Kine 1020: Exam Review
Why is Strength Important?
Performance-Related
 Sport
o Greater power, speed and balance
o Reduce demands on cardiovascular system
 Job/Occupational Requirements
o Reduced risk of injury
o Productivity
Health-Related
 Lower risk of functional limitations
o Avoid injuries/infirmity
o Predictor of advanced age disability
o Reduces chronic low back pain
 Lower Risk of Chronic Diseases
o Improved blood sugar control
o Retard/prevents osteoporosis
o Increase metabolic rate
 Psychological Heath
o Improved self-­­image
o Emergencies
 Emergencies
HEALTH-RELATED
 Maintaining or improving muscular strength later in life reduces the
percentage of functional limitations by over 50% for both men and women.
 Peopleawith greater muscle strength during midlife are at a lower risk
of becoming disabled because of their greater reserve of strength rega
rdless of chronic conditions that may develop.
Decreasing Muscle Strength With Aging



Sarcopenia is the loss of muscle mass and strength due to aging process
o ~1-2% muscle mass per year past 50 yrs of age – loss of strength varies
and may be greater
Prevalence
o Impacts 10-25% of the population under 70 yrs of age and ~40% above
80 yrs of age
o By 80 yrs a loss of 30-40% of the muscle fibers (hypoplasia of muscles
containing Type II muscle fibers)
Concerns
o Risk of functional limitations
Sarcopenia is a result of Programmed Cell Death – Apoptosis
Characterized by:
 DNA fragmentation; and
 Nuclear condensation leading to formation of apoptotic bodies (these are
engulfed by macrophages but do not induce an inflammatory response)
Potential Causes of Sarcopenia
I)
Activation of apopotic pathways – caspases (enzymes that breakdown
and degrade proteins and DNA)
II)
Loss of hormonal adaptations (decrease in testosterone and growth
hormone)
III)
Loss of neurological influences (selective loss of type II motor units
resulting in cluster of Type I muscle fibers with age)
Activation of proteolytic pathways – proteases (enzymes that breakdown and
degrade proteins) by:
I.
Caspase-dependent
a) Ionic Imbalance (accumulation of intracellular calcium)
b) Oxidative stress (accumulation of reactive oxygen species (ROS)
which are considered damaging)
c) Mitochondrial dysfunction (a decline in ATP levels, increase in oxygen
free radicals – membrane leakage)
II.
a) Mitocohondial dysfunction – apoptosis-inducing factor (AIF) – results
in DNA fragmentation
Inpact of Training (strength and endurance) on Apoptotic Pathways in the
Elderly
 Improved calcium handling – therefore not as much accumulation
 Increased Bcl-2/Bax ration (therefore less cytoch-c leakage)
 Decreased Apaf-1
 Reduced AIF
Muscles Diseases: Definitions and Types
Any disorder or disease that affects the human muscle system:
a) Primary Muscle Disease – the pathology originates with the muscle (internal
membranes/metabolic) disorders; [examples – McArdle’s Disease; Forbe’s
Disease]
b) Secondary Muscle Disease – the pathology originates in other systems:
 Nerve – neuromuscular disease/disorder [Parkinson’s Disease;
muscular dystrophy]
 Bone/joint – musculoskeletal disease/disorder
 Inflammatory System – inflammatory muscle diseases/disorders
[Dermatomyositis]
 Immune System – autoimmune muscle diseases/disorders [Multiple
Sclerosis; Myositis; Muscle Rheumatism]
Muscle Diseases: Symptoms/Indicators
1) Muscle atrophy (decrease size) and accompanying muscle weakness
2) Pain – defects in cardiovascular system, inflammatory system
3) Tetany – involuntary contractions (spasms) because of changing calcium
levels – generally larger muscles of arm and legs;
4) Twitching – single motor unit firing due to loss of nerve cells – typically close
to surface of the skin
5) Muscular hypertrophy and accompanying increase in stiffness (myotonia
congenital); increase size due to more fat in muscle – form of muscular
dystrophy
6) Biochemical parameters
 Reduced muscle glycogen; mitochondrial oxidative potential;
 Increased myoglobin, acid maltase; CK…
Muscle weakness  failure to develop an expected force which can be attributed
any one of the processes requires for force generation. This is associated with all
types and examples of muscle diseases/disorders
Classifications:
a) Upper motor neuron disease
 Muscle weakness typical of upper motor neuron disease includes:
I)
CV-stroke producing weakness of one side of the body. The arm is
typically flexed, the leg is extended, and the limbs have increased tone.
Some movement may be preserved, although the use of the hand is
particularly limited.
II)
With upper motor neuron disease the muscle bulk is usually well
preserved (different than lower motor neuron)
III)
Other causes of upper motor neuron disorders include tumors and
spinal cord injury
b) Lower motor neuron disease – flaccid muscle weakness
1. Spinal Cord – muscle wasting is prominent  shrinkage and eventual death of
neurons  denervation of muscle.
I)
II)
III)
IV)
Motor neurons lying in the spinal cord  most common amyotrophic
lateral sclerosis and Lou Gehrig disease
Generally between 50 and 70 years of age and have upper and lower
motor neuron weakness – paralysis progresses rapidly, and death
within three years.
Infant amyotrophic lateral sclerosis is fatal within one year
No cause is yet known for any of these diseases, and no cure is
available
2. Peripheral Nerves Diseases (peripheral neuropathies or polyneuropathies)
 Symptoms usually begin in the hands and feet and progress toward the body
– also associated with sensory disturbances
I)
Peripheral neuropathies – degeneration of the axons (core of nerve
fibres).
 Axons can regenerate but only at a rate of one to two
millimetres per day. Thus, after injury to a nerve at the elbow
the hand will not recover for six to nine months.
 Damage to blood vessels (physical and/or chemical) tend to
cause axonal types of neuropathy.
II)
Myelin Sheath – peripheral neuropathy caused by degeneration of
the myelin sheaths (covering of axons) – demyelinating neuropathies
 Symptoms are similar to axonal neuropathies but since the
axons remain intact, the muscles rarely atrophy.
 Recovery from demyelinating neuropathies can be rapid
 Other causes of peripheral neuropathy include diabetes
mellitus nerve trauma, inherited factors, and chronic renal
failure
c) N-M junction disease
I)
These diseases are associated with weakness and fatigability with
exercise.
II)
Diseases of the neuromuscular junction typically involve the
generation of an end-plate potential that is too low to propagate an
action potential in the muscle fibre.
III)
Diseases of neuromuscular transmission may be acquired or inherited
and may be the result of autoimmune disorders, such as myasthenia
gravis congenital disorders; toxins such as those present in botulism
Muscle weakness  Etiology
Muscle contraction results from a chain of events that begins with a:
I)
Nerve impulse traveling in the upper motor neuron from the cerebral
cortex in the brain to the spinal cord
II)
The nerve impulse then travels in the lower motor neuron from the spinal
cord to the neuromuscular junction;
III)
Where the neurotransmitter acetylcholine is released. Acetylcholine
diffuses across the neuromuscular junction, stimulating acetylcholine
receptors to depolarize the muscle membrane
IV)
The result is the contraction of the muscle fibre (actin/myosin)
 Contraction depends on the integrity of each of these parts;
disease or disorder in any part causes muscle weakness.
Muscle Diseases: Muscular Dystrophies
The muscular dystrophies are a group of hereditary disorders (n=9) characterized
by progressive muscular atrophy and weakness. In most varieties the muscles of
the limb girdles – the pelvic and shoulder muscles – are involved.
There is a progressive loss of muscle size and strength which is caused by loss of
muscle proteins later changing to muscle fiber death and tissue death
Assessments include:
I)
Measurement of the activity of creatine kinase in the blood
II)
Analysis of a muscle biopsy (structural), and
III)
Recordings from an electromyography frequently establish that the
muscle weakness is due to primary degeneration of the muscles
Nine Types of Muscular Dystrophy
Steinert’s Disease or Myotonic Muscular Dystrophy:
 It is the type of muscular dystrophy which is most common in adults, as its
name tells, in this disorder the muscles remain in spasms or become stiffened
after slight use or exercise, and lower temperatures increase these
symptoms.
 This type affects both males and females
Duchenne Muscular Dystrophy:
 It is the type which is most common in children and it only affects males
between 2-6 years of age, decrease in the mass of muscle is progressive and
in most cases the children are wheelchair ridden by the start of their teens
years
 Usually do not survive more than 20 years
Becker Muscular Dystrophy:
 This type similar to Duchenne but the symptoms are milder and can appear
till 25 years of age. Usually the affected people can live and enjoy life and are
also able to walk but they have some heart problems and is present only in
males.
Emery-Dreifuss:
 It is the type which affects from childhood to teen years and is present only
in the males
 It affects the muscles of pectoral region to upper arms and lower parts of legs
 And along with that patients have extreme heart problems that are usually
fatal
Limb-Girdle:
 It is the type which affects from teenage years to adulthood and is present in
both males and females
 As the name indicates, in this type the problem starts from hip (pelvic girdle)
region and then reaches to the shoulders (pectoral girdle) and later legs and
arms are also affected
 The sufferers are unable to walk and most patients live past mid adulthood
Fascioscapulohumeral Muscular Dystrophy:
 As the name indicates in this type of muscular dystrophy the muscles of face,
scapula (shoulder blade) and humerus (shoulder joint and elbow joint) are
affected
 It affects both males and females but about half of the sufferers are able to
walk throughout their life
 And almost all the patients live a normal life span
Oculophyrangeal Muscular Dystrophy:
 It is the type of muscular dystrophy which affects primarily the muscles of
eyes and throat which occur around 40s to onward ages
 Symptoms include the weakness of eyes and facial muscles which could later
cause swallowing problems
 This type predisposes the patients to pneumonia and choking
Muscle Diseases: Myasthenia Gravis
Myasthenia gravis is an acquired autoimmune disorder that involved a failure in the
transmission of nerve impulses to the muscles and is characterized by persistent
muscular weakness and a tendency of muscles to be easily fatigued.
Symptoms include:
 Weakness is particularly of the face, limbs, and neck
 Double vision
 Difficulty swallowing and breathing
 Excessive muscle fatigue during exercise with partial recovery after rest
Disease can be controlled by:
1) Treatment with high doses of corticosteroids (which depress the immune
response)
2) Anticholinesterase medications (which stimulate the transmission of nerve
impulses)
Muscle Diseases: Myotonic Diseases
Myotonia is a difficulty in relaxing (slow relazation) a muscle after contraction (i.e.,
relaxing the hand after a handshake).
Causes:
 Continuing electrical activity of the sarcolemma (the membrane of striated
muscle fibres) – multiple firing of the nerve is most common form
 Problem lies in abnormal ion channels or ion pumps in the
sarcolemma
 Delayed disengagement of the thick and thin filaments of myosin and actin
Physical inactivity and cold enhance the condition.
Muscle Diseases and Disorders: Fibromyalgia
Fibromyalgia is a common syndrome in which a person has long-term, body-wide
pain and tenderness in the joints, muscles, tendons, and other soft tissues.
Fibromyalgia has also been linked to fatigue; sleep problems, headaches,
depression, and anxiety
Causes and Incidence:
 The cause is unknown. Possible causes include:
I)
Physical or emotional trauma
II)
Abnormal pain response – EEG  areas in the brain that are responsible
for pain may react differently in fibromyalgia patients
III)
Sleep disturbances
IV)
Infection, such as a virus, although none has been identified
Fibromyalgia is most common among women aged 20 to 50
Symptoms:
 Pain is the main symptom of fibromyalgia – ranging from mild to severe.
I)
Painful areas are called tender points. Tender points are found in the soft
tissue on the back of the neck, shoulders, chest, lower back, hips, shins,
elbows, and knees. The pain then spreads out from these areas.
II)
Pain may feel like a deep ache, or a shooting, burning pain
III)
Joints are not affected, although the pain may feel like it is coming from
the joints
 Tend to wake up with body aches and stiffness
 Pain can improve during the day or stay all day
 Pain may get worse with activity, cold or damp weather, anxiety, and stress
Fatigue, depressed mood, and sleep problems are seen in almost all patients with
fibromyalgia – difficulty falling and staying asleep; constant feeling of tiredness
Assessment:
 To be diagnosed with fibromyalgia, you must have had at least 3 months of
widespread pain, and pain and tenderness in at least 11 of 18 areas,
including: arms (elbows), buttocks, chest, knees, lower back, neck, rib cage,
shoulders, thighs
Treatment:
 The goal of treatment is to help relieve pain and other symptoms, and to help
a person cope with the symptoms
 The first phase of treatments may involve one or more of the following:
I)
Physical therapy
II)
Exercise and fitness program
III)
Stress-relief methods, including light massage and relaxation
techniques
Skeletal Muscle: Adaptations, Strength Training and Conditioning
Outline
 Muscular Adaptations
 Acute – injury and damage
 Chronic – fibre transitions, hypertrophy
 Timing
 Principles of Strength Training
 Program Design Characteristics
Strength/Resistance Training and Muscular Adaptations
Acute changes – are associated with
Skeletal Muscle Fatigue
a) The inability to maintain the required power output which is related to a
decline in both force and velocity.
b) A condition in which there is a loss in the capacity for developing force
and/or velocity of muscle resulting from muscle activity under a
demand/load which is reversible by rest
c) The inability to maintain the required power output which is related to a
decline in force, velocity and power, which is reversible
Acute Changes – Characteristics of Fatigue: Eccentric Contractions
 Decreased strength/power output
 Muscle damage (injury)
 Delayed onset muscle soreness (DOMS)
 Restricted range of motion (ROM)
 Increased blood proteins
Many mechanisms have attempted to explain the fatigue process
Fatigue – possible sites/causes
Central
1)
2)
3)
4)
Planning of voluntary movement
Motor cortex and supraspinal outputs
Upper motor neurons
Lower motor neurons
Peripheral
5) Neuro-muscular (NM) junction and sarcolemma
6) Sarcoplasmic reticulum (Ca2+ movements)
7) Actin-myosin interaction
8) Metabolic supple (all 3 systems) and accumulation
Neuro-Muscular (NM) Junction and Sarcolemma: High Intensity Contractile
Activity
A) Neuromuscular junction:
 No evidence that N-M blockage (either release or uptake of
acetylcholine) is a problems
B) Sarcolemma and t-Tubule Systems:
 Action potential propagation – is changed
I)
Fatigue is associated with a +10mV change in membrane potential;
resting membrane electrical potential goes from -80 to -70mV with heavy
exercise
II)
Fatigue associated with a drop in the amplitude of the action potential
(peak of excitation); therefore not sufficient to activate channels in Ttubule system – caused by potassium (K+) leaking out of muscle cell
(which is accompanied by Na+ leaking in)
III)
Na+-K+ pump has been suggested – decrease in ATP or increase in ROS
Sarcoplasmic Reticulum (Ca2+ movements)
Fatigue with heavy exercise associated with:
 A reduction in SR calcium concentration as a result of decreased SR Ca2+
ATPase pump (SERCA) and/or because more calcium remains bound in SR
(possibly linked/bound to phosphate)
I)
Reduced SERCA activity due to:
 Lower [ATP]
 Inefficient or Leaking – because of action of ROS
II)
Increased Binding due to:
 Increased inorganic phosphate which comes from increasing
muscle contractions
 End result less calcium for releaseupon stimulation/excitation and
conversely more calcium remains in the cytoplasm with heavy exercise
(fatigue)
Muscle Weakness and Low Frequency Fatigue (LFF)

The Ca2+ release channel (ryanodine receptor – RyR) does not release
sufficient calcium – ‘less activation’
Actin-Myosin – Contractile Protein Interactions
Fatigue with heavy exercise associated with:
I)
Increasing inorganic phosphate (pi)
 Which delays detachment phase of A-M cross-bridges
II)
Increasing hydrogen ions levels will decrease the pH
 Heavy exercise from ~7.2 to ~6.8 (more acidity)
 Myosin ATPase activity is reduced at lower pH
Fatigue with heavy exercise associated with:
I)
Loss of contractile protein(s)
 ~60% reduction in each of myofibrillar proteins troponin-I,
tropomyosin
II)
Loss of cytoskeletal (structural) proteins
 ~%0% loss of alpha-actinin (z-line)
 ~80% loss of desmin (myofibril-linking protein)
Cause:
 Myofibril protein losses a result of increased protease activity – calcium
activated neutral protease
 Calpain (CANP1; CAPN2)
Metabolic Supply (3 systems) and Accumulation
Fatigue with heavy exercise associated with:
A) Phosphagen Sources
I)
Reduced levels or lower supply of creatine phosphate (CP) or
phosphocreatine (Pcr) – can be ~80% depleted
B) Anaerobic Glycolysis
I)
Lower supply – reduced glycofen concentrations
II)
Build up or accumulation of intracellular muscle lactate (vs lactic acid)
C) Aerobic – oxidative phosphorylation
I) Accumulation or increased ROS
Chronic Impact of Fatigue with Heavy Strength/Resistance Exercise
Resistance training  Muscle hypertrophy
Endurance training  Mitochondrial biogenesis
Muscular Adaptations to Strength/Resistance Training
Muscular Adaptations – remodeling
A) Muscle Fibre Transitions
B) Muscle Hypertrophy
C) Timing of Muscular Adaptations
Muscular Adaptations – Remodeling
 Formation of new muscle fibres is critical to normal muscle function –
‘turnover’
 Number and type of muscle fibres genetically determined
 Replace old fibres with new fibres – remodling
 Formation of new muscle fibres is called myogenesis;
 Satellite cell  myoblast  myotube  muscle
 Activators include myoD and myogenin
 Inhibitors include myostatin
Stimulation of myogenesis with training?
 Resistance Training
 Increases myoD and myogenein expression (peak ~36hr)
 Reduces myostatin

Endurance Training
 Modest impact on regulators of myogenesis
Muscular Adaptations – Muscle Fibre Transitions (identified through MHC)
Transformations
I)
MHC – T1/2 is ~30 hrs
II)
MHC changes after 2-3 workouts
III)
More oxidative
Muscular Adaptations – Hypertrophy
 Increase in size of muscle (also muscle fibre) with
strength/resistance/anaerobic training
 Increase in muscle fibre size due to more protein (accretion) as a result of
increased protein synthesis
 Therefore hypertrophy resulting from training is a result of protein
degradation and protein synthesis
 Cucles of degration (PD) and synthesis (PS) are critical for hypertrophy (and
transitions)
 PD – peak at end of exercise and slows down in recovery lasting ~24hrs
 PS – little increase immediately after exercise and reaches peak ~36-48hrs of
recovery
 Factors promoting PS
 Are there muscle fibre specific adaptations?
Muscular Adaptations – Hypertrophy and Muscle Fibre Types
Resistance Training
 Both types increase (Type II>I)
 3-6 months:
 increase in Type II ~35%
 increase in Type I ~20%
 Athletes vs untrained:
 Type II ~132% then UT
 Type I > ~60% then UT
Factors Promoting Protein Synthesis:
 Intensity and volume of the workload
 Principles of strength/resistance training
 Nutrient intake
 Type
 Timing
 Hormonal Environment
Intensity and volume of the workload
I)
Contraction Type – eccentric > concentric:
Type I  CON(0%); ECC(25%)
Type II  CON(5%); ECC(40%)
*linked to increased protease activity  damage:
leading to increased organelle disassembly (i.e., sarcomere), protein
targeting (E3-ligases)  cell ‘clean-up’
II)
Tension – greater tension > membrane disruption results in
 Release of growth factors (calcineurin) and
 Increase in signaling pathways (kinases; AkT; mTOR) for gene
transcription and PS
III)
Metabolic Stress – greater anaerobic contribution to energy (ATP)
production  greater growth hormone response
Associated with:
 High tension – restricted or occluded blood flow
 Moderate loading, high volumes and short rest intervals
Nutrient Intake
I)
Water (cellular hydration is associated with decreased protein
degradation and increased protein synthesis
 Creatine loading – results in cellular hydration
II)
Carbohydrates – increasing intake  insulin
 Strength athletes – 55%-65% CHO; or 6g/day
III)
Protein (amino acids – 9 essential increased in diet (intake) or
supplementation
 Diet recommend range of 1.7 to 2.2 g/kg
 Supplementation – brain-chained amino acids; whey protein
Hormonal Environment
I)
Androgenic – testosterone
II)
Anabolic – steroids; testosterone esters; growth hormone; testosterone
enhancers (banned, unethical substances)
Structural Changes
1. Increased number of myofibrils
2. Increased density (amount) of the sodium-potassium pump (Na2+-K+ATPase); sarcoplasmic reticulum; and t-tubule
3. Results in an improved calcium handling (important for power/speed
activity)
4. Hyperplasia (increase in muscle fibre number) – human?
Strength/Resistance Training: Principles of Program Design
 Progression (habituation) is a long term goal of all programs
 No training/workout equals no benefits
 Ten Success Factors
 Muscle Action(s)
 Repetitions
 Set
 Volume
intensity
frequency
 Exercise Selection
 Exercise Order
 Rest Periods/Intervals
 Repetition Velocity
Muscle Actions
 ECC>CON – both are considered dynamic actions with constant external
resistance (i.e., isoinertial) results in variable force production throughout
the range of option (ROM)
 ISOM (isometric) – no movement with constant external resistance
 ISOK (isokinetic) – variable external resistance – force production across the
ROM is constant
Repetition
 Complete movement cycle – ie, moving a weight up and down
Set
 A specified group or number of repetitions
Volume
 Total amount of work performed during a workout
Intensity
 Magnitude of loading (weight lifted) – related to RM (maximum weight lifted
in 1 effort) 1RM or 90% of 1RM
Frequency
 Number of training sessions per day or week
Exercise Selection
 A selected group of exercises to be performed in a session or training
program
Exercise Order
 Sequence of exercises
Rest Periods/Intervals
 Amount of rest taken between sets, repetitions and/or exercises
Repetition Velocity
 Velocity at which reps are performed
Five Basic Principles – generic to all programs:
 Progressive Overload
 Specificity
 Variation
 Individualization
 Reversibility
Principle of Progressive Overload
 Refers to gradual increase in physical stress/demand on the whole body
and/or segments
 Without PO muscles accommodate or become ‘stale’ (i.e.,
accommodation) resulting in minimal benefits
 PO required for muscular adaptations – ‘training stimulus’
 ‘Success’ factors are applied to the concept of progressive overload –
‘needed for success’
 Any combination of success variable can be applied – goal of individual
program must be identified
 National Strength and Conditioning Association
 American College of Sports Medicine
Anatomy of the Respiratory System
CONDUCTIVE ZONE (no gas exchange):
 Mouth/nose --? Trachea  larynx  bronchi --? Bronchioles  humidifies,
warms and filters are
RESPIRATORY ZONE (gas exchange):
 Bronchioles  alveoli
Lung Function Tests
 Routine spirometry tests basic lung function
Munute Ventilation (rest) = Breathing Freq (breath/min) * Tidal Volume (L)
= 12-15 (breath/min) * 0.5 (L)
= 6.0-7.5 L/min
Sinoatrial (SA) Node  “pacemaker” of the heart
P wave  activation of the atria
QRS Complex  activation of the ventricles
T Wave  recovery wave
Why do we need the atria?
 Walls are thin so blood can easily return into the heart
 Atria contractions, ‘over’ fill the ventricles so that they are slightly stretched
and allow for a better contraction and ejection fraction (Frank-starling
Mechanism – elastic recoil). Not possible with the low venous blood
pressure alone
 Ventricle walls are much thicker so that it can generate the blood pressure
necessary to distribute blood around the body
Normal Resting Values
Heart Rate (HR): 50-80 bpm
Stroke Volume (SV): 60-80 mL/beat
Elite Values
Heart Rate: 30-40 bpm
Stroke Volume: 90-110 mL/beat
Composition of Inhaled Air
21% Oxygen
78% Nitrogen
How Does Oxygen Travel in the Blood?
 Red blood cells contain several hundred hemoglobin molecules which
transport oxygen
 Oxygen binds to heme on the hemoglobin molecule
 Carries 98.5% of all oxygen molecules
 Holds up to 4 oxygen molecules
 Also carries other gasses (CO2, CO, NO, etc.)
What Happens With Exercise?
 1 L O2= 5 kcal
 The oxygen intake reaches a steady state to meet the energy demands using
aerobic metabolism
 This process takes time
 Where does the ‘extra’ energy come come?
What is a MET?
 1 MET = 3.5 mL O2/kg/min


Amount of energy you use at rest
Marker of exercise intensity
What Happens with Exercise?
Fick’s Equation: VO2 = Q x (CaO2 – CvO2)




Heart Rate: Vagal (parasympathetic) withdrawal  ~100-110 bpm (quick)
 Sympathetic activation  HRmax(slower)
Stroke Volume: Frank-Starling mechanism (elastic recoil)
 Reduced peripheral resistance
Age-predicted heart rate maximum = 220-age
 Usually accurate within 10-15 beats per minute
 Used to predict exercise intensity much easier than measuring oxygen
uptake (VO2)
Stroke Volume: Increases with exercise
 Greater contractility
 Reduced peripheral resistance (vasodialation)
Increased ejection fraction (heart empties more)
 Elite athletes have higher stroke volumes
Exercise and Oxygen Extraction
Extraction is related to the diffusion gradient, diffusion area and barriers to
diffusion
You deliver more oxygen and extract a greater proportion
What Limits Maximal Exercise?
VO2 = HR x SV (CaO2 – Cv O2)
Would we increase VO2max if we could make:
1. The heart beat faster
2. The heart beat more blood per beat
3. Deliver more oxygen
 Increases Hb in some but not all (increases oxygen delivery)
 Blood doping definitely works
4. The muscles take up more of the oxygen that is delivered to it
 More capillaries (increases diffusion area)  unlikely
Q Limits Maximal Exercise
 Muscle capacity for blood flow is greater than the heart’s ability to give it
Immediate Energy Sources Anaerobic – Alactic System
ATP = Adenosine Triphosphate
 7.3-11 kcal
ATP  ADP + Pi + Energy (2-3 sec)
PCr + ADP  ATP + Cr (6-8 sec)
Energy Systems for Exercise
Energy Systems
Immediate: ATP-PCr (ATP
& phosphocreatine)
Short Term: Glycolytic
(Glycogen-Lactic Acid)
Long Term: Oxidative
Mole of ATP/min
4
Time to Fatigue
5 to 10 sec
2.5
1 to 2 min
1
Unlimited Time
Glycolysis – Anaerobic


Glycolysis does not require oxygen (anaerobic)
ATP-PCr and glycolysis provide the energy for ~2 min of all-out activity
Pyruvate Metabolism Anaerobic



Without oxygen present, pyruvate produced by glycolysis becomes lactate
lactic acid)
Lactate can be transported by blood to liver and used in gluconeogenesis
(produce glucose)
Too much lactate forms lactic acid and lowers the pH impairing enzyme
activity
The Oxidative System





The oxidative system uses oxygen to generate energy (aerobic)
Oxidative production of ATP occurs in the mitochondria
Can yield much more energy (ATP then anaerobic systems)
The oxidative system is slow to turn on
Primary method of energy production during endurance events
Anaerobic and Aerobic Energy Production


Glycolysis: Breakdown of glucose (anaerobic: 2 ATP)
Krebs Cycle: production of ATP, NADH, FADH, (aerobic: 38 ATP)
Common Criteria Used to Document Successful VO2max Test


Primary Criteria
 Plateau in VO2 despite increasing work rate
Secondary Criteria
 HR >90% of age predicted max
 Blood lactate > 8 mmol/L
 PRE > 17
 RER > 1.10
RPE – Rating of Perceived Exertion (Borg Score)
 6-20
Respiratory Exchange Ratio
Respiratory exchange ratio (RER)  measurable
RER = VCO2(expired)/VOz(consumed)  Indicates type of substrate being
metabolized: 0.7 (100% Fat) to 1.0 (100% Carbs)
Respiratory Quotient (RQ)  theory
What Happens During Maximal Exercise?
 RER goes up with exercise due to increased carbon dioxide production
relative to oxygen consumption
 Related to buffering of lactic acid production
How Do We Counteract Too Much Lactic Acid?
 Bicarbonate (released from kidneys) helps to buffer the acid
H+ + HCO3-  H2CO3  CO2 + H2O
What is Tvent?
Ventilatory Threshold: is the point in which the ventilation increases
disproportionately to oxygen uptake
Why Should I Care About Tvent?





At intensities higher than Tvent there is an abrupt increase in blood lactate
levels and the individual cannot maintain steady state exercise
More trainable than VO2max
Occurs at 50-60% of VO2max in untrained endurance individuals
Occurs at 80-90% of VO2max in elite, world-class endurance athletes
Allows the individual to be capable of maintaining a higher level of steady
state during the endurance exercise

A better indicator of endurance performance than VO2max as it tells you how
much of your VO2max you can use a steady state
Cardiorespiratory Fitness Training
1. Frequency of Training
 Optimal 3-5 days/week
 No benefits with < 2 days
 Benefits will plateau at 5 days
2. Intensity of Training
 Lower intensity will only increase fitness in individuals who are unfit
 Lower intensity = Longer duration vs Higher intensity = Shorter
during
 Higher intensity prone to injury and over training
3. Time (Duration) of Exercise
 20-60 mins of continuous or intermittent aerobic activity in a day
 Lower intensity exercise (40-65% VO2max) should be conducted over
a longer period of time (>30 mins)
4. Type (Mode) of Training
 Any activity that uses large muscle groups, is rhythmic and aerobic in
nature, and can be maintained continuously
How Much Can I Improve My VO2max?
 Studies > 5 months
 3-5 days per week
 20-25% Improvement
 There is substantial inter-individual differences
Endurance Strategies
 Carb loading
 Fat loading
 PCr
 Sodium Bicarbonate
Inventory of Fuel Supply
 Carbohydrate
 Muscle Glycogen 350g (1400 kcal)
 Liver Glycogen 60g (240 kcal)
 Plasma glucose 10g (40 kcal)
 Protein
 Whole body (24 000 kcal)
 Fat
 Muscle 500g (3850 kcal)
 Adipose tissue 14kg (107 800 kcal)
Carb Loading and Performance
 No benefit for events less than 90 min
 Extra water weight
 Bloating
Events longer than 90 mins
 Postpone time to fatigue by 20%
 Improves time to go a set distance by 2-3%
Replenishment of Glycogen
 Beginning immediately post-exercise (Golden hour)
 Continue until 500g ingested or a large, high-carbohydrate meal is consumed
 Moderate to high glycemic index CHO are more effective in regenerating
glycogen stores than low GI
 Glycogen stores replenish at a rate of about 5 to 7% per hour
High-fat Diet and Performance
 >30% fat
 Many studies use >50%
Theory: use more fat and spare glycogen
Acute Effects of a High-fat Diet
 Lower muscle and liver glycogen stores
 Lower whole-body CHO oxidation
 Increased rating of perceived exertion
Creatine Supplementation
 Found in dietary meat
 90% stored in skeletal muscle (60% as PCr)
 70%of people will increase creatine stores with supplementation (20g/day)
 Aid in high intensity activities <30 sec
 Power/strength (5-15%)
 Single (1-5%) and repetitive (5-15%) sprint performance
 Jumping, cycling, but not running
 No help for endurance events
Sodium Bicarbonate Ingestion
 Help with buffering acid
 0.3-0.5g/kg/BM
 Improve mean power by 2% in high-intensity races
 Large variation
 Risk: GI discomfort
Caffeine and Aerobic Exercise




Helps with endurance events
Improves endurance time trials by 10-15%
May also help with power and resistance training (60-180 sec)
Banned substance
Preventing Heart Problems
 Physical activity
 Diet
 Fat – good and bad
 Fish
 Vegetables and fruit
 Fiber and whole grains
 Soy
 B vitamins
 Moderate alcohol consumption
Modifiable Risk Factors for Cardiovascular Disease
 Tobacco Smoking
 Physical inactivity
 Overweight
 Less than recommended consumption of fruits and vegetables
 High blood pressure
 Diabetes
Risk Factors You Can’t Control
 Heredity
 Race and ethnicity
 Age and gender
 Male pattern baldness
Lipoprotein Profile
Total cholesterol = LDL + HDL
Cholesterol + Triglycerides (TG) inside lipoproteins
TG can also be carried free in the blood by albumin (protein carrier)
Consequences of High Blood Pressure
 Eye damage
 Heart attack
 Kidney failure
 Stroke
 Damage to artery walls
Signs of a Heart Attack







Tight ache, heavy, squeezing pain, or discomfort in the centre of the chest,
which may last 30 minutes or more and is not relieved by rest
Chest pain that radiates to the shoulder, arm, neck, back, or jaw
Anxiety
Sweating or cold, clammy skin
Nausea and vomiting
Shortness of breath
Dizziness, fainting, or loss of consciousness
So You Have Chest Pain
What do the doctors do?
 EKG or ECG (electrocardiogram)
 Stress Test
 Angiography
EKG or ECG (electrocardiogram)
 A simple test that detects and records the electrical activity of your heart
 Shows the strength and timing of electrical signals as they pass through each
part of your heart
 Certain electrical patterns suggest whether CAD is likely, and can show signs
of a previous or current heart attack
 However, some people with angina have a normal EKG
Post Myocardial Infarction
 Hyperacute phase = immediately after a heart attack
 Fully evolved phase = a few hours to days after a heart attack
 Resolution phase = a few weeks after a heart attack
 Stabilized chronic phase is the last phase and typically has permanent
pathological changes compared to a normal ECG tracing
Stress Tests
 Exercise or medicine is given to make your heart work hard and beat fast
while doctor measures blood pressure and EKG
 When your heart is working hard, it needs more blood and oxygen. Arteries
narrowed by plaque can’t supply enough oxygen-rich blood to meet your
heart’s needs
 Can show possible signs of CAD, such as:
 Abnormal changes in heart rate or blood pressure
 Symptoms such as shortness of breath or chest pain
 Abnormal changes in your heart rhythm or your heart’s electrical
activity (ECG)
Angiography






Uses dye and x-rays to show the insides of your coronary arteries
A long, thin, flexible tube (catheter) is put into a blood vessel in your ar,
groin, or neck
The tube is then threaded into your coronary arteries, and the dye is released
into your bloodstream
X-rays are taken while the dye is flowing through the coronary arteries
Usually done in a hospital when you are awake
The figure shows a stenosis (narrowing) in the left anterior descending
coronary artery causing reversible myocardial ischemia in a patient with
stable angina
Treatment for Angina
1. Lifestyle Changes
 Better diet
 Physical activity
 Lose weight
 Quit smoking
 Slow down or take rest breaks if angina comes on with exertion
 Avoid large meals and rich foods that leave you feeling stuffed if
angina comes on after a heavy meal
 Try to avoid situations that make you upset or stressed if angina
comes on with stress
2. Medications
 Nitrates (most common – nitroglycerin): relax and widen blood
vessels. This allows more blood to flow to the heart while reducing its
workload
 Nitroglycerin dissolves under your tongue or between your
cheeks and gum. Is used to relieve angina episode
 Blood pressure and cholesterol medicines
 Other medicines that:
 Slow the heart rate
 Relax blood vessels
 Reduce strain on the heart (ie. Diuretics)
 Prevent blood clots from forming
Angioplasty


Angina (chest pain) can occur when blood flow to the heart is reduced
Angioplasty is a procedure in which a balloon is blown up in an artery to
push away blockages and widen the opening of the artery to increase blood
flow to the heart
Coronary Graft Bypass


Sometimes if the blockage is too severe, the physician will try to bypass
(avoid) the blocked area using the Saphenous vein (leg) or the Internal
Mammary Artery
During the surgery, multiple blockages can be bypassed
Minimally Invasive CABG


Uses a smaller incision and accesses the heart from between the ribs. Can be
done without stopping the heart
The MIDCAB approach is usually reserved for cases requiring one or two
bypasses; typically bypassing arteries on the front of the heart, such as the
left anterior descending (LAD) coronary artery
TECAB surgery: Totally endoscopic coronary artery bypass





Only needs a few openings each about the size of a dime
The procedure is carried out by a surgical robot (“da Vinci”)
A tiny fiber optic video camera is mounted onto a robot arm and is controlled
by foot pedals
The procedure is performed by a surgeon operating two more mechanical
arms using a joystick, or with rings the surgeon can insert his fingers into to a
operate the robot’s “fingers”
The entire procedure is carried out watching a video monitor
Deep Vein Thrombosis
Symptoms:
 Swollen area of the leg
 Pain or tenderness in the leg, usually in one leg and may be felt only when
standing or walking
 Increased warmth in the area of the leg that is swollen or in pain
 Red or discolored skin
 Not Fatal
Causes:
 Stagnant blood (i.e. Immobility – Prolonged sitting, casting, hospitalization,
surgery, pregnancy, obesity)
 Hypercoagulability *coagulation of blood faster than usual)
 Medications (i.e., birth control, estrogen)
 Smoking
Genetic predisposition
 Polycythemia (increased number of red blood cells)
 Cancer
 Trauma to the vein or leg
Treatment:
 Anti-coagulants (heparin and warfarin)
 Compression stockings (swelling)
 Vena cava filter (surgery)
Pulmonary Embolism
Symptoms:
 Chest pain when taking a deep breath
 Shortness of breath
 Fainting
 Dizziness
 Sweating
 Anxiety
 Death
Some people find out that they have deep vein thrombosis only after the clot has
moved from the leg and traveled to the lung (pulmonary embolism)
Treatment:
 Anticoagulants
 Oxygen
 May need to have surgery to remove embolism and/or filter blood of clots
Stroke
HEMORRHAGIC STROKE:
 20% of stroke
 Caused by ruptured blood vessels followed by blood leaking into tissue
 Usually more serious than ischemic stroke
Subarachnoid hemorrhage
 A bleed into the space between the brain and the skull
 Develops most often from an aneurysm, a weakened, ballooned area in the
wall of an artery
Intracerebral hemorrhage
 A bleed from a blood vessel inside the brain
 Often caused by high blood pressure and the damage it does to arteries
ISCHEMIC STROKE
 80% of stokes
 Caused by blockages in brain blood vessels; potentially treatable with clotbusting drugs

Brain tissue dies when blood flow is blocked
Embolic Stroke
 Caused by emboli, blood clots that travel from elsewhere in the body to the
brain blood vessels
 25% of embolic strokes are related to atrial fibrillation
Thrombotic stroke
 Caused by thrombi, blood clots that form where an artery has been narrowed
by atherosclerosis
 Most often develops when part of a thrombus breaks away and causes a
blockages in a “downstream” artery
Causes of Cerebral Aneurysms




A cerebral aneurysm is a weak or thin spot on a blood vessel in the brain that
balloons out and fills with blood
More common in women than men
Most cerebral aneurysms do not show symptoms until they either become
very large or burst
Larger aneurysms may press on tissues and nerves
Causes:
 Congenital (Genetic inborn abnormality in an artery wall)
 Trauma or injury to the head
 High blood pressure
 Infection
 Tumors
 Atherosclerosis
 Cigarette smoking
 Drugs (oral contraceptives or cocaine)
Symptoms of an unruptured aneurysm:
 Pain above and behind the eye
 Numbness, weakness, or paralysis on one side of the face
 Dialated pupils
 Vision changes
Symptoms of a ruptured aneurysm (hemorrhage):
 Sudden and extremely sever headache
 Nausea and vomiting
 Stiff neck
 Loss of consciousness
Diagnosing Cerebral Aneurysms
Computed Tomography Angiography (CTA)
 Noninvasive X-ray to review the anatomical structures within the brain to
detect blood in or around the brain. Involves the injection of contrast dye and
provides the best pictures.
Angiogram
 An invasive procedure where a catheter is inserted into an artery and passed
through the blood vessels to the brain. Once the catheter is in place, a
contrast dye is injected into the bloodstream and the x-ray images are taken.
Magnetic resonance Angiogram (MRA)
 A noninvasive test, which uses a magnetic field and radio-frequency waves to
give a detailed view of the soft tissues of your brain and blood vessels. Can
use contrast dye.
Treatment for Cerebral Aneurysms
Microvascular clipping
 The most common treatment for an aneurysm
 Using general anesthesia, an opening is made in the skill, called a craniotomy
 The brain is gently retracted so that the artery with the aneurysm may be
located
 A small clip is placed across the neck of the aneurysm to block the normal
blood flow from entering the aneurysm
 The slip is made of titanium and remains on the artery permanently
 Shown to be high effective, and in genera, the aneurysm do not return
Occlusion and Bypass
Occlusion  clamp off (occlude) the entire artery that leads to the aneurysm. This
procedure is often performed when the aneurysm has damaged the artery
Bypass  a small blood vessel is surgically grafted to the brain artery, rerouting the
flow of blood away from the section of the damaged artery. Sometimes accompanies
the occlusion surgery.
Endovascular Therapy (Coiling)


Minimally invasive (no pen surgery)
Once the individual has been anesthetized, the doctor inserts a hollow plastic
tube (a catheter) into an artery (usually in the groin) and threads it, using
angiography (x-ray), through the body to the site of the aneurysm




Usually a guide wire, detachable coils (spirals of platinum wire) or small
latex balloons are passed through the catheter and released into the
aneurysm
Tiny platinum coils are threaded through the catheter into the aneurysm,
blocking blood flow into the aneurysm and preventing rupture (blood clots)
This endovascular coiling, or filling, of the aneurysm is called embolization
and can be performed under general anesthesia or light sedation
Unclear if coiling or clipping is better
Stroke Symptoms







Sudden weakness or loss of strength
Numbness of face, arm, or leg
Loss of speech, or difficulty speaking or understanding speech
Dimness or loss of vision, particularly double vision in one eye
Unexplained dizziness
Change in personality
Change in patter of headaches
Risk Factors for Strokes





Age hypertension
High red blood cell count
Heart disease
Blood fats
Diabetes mellitus
How to Prevent a Stroke






Quit smoking
Keep blood pressure under control
Eat a low saturated-fat, low cholesterol diet
Avoid obesity
Exercise
Get enough vitamin B
Common Lung Diseases





Asthma
Chronic obstructive pulmonary disease (COPD)
Bronchitis
Emphysema
Pulmonary fibrosis
Main Types of Lung Disease
Pulmonary circulation diseases  Clotting, scarring, or inflammation of the blood
vessels
 Less capable of taking up oxygen and releasing carbon dioxide
 May also affect heart function
 Ie. Pulmonary embolism, pulmonary arterial hypertension, pulmonary
hemorrhage
Restrictive Lung Tissue Diseases  affect the structure of the lung
 Ie. Pulmonary fibrosis, sarcoidosis, severe obesity
 Like “wearing a too-tight vest”, can’t take a deep breath
Airway diseases  narrowing or blockages of the airways
 i.e. asthma, bronchitis, emphysema, chronic obstructive pulmonary disease
(COPD)
 like “trying to breathe out through a straw”
Restrictive Lung Disease
 Reduced lung compliance (Stiff lung)
 Increased work of breathe (increased lung oxygen demand)
 Reduced tidal volumes (shallow breaths)
 Increased expiratory flow rates
 Increased respiratory rate
 Non-uniform distribution of ventilation (some alveolar units are not exposed
to gas)
 Fibrosis also impairs gas transfer at the alveolar-capillary surface
 Poor gas exchange
Scoliosis
 A severe lateral curve in the spine  deformation in the chest wall  limited
chest movement --? Reduced lung volumes
Pulmonary Fibrosis
 Can be caused by infections, environmental agents like asbestos and silica,
and chronic inflammation
Sarcodosis
 An immune disease that causes lumps of fibrous tissues called granulomas on
the skin and organs
Exercise in Restrictive Lung Disease Patients
 Ventilation increased by increased respiratory rate as opposed to tidal
volume
 4x O2 requirement; Plus reduction in maximal stroke volume
 greater competition between respiratory and locomotive muscles for a lower
total O2 supply
The Airways in Asthma
 ~5% of population
 Normal airways at rest
 Usually bronchioles do not contribute to airway resistance because their
total x-sectional area is 2000 times that of the trachea
 Asthma is associated with bronchoconstriction, edema and mucus
Common Asthma Triggers
 Animals
 Dust
 Cold weather
 Chemicals in the air or in food
 Exercise
 Mold
 Pollen
 Respiratory infections, such as the common cold
 Strong emotions (stress)
 Tobacco smoke
Asthma Outcomes
 Airway inflammation
 Airway remodeling
 Airway hypersensitivity
 Reversible airflow obstruction
 Lower forced expiratory volume
Emergency Asthma Symptoms
 Bluish color to the lips and face
 Decreased level of alertness
 Extreme difficulty breathing
 Rapid pulse
 Severe anxiety due to shortness of breath
 Sweating
Asthma Treatment
 Relievers (Quick Acting Bronchodilators)
 Controllers (Longer Acting Anti-inflammatory/bronchodilators
 Inhaled Corticosteroids (reducing inflammation)
Asthma and Training


Asthma prevalence among elite athletes is similar if not higher than in nonathletes
Effect of training:
 No effect on resting lung function
 Increased cardiorespiratory fitness
 Quality of life?
 Alterations in symptoms?
Chronic Obstructive Pulmonary Disorder (COPD)
COPD = Bronchitis + Emphysema


Normally, hypoxia in the muscle causes vasodialation
 Increased blood flow
 Increased oxygen supply
BUT hypoxia in pulmonary blood vessels
 Vasoconstriction
 Pulmonary hypertension
 Increased afterload on right ventricle
Can cause Right Ventricle Heart Failure
Impact of COPD
 5th leading cause of death
 Major cause is smoking (environment, infections)
 Symptoms:
 Shortness of breath
 Cough
 Wheezing
 Fatigue
 Weight loss
 Chest and stomach pain
 Anxiety
Emphysema (smoker’s lung)
 Irritation  lung tissue (airways and alveolar) damage
 Alveoli loss elastic recoil, and so the individual needs to work to push air out
of their lungs
How to Exercise Test
 Small work increments
 Assess oxygen desaturation
 Perceived dyspnea, leg discomfort (0-10 scale)
 Asthma or COPD patients
 Often have ventilatory limitations to exercise and/or oxygen
desaturation
Exercise Prescription in COPD
 Interval training higher work rates are achieved with lower symptom scores
 Hence, may be more comfortable in patients with severe dynamic
hyperinflation
 Small muscle group training lowers the ventilatory burden of exercise
 Not limited by the central cardiorespiratory limitations, can achieve
significantly higher relative work rates
 Resistance training (weight lifting) is a way training small muscles
 Combo of resistance + endurance exercise is advised in clinical rehab
 O2 should be monitored during initial training sessions and should be >90%
Exercise in Cystic Fibrosis
 Aerobic Exercise is best
 Need to be careful about dehydration and loss of salt through sweating
 Drink lots of water
 High salt solutions (replace salt lost)
What are Natural Health Products?
 Vitamins/minerals
 Homeopathy
 Herbal/plant remedies
 “Traditional” medicine
 Amino acids/essential fatty acids
 Probiotics
 Some personal care products
Food  any article manufactured, sold or represented for use as a food or drink for
human beings, including chewing gum
Drug  includes any substance or mixture of substances manufactured, sold or
represented for use in:
 The diagnosis, treatment, mitigation or prevention of a disease, disorder or
abnormal physical state, or its symptoms, in human beings or animals
 Restoring, correcting or modifying organic functions in human beings or
animals
 Disinfection in premises in which food is manufactured, prepared or kept
Natural Health Product  natural health products are naturally occurring
substances that are used to restore or maintain good health
Risks of Using NHPs





Manufacturing problems
Unproven claims
Not enough information for people to make an informed choice
Interaction with prescription drugs or other natural health products
Unwanted side effects
Case Study: Oscillococcinum
 Approved in Canada
 Treatment for colds and the flu
Case Study: Horny Goat Weed
 The leaf of the plan Epimedium sagittatum
 Approved by Health Canada’s Natural Health Product Directorate with the
following recommended use:
 Traditional Chinese Medicine used to tonify the kidney and fortify the
yang, for symptoms such as frequent urination, forgetfulness,
withdrawal, and painful cold lower back and knees
Common Health Foods/Products










Garlic  Level III evidence – half to one clove (or equivalent) daily has
cholesterol-lowering effect of up to 9%
Aged garlic extract  Level III evidence – 7.2g has anticlotting, as well as
modest reductions in blood pressure effects
Ginseng  four studies suggesting a benefit on glycaemia if consumed
chronically. None for improving circulation.
Ginger  Level II evidence – ameliorating arthritic knee pain; however less
effective than ibuprofen.
Chamomile  has moderate antioxidant and antimicrobial acitivies, and
significant antiplatelet activity in vitro
 Antiinflammation, antimutagenic and cholesterol-loweing activities
from animals studies
 Human studies are limited, and clinical trials examining the purported
sedative properties and chamomile tea are absent
Ginkgo  of questionable use for memory loss and tinnitus, but has some
effect on dementia and intermittent claudication (pain/cramping in legs)
St. John’s wort  efficacious for mild to moderate depression, but serious
concerns exist about its interactions with several conventional drugs
Echinacea  may be helpful in the treatment or prevention of upper
respiratory tract infections, but trial data are not fully convincing
Kava  an efficacious short-term treatment for anxiety
None of these herbal medicines is free of adverse effects. Because the
evidence is incomplete, risk-benefit assessments are not completely reliable,
and much knowledge is still lacking
Health Canada’s Evidence for Homeopathic Medicines: Guidance Document
 “safety, efficacy, and quality”
 clinical trials to “traditional use”
H1N1
 From August 30 to December 29, 2009, a total of 6 951 hospitalized cases
and 324 (4.7%) deaths were been reported…
Pathogens and Infectious Disease
 Infections directly contribute to at least ¼ of all death rate.
 Most common infectious killers are URTIs, HIV/AIDS, and diarrhea
 TB, malaria and measles also kill many people in developing nations
Infectious Diseases  Definitions
 Disease  a pathological condition of the body (or parts of the body)
characterized by an identifiable group of signs and symptoms
 Infectious disease  a disease caused by an infectious agent such as
bacterium, virus, protozoan, or fungus that can be passed on to others
 Infection  occurs when an infectious agent enters the body and begins to
reproduce; may or may not lead to disease
 Host  an organism infected by another organism or pathogen
 Virulence  the relative ability of an agent to cause rapid and severe
disease in a host
Classifications of Agents of Infection
 Bacteria
 Viruses
 Protozoa
 Fungi
 Parasitic worms (helminthes)
 Prions
Virus and Bacteria
Response to Antibiotics
Virus
20-400
Animals, plants, bacteria.
Once in a host, viruses
usually target specific
tissues
Unaffected by antibiotics
Reproduction
Uses host DNA/RNA to
Size in nm
Typical Host
Bacteria
400 to thousands
Animals, plants. Can affect
whole organism
Susceptible to antibiotics.
Antibiotics target specific
kinds of bacteria. Some
bacteria are resistant
Reproduces without using
Structure
reproduce
Simple structure
consisting of a core
reproductive molecules
(DNA/RNA), usually about
8 genes, surrounded by a
protective protein coat
the DNA and RNA of host
Complex unicellular
structure containing a
variety of organelles for
different functions
(energy production,
reproduction, protein
synthesis)
Hemagglutinin  allows virus to enter host’s cells
Neuraminidase  allowed virus to escape the host’s cells
SARS  Severe Acute Respiratory Syndrome
 Spread person to person
 Water droplet transmission
 Symptoms:
 Fever > 38.0 C, cough, shortness of breath or difficulty breathing
Examples of Viruses and Bacteria
Viruses
Influenza viruses
Rhinoviruses and adenoviruses
Herpes
Papilloma virus
Hepatitis
Retroviruses (contain viral RNA and
reverse transcriptase to make copies of
viral DNA from viral RNA
Bacteria
Escherichia coli (Latin for from the
colon)
Tuberculosis
Tetanus
Gonorrhea
Scarlet fever
Diphtheria
Prions
 A protein
 Bovine spongiform Encephalopathy (BSE) (Mad Cow Disease)
 Symptoms: abnormal behaviour, loss of coordination, tremors, rigidity,
irritability, and progressive dementia
 Death usually occurs within 3-12 months from the onset of symptoms
What Else Spreads Disease?
 Parasites
Malaria is caused by a parasite (protozoa) called Plasmodium, which is transmitted
via the bites of infected mosquitoes.
How Do You Catch an Infection?




Animals and insects
People
Food
Water
Infections
 Pathogens are everywhere
 Contact is generally from person to person for viruses and via persons,
animals, plants, food, soil and water for bacteria
 Our immune system protects us somewhat from infection
Chain of Infection
Pathogen  Reservoir  Portal of exit  Means of transmission  Portal of entry
 New host
What Determines if You Get a Pathogen?
 Is the pathogen in the environment around you?
 What is the amount of pathogen?
 Is there a point of entry?
 How strong is you immune system?
Stopping an Epidemic
 Case Study:
 The West Nile Virus
 The West Nile Virus is a mosquito-borne virus that can cause encephalitis.
First appeared in 1937.
 “polio-like” condition called sudden limb paralysis
 Reduced spread by reservoir
Lines of Defense
 Physical and chemical borders
 Skin
 Mucus membranes
 Fluids (tears, saliva)
 Cilia
 Coughing, sneezing
Lymphatic System
 Vessels/glands that pick up fluid, protein, lipids, etc.
 Contain WBCs that trap and destroy and filter pathogens
 Swollen glands
The Inflammatory Response

Following injury or infection inflammation occurs:
 Histamine causes blood vessels to dilate and fluid to accumulate
 Heat
 Swelling
 Redness
 Macrophages and neutrophils attack the infection
 Pus (collection of dead white blood cells and debris)
Inflammatory Response to Bacteria
1) Damaged tissues release histamines, increasing blood flow
2) Histamine causes capillaries to leak, releasing phagocytes and clotting factors
3) Phagocytes engulf bacteria, dead cells, and debris
4) Platelets move out of the capillary to seal the wound
The Immune System



Two kinds of responses
 Innate (natural)
 Acquired
 Both recognize the invader based on the invaders antigen
ANTIGEN: A marker on the surface of a foreign substance that the immune
system recognized as nonself that triggers the immune response.
Several cells respond
INNATE IMMUNITY
 Refers to antigen-nonspecific defense mechanisms that a host uses
immediately or within several hours after exposure to an antigen. This is the
immunity one is born with
 Neutrophils and macrophages are cells of the immune system
designed to recognize a few highly conserved structures present in
many different microorganisms
ACQUIRED IMMUNITY
 An antigen-specific defense mechanisms that takes days to become
protective and are designed to remove a specific antigen
 This is the immunity one develops throughout life
 The downside to the specificity of adaptive immunity is that only a
few B-cells and T-cells in the body recognize any one antigen
Acquired Cell-Mediated Immunity
 Lymphocytes (B- and T-cells)
 B-cells are characterized by the presence of immunoglobulins on their
surface, and upon stimulation with antigen, they are transformed into
antibody secreting plasma cells
 T-cells have the dual function of regulating the immune response
(helper T cells) and also generating specific cell mediated immunity
(killer and suppressor T cells).
Phase 1: Viruses invade the body through a break in the skin or another portal of
entry. They take over body cells in order to replicate.
Macrophages recognize the invaders by the antigens on their surface. They consume
the viruses and display their antigen.
Helper T cells read this information and rush to respond.
Phase 2: Helper T cells trigger the production of killer T cells and B cells
Phase 3: Killer T cells and natural killer cells destroy infected body cells. B cells
produce antibodies that bind to viruses and mark them for destruction by
macrophages
Phase 4: When the danger is over, suppressor T cells halt the immune response.
Memory B and T cells are reserved so that a quick response can be mounted for
future invasions by this virus.
Symptoms and Contamination



Incubation
 Viruses or bacteria are multiplying
 Generally no symptoms but may be contagious
Prodromal period
 Generally feel some symptoms (fever, runny nose, sore throat)
 Symptoms are related to the immune response
Clinical period
Immunization
 Primes the immune system for future pathogens
 Immune system can then quickly produce antibodies to the organism
 E.g. Diphtheria, Hep A and B, Influenza, MMR
Reproductive and Urinary Tract Infections
 Vaginal Infections:
 Trichomoniasis
 Candidiases
 Bacterial vaginosis
 Urinary Tract InfectionsL
 Urethritis
 Cystitis
 Pyelonephritis
Cancer Cycle
1) Tumor development begins with a cell gets a genetic mutation
2) Hyperplasia occurs but cells look normal. After a period of time some cells
mutate further.
3) Cells continue to reproduce and descendants appear abnormal in shape
(dysplasia). After time, a rare mutation that alters cell’s behavior occurs.
4) Affected cells are abnormal in growth and appearance but the tumor is still
contained (in situ cancer).
5) If genetic changes allow the tumor to begin invading underlying tissues and
to shed cell into lymph or blood. The escaped cells establish new tumors
(metastases). These may be lethal.
Stages of Cancer
 Cancer stage is based on the size of the tumor, whether the cancer is invasive
or non-invasive, whether lymph nodes are involved, and whether the cancer
has spread…
 Cancer specific
 Usually stage 0, I, II, III, IV
Risk Factors for Breast Cancer
 Age (55 or older)
 Family History
 Age at menarche
 Age at birth of first child
 Breast biopsies
 Estrogen
Family History
 About 5% to 10% of breast cancers are thought to be hereditary, caused by
abnormal genes passed from parent to child
 If you’ve had one first-degree female relative (sister, mother, daughter)
diagnosed with breast cancer, your risk is double. If two first-degree
relatives have been diagnosed, your risk is 5 times higher than average
 BRCA1 or BRCA2 gene
 Abnormal CHEK2 gene
Overweight/Obesity and Cancer
 Overweight and obese women (BMI >25) have a higher risk of being
diagnosed with breast cancer compared to women who maintain a health
weight, especially after menopause
 Being overweight also can increase the risk of the breast cancer coming back
(recurrence) in women who have had the disease

This higher risk may be because fat cells make estrogen and other adipokines
that influence the rate at which cancers develop and grow
Cancer Prevention and Nutrition
 Tea, coffee
 Berries, grapes, wine
 Fiber, whole grains
 Spices
 Vitamins, minerals
 Antioxidants, polyphenols, isoflavanoids
 Berries, nuts
 Cruciferous, vegetables
Exercise and Breast Cancer Prevention
 Research shows a link between exercising regularly at a moderate or intense
level for 4 to 7 hours per week and a lower risk of breast cancer
 Exercise consumes/controls blood sugar and limits blood levels of insulin
and IGF1, a hormone that can affect how breast cells grow and behave
 People who exercise regularly tend to be healthier and are more likely to
maintain a health weight and have little or no excess fat compared to people
who don’t exercise
Exercise Reduces Risk for Other Cancers
 Colorectal cancer
 Endometrial cancer
 Lung cancer
 Prostate cancer
Breast Exam/Detection
 Mammography (age 40 or earlier)
 Clinical Breast Exam
 Regular Breast Self Examination
Seven Warning Signs of Cancer
 Change in bowel habits
 A sore that doesn’t heal
 Unusual bleeding or discharge
 Thickening of lump in breast, testes, or elsewhere
 Indigestion or difficulty swallowing
 Obvious change in a wart or mole
 Nagging cough or hoarseness
Reduce Cancer Risk
 Cancer-Smart Nutrition




Tobacco Smoke
Health weight
Reduce exposure to carcinogens
Early Detection
Risk Factors for Skin Cancer
 Fair skin, light eyes, or fair hair
 A tendency to develop freckles and to burn instead of tan
 A history of childhood sunburn or intermittent, intense sun exposure
 A personal or family history of melanoma
 A large number of nevi, or moles or dysplastic moles
Metastasis
 Attachment: A primary tumor attaches to a blood vessel (or lymph node)
 Once Cancer cells are attached, they may pass through the lining of the lymph
or blood vessel.
 Cancer cells move into the circulation system and spread to other parts of the
body, colonizing other organs. This traveling and reproducing is called
metastasizing.
 The cancer cells may then move through the blood and lymph system to form
a secondary tumor, or metastasis, at another site in the body.
Treatment
 Depends on the stage and extent of the disease
 Chemotherapy
 Radiation therapy
 Surgery
 Other (angiogenesis inhibitors, biological to boost the immune system,
targeted cancer therapies and drugs that block growth)
Pedometers
 Measures the # of steps to determine “steps per day” – some also estimate
the distance traveled and energy expended
 Worn on a belt or waistband and responds to vertical movements
 Studies of the # of steps measured by pedometer versus steps counted on a
treadmill show good congruency
 Pedometers do not capture all PA
 There are varying qualities of pedometers
 Purposeful walking, 30 mins = 3000-4000 steps of 200 calc
 The average office worker takes ~5000 steps/day
 Pedometers provide motivation by promoting daily walking
Steps Necessary for Good Health



10 000 steps/day (60-90 min of moderate PA – 4mph has an approximate
energy expenditure of 400-600 kcal (depending on speed, stride length and
body weight)
another recommendation for health is 2 000 steps beyond your normal daily
routine
for weight loss, the recommendation is 20 000 steps/day
Popular Exercise Class
 Aerobic Floor Classes
 Step Aerobics
 The Ramp
 Spin Cycle
 Yoga
 Pilates
Yoga




Developed in India ?5000 y ago, “spiritual discipline”
Currently a “fad” fitness workout
Concentrates on posture, breathing & “focused awareness”
Aim to develop both physical & mental conditioning
Pilates
 Developed in Germany >100 y ago
 Currently a “fad” fitness workout
 Core stabilization with concurrent dynamic exercise
 Aim to develop both physical & mental conditioning
Exercise Facilities – Things to watch for
 Time and location restrictions
 High-pressure sales
 Misrepresentation in sales presentation
 Very little privacy
 Promotional gimmicks
 “Special Reduced Price”
 “Free Visits”
 “Before and After pictures”
 “Bait and Switch”
 “Guarantees”
 “Cancellation”
 Cost and credentials of Personal Trainers
Canadian Community Health Survey
 Physically inactive decreased from 62 to 56%
 Obesity increased (13 to 16%)


High blood pressure increased (19 to 25%)
Diabetes increased by 25% (6.6t to 8.2%)
Why Test Athletes?
 Establish normative standards
 Determine strengths and limitations
 Monitor development and training responses
 Provide information about health status
 Provide athlete with greater body awareness
Effective Testing
 Relevance to sport
 Validity and reliability
 Sport specific
 Controlled administration
 Repeated regularly
 Performance interpretation
Objectives
 Perform needs analysis for soccer and rowing
 Describe the development of testing protocols
 Provide overview of performance characteristics
 Offer views on interpreting performance outcomes
Most popular sport in the world
 265 million soccer players worldwide
 Canada
 7000 clubs and 55000 teams
 Players ~850 000
 Men ~490 000
 Women ~360 000
Testing Protocol
 Sport characteristic
 Headers
 Changes in direction
 Sprints of 23 seconds
 100-200 sprints/hi intensity runs
 10-12K traveled
 Matched Test
 Jump ability
 Agility
 Linear sprint
 Repeated sprint ability

Aerobic fitness
Agility
 The ability to change directions rapidly
 Variety of tests to assess agility
 Most common to soccer: Pro-agility, Illinois, and Balsom tests
Repeated Sprint Ability
 Various protocols:
 10-12 x 20m with 10 sec rest
 15-20 x 35m on a 30 sec cycle
 Outcomes:
 Average time
 Total time
 Fatigue index
Rowing Cycle
 Catch  oar(s) place in the water
 Drive  legs extend and arms flex
 Finish  oar(s) come out of the water
 Recovery  arms extend and legs flex
Testing Protocol
 Anthropometry
 100 metre
 60 second
 2K
 6K
 60 minute
Summary
 Soccer
 Field based testing
 Aerobic ability 10-12K
 Anaerobic ability 100+ events over 90 minutes
 Anthropometry-minimal importance
 Rowing
 Laboratory based testing
 Aerobic ability 2K
 Anaerobic ability – start and finish
 Anthropometry – extremely important
Application of Fitness Assessment in Sport
1) Recognize that you are not the coach
2)
3)
4)
5)
6)
Convince coach and/or team officials of importance of fitness testing
Determine the fitness components and how to evaluate them
Construct appropriate battery of tests
Recognize practical limitations
Interpretation of Feedback of Results
Convince coach and/or team officials of importance of fitness testing
 Why Physical Fitness?
1) Decreased Work Rate
2) Decreased Concentration
3) Decreased Technical Performance
4) Decreased Tactical Judgment
5) Increased Susceptibility to Injury
 Uses of Test Results
1) Establish norms to aid in athlete selection
2) Provide baseline data for training
3) Monitor effectiveness of a training program
4) Motivate athlete for training and competition
Determine the fitness components and how to evaluate them
 Knowledge/Experience of Coach
 Scientific Analysis
1) Time motion analyses
2) Descriptive Match Data
3) Physiological Assessment during competition and in the Lab
Construct appropriate battery of tests
1) Laboratory Tests
2) Laboratory-Like Tests
3) Field Tests
Interpretation and Feedback of Results
1) Equipment/Facilities
2) Support Personnel
3) Number of Athletes
4) Level of Competition
5) Cost
6) Frequency of Testing
Effective Testing
 Relevance to sport
 Validity and reliability
 Sport specific
 Controlled administration
 Repeated regularly

Performance interpretation
Interpretation and Feedback of Results
1) Coach
2) Athlete
NHL Entry Draft
 1st week of May in Toronto
 top 110 players ranked by the NHL are invited
 All teams can come interview them
 Doctors – heart (ECG), lungs, vision, concussion, medical history
 Fitness tests – grip strength, push-pull, push-ups, curl-ups, long jump,
vertical jump, bench press, Wingate, neurological assessment, VO2max on bike
Tennis Fitness Testing Protocol
1. Body Composition - ideal weight, skinfolds
2. Aerobic Fitness – VO2max on Treadmill
3. Anaerobic Fitness – Cunningham-Faulkner Treadmill Run with postexercise lactate
4. Strength and Power – grip strength, leg power (vertical jump), universal
(bench press, squat, etc)
5. Muscular Endurance – chin-ups, push-ups, sit-ups
6. Flexibility – overhead goniometer (shoulder, trunk and hip extension),
Flexibility Stool (trunk flexion)
7. Visual Acuity – peripheral vision, depth perception, reaction time
(forehand and backhand)
8. Hematology – hemoglobin, hematocrit
The Female Athlete Triad



Low energy availability
Amenorrhea
Osteoporosis
Christy Henrich
 1988 – at a meet in Budapest a U.S. judge told Christy Henrich one of the
world’s top gymnastics, that she was too fat and needed to lose weight if
she hoped to make the Olympic squad
 Age – 16 years old
 Height – 147cm (4’10”)
 Body mass – 42kg (93lbs)
 BMI – 19.8 kg/m2
 Resorted to anorexia and bulimia to control her weight
 Lowest body mass 22kg (47lbs)


BMI – 9.8 kg/m2
Only July 2th, 1994, at the age of 22, she died of multiple organ failure
Heidi Guenther
 Ballet dancer told to lose 5 pounds by her ballet company at 5’5” and 115
lbs
 Struggled with anorexia
 Died at the age of 22 weighing 93 lbs when her heart suddenly stopped
Definitions – Reproductive



Eumenorrhea  ovulatory cycle with menses occurring every 24-34 days
(10-13 cycles per year)
Oligomenorrhea  irregular menses occurring more than 35 days and
less than 90 days apart
Amenorrhea – no senses for at least 90 days
Alex DeVinny
 2003 State champion in 3200 m
 at 9 had issues with eating
 at 17 had not yet began menstruating
 at 20 died of cardiac arrest as a consequence of anorexia (weight 32kg)
Bone Regulation


Osteoclasts  cells that break down bone
Osteoblasts  cells that build bone
Resting Bone surface  resorption  reversal  bone formation  mineralization
Importance of Estrogen
 Suppresses bone resorption
 Allows skeleton to ‘hear’ physical activity
Risk factors for triad
 Calorie restriction
 Exercise for prolonged periods of time
 Involved in sport emphasizing body appearance
 Pressure to lose weight to improve performance
 Competitive nature
 Complete involvement with sport
 Trains even when injured or sick
 Traumatic event, injury, poor performance, changing in coaching
personnel

Other life stressors
Symptoms of Triad
 Menstrual irregularities
 Fatigue
 Problems controlling body temperature
 Problems with sleep
 Reduced bone mass
 Frequent injuries
Bona Fide Occupational Requirement (BFOR)
 Physically demanding occupations in which failure to perform the job or
ineffective job performance can result in loss of life or property
1) The standing must be for a purpose rationally connected to job performance
2) The standard must have been adopted by the employer in good faith and
belief that it was necessary for the fulfillment of the work-related purpose
3) The employer must show that the standard is reasonably necessary to
accomplish the work-related purpose (demonstrate that it is impossible to
accommodate the worker without imposing undue hardship on the
employer)
Workers’ Compensation
 Ontario’s Workplace Safety and Insurance Board (WSIB) decides
whether or not a worker receives compensation, and decides what the
worker gets compensation for. Depending on the injury or illness, a
worker can receive:
 85% of lost wages
 Health care costs
 Transportation costs to medical treatment
 Payment for pain and suffering
 Return to work plan