oxygen uptake is measured until the athlete fatigues.
The maximal oxygen uptake is usually related to the body weight of
a subject.
Task: Interpret the figure on
the left.
Rowell (1993)
Lactate threshold
Determining the maximal oxygen uptake give a good indication about
the talent of an individual for endurance sports. A second test is to
determine the “lactate threshold”. The power output at the lactate
threshold is usually better correlated with actual endurance
performance than the maximal oxygen uptake.
Lactate is generated from pyruvate by lactate dehydrogenase. Its
concentration depends on the rate of glycolysis (which is the rate of
pyruvate production) minus the rate of pyruvate oxidation by
oxidative phosphorylation.
The rate of glycolysis increases with
exercise intensity. Endurance athletes
Glucose, glycogen
have many mitochondria and can thus
combust more pyruvate by oxidative
Pyruvate
phosphorylation. That is why lactate is
Oxidative
lower in endurance athletes at any given
Lactate phosphorylation intensity than in untrained subjects.
Athletes reach 4 mM lactate at higher workloads
Athletes again perform a graded exercise test. Small blood samples are
obtained from the earlobe or fingers. The relationship between power
and [lactate] is plotted and the power at 4 mM lactate determined. The
higher the power at 4 mM the more endurance trained the subject.
[Lacate] mM
8
Task: Interpret the
figure on the left:
Which
subject
is
more
endurancetrained?
6
4
2
0
100
Power (W)
200
300
Determinants of endurance performance
Task: Interpret the schematical drawing below. What do the
abbreviations mean?
Endurance training
Part 2
Adaptation to endurance training
Homo sapiens: did we evolve as endurance runners?
Bramble DM and Lieberman DE. Endurance running and the evolution
of Homo. Nature 432, 345-352, 2004. In this landmark paper,
Bramble and Lieberman argue that the anatomy of human beings has
been selected for endurance running. The compare human beings
and argue that human beings are actually very good at covering long
distances when compared to numerous other species. Many skeletal
features are advantageous for endurance running especially when
compared to close species. They hypothesize that endurance running
helped hominids to exploit protein-rich resources such as meat,
marrow and brain.
If the evolutionary pressure
was favouring an endurance
running human then our
anatomy, biochemistry and
muscle function may have all
been selected for endurance
running.
Human
A. afarensis
Chimpanzee
No comment
Adaptation is the key mechanism of training
Evolution is one mechanism by which a species adapts to its
environment (i.e. natural selection of genotypes; survival of the
fittest; Darwin 1809-1882).
A second mechanism is the functional adaptation of organs. Roux
(1881) suggested that the functional adaptation of cells is regulated
locally, governed by stimuli, in a self-organisational process. He
explains that cells can adapt to signals with specific adaptations.
Functional adaptation is the key mechanism by which training induces
specific changes in the structure or size of our organs. It is
responsible regulating the growth of the athlete’s heart, of increases
in muscle “fitness” and size and strength of bones in response to
exercise.
Task: Describe 3 functional adaptations of tissues to
stimuli other than exercise.
W. Roux
How does adaptation work?
There has been much speculation about how adaptation to training
may work. One example is the “supercompensation” theory that has
been proposed by Yakovlev (1967). It is an important model but fails
to explain the underlying mechanisms. In addition, it does not apply
to all systems (for examples, a heart always “trains” but still
hypertrophies in response to exercise).
System status
Molecular exercise physiology has dramatically changed our
knowledge about how adaptations occur: Molecular exercise
physiologists have discovered several signals, the communication of
these signals and their link to adaptive responses.
Supercompensation
Return to normal
Compensation
Training
Time
Yakovlev (1967)
Specific adaptations to endurance training
Endurance training induces performance-enhancing adaptations
mainly in the cardiovascular system and in the exercising muscles.
However, other tissues such as bones, tendons, the immune system,
liver and brain adapt as well. The following slides show some
examples for adaptations.
Better antioxidant
defence
Better glucose
Increased fatigue
uptake and
resistance
higher glycogen
concentration
Higher rate of
fat metabolism
Cardiac hypertrophy (athlete’s
heart) facilitating greater stroke
volume and maximal cardiac
output
Cardiovascular system
Slower motor
proteins
Lower rate of
maximal ATP
More capillaries
hydrolysis
(angiogenesis)
More mitochondria
(mitochondrial biogenesis)
Muscle
Athlete’s heart
This study shows the increase in heart volume over time in
competitive swimmers. Note the decrease in heart volume in
swimmers that end their swimming career.
Rost (1997)
Athlete’s heart
The volume of a normal heart is 750-800 ml whereas endurancetrained athletes reach 900-1200 ml. The figure shows the largest
healthy heart reported in literature. It was 1700 ml and belonged
to a world champion in professional cycling.
Hollmann (1965)
Athlete’s heart
The larger the heart of the athlete, the larger the stroke volume of the
heart. Because maximal heart rate does not change much with
training, the stroke volume largely determines the cardiac output
during maximal exercise. Maximal cardiac output and maximal oxygen
uptake correlate (see figure).
It seems likely that the size
of the heart (or its maximal
stroke volume) is a key
determinator
of
maximal
oxgygen uptake.
Ekblom (1969)
Mitochondrial biogenesis
Exercise also increases the number of mitochondria in muscle
fibres. The figures shows a large increase in mitochondria (stained
dark) in a muscle that was electrically stimulated for several
weeks. Such stimulation may be viewed as an extreme exercise
stimulus.
Control
Increased mitochondrial density
after chronic electrical stimulation
Salmons, Jarvis, Higginson, Manolopoulos,
Woods,
Wackerhage,
unpublished
data
(2001)
Endurance training increases fat metabolism
After a period of endurance
training,
total
energy
expenditure
is
unchanged
(because the exercise still
requires the same amount of
energy).
Fat
combustion,
however, is increased whereas
carbohydrates or glycogen are
saved.
Hurley et al. (1986)
Fast-to-slow exchange of motor proteins
Chronic electrical stimulation
also exchanges faster with
slower motor proteins. The fast
myosin
heavy
chain
IId/x
(MHCIId/x; ) and MHCIIb ()
motor proteins decrease and
the intermediate MHC IIa ()
motor protein increases.
Exercise usually only leads to a
small decrease of the fast MHC
IIx and a small increase in the
MHC IIa motor proteins.
Jaschinski et al. (1998)
It is unclear whether exercise is just a lower “contraction” dose than
chronic electrical stimulation or whether different mechanisms are
involved.
Angiogenesis
Another adaptation of endurance training is the increase in the
number of capillaries that nourish a muscle fibre. The capillary-tofibre ratio correlates with the maximal oxygen uptake and increases
with training.
Brodal et al. (1977)
Task: Critically examine the figure above. Does it proof the effect
of training on capillary growth? Does it proof that more capillaries
per fibre increases maximal oxygen uptake?
Endurance training
Part 3
Endurance training methods
Endurance training
Today’s endurance training methods have not been scientifically
developed. They are the result of subjective interpretations of trial
and error “experiments”. Things that usually work well have been
kept while training regimes that did not work have been abandoned.
Endurance athletes usually train at various intensities with a focus
on low to medium intensities. The total training volume depends on
the sport. Swimmers and cyclists often train up to 6 hours a day
whereas runners can run little more than 2 h probably because of
the eccentric form of exercise.
Athletes also periodise their training. The usual strategy is to train
high volume first and then to reduce volume and to increase training
intensity. Here, I will restrict myself to explain some major
endurance training forms.
Long slow distance (LSD)
A key endurance training method is long
slow distance training. It is used
especially by Marathon runners, cyclists,
triathletes, cross country skiers and
athletes competing in similar sports.
Duration: 30 min-6 h
Intensity: 50-60% of VO2max or
HRreserve (some recommend higher
intensities).
Examples: 20 mile run, 100 mile cycle
ride.
Effects: Decrease in muscle and liver
glycogen
(which
stimulates
supercompensation),
high
energy
turnover and fat combustion.
Medium and high intensity continuous training
LSD training is the major training form but alone
is insufficient. Medium and high intensity
continuous
training
prepares
athletes
for
maintaining a high pace.
Duration: 20 min-70 min
Intensity:60-85% of VO2max or HRreserve.
Examples: 60 min run at 75% of HRreserve.
Effects: Higher rates of fat and carbohydrate
combustion than LSD; train motor units that are
not normally activated during LSD; exercising
closer to race pace (depends on race distance).
Interval and fartlek training
A small percentage of the total training
load; especially used closer to competitions.
Duration: up to 60 min (exercise training)
or 90 min (runner’s fartlek).
Intensity: >85% of VO2max or HRreserve.
Examples: 10 X 1000 m running; 70 min
fartlek (running all uphill sections at high
intensity).
Effects: Close to 100% carbohydrate
oxidation;
medium
to
high
lactate
concentrations reached; innervation of
intermediate and fast motor units; race
pace or above.
Adaptation is the key mechanism of training
Task:
1) A popular but unproven assumption is that a system adapts
more if it is used more. Assuming this assumption was true,
explain whether long slow distance or high-intensity endurance
training is best to:
a) increase mitochondrial biogenesis;
b) increase angiogenesis;
c) increase heart volume;
d) increase fat oxidation.
2) We now know that adaptations are regulated by
signals/stimuli that occur within an exercising muscle. Name 5
signals/stimuli that change with exercise in muscle.
The End