4/21/2014

1
Systems Review
Review of Training Principles
1. Overload Principle
2. Specificity Principle
3. Individual Differences Principle
4. Reversibility Principle
Metabolic Adaptations
Larger and more numerous
mitochondria in endurance trained
skeletal muscles
What does this directly result in?
Increase in mitochondrial proteins by a
factor of 2 can increase VO
2
max up to 10-
20%
Metabolic Adaptations
Improved Fat metabolism increase in a individuals
ability to mobilize, deliver, and oxidize fatty acids for
energy use during submaximal exercise
Contributing factors:
1. Greater blood flow within muscles.
2. Greater fat mobilizing and metabolizing enzymes
3. Enhanced mitochondrial capacity
4. Blunted catecholamine release for the same
absolute power output (blunts SNS) helps
conserve glycogen stores
Metabolic Adaptations
Improved carbohydrate metabolism
greater capacity to oxidize
carbohydrates during maximal exercise
Submaximal exercise reduction of
glycogen fuel turnover in favor of fatty
acids
Metabolic Adaptations
Muscle changes
Maximization of muscle fibers aerobic
potential
Enhancement of slow twitch muscles over
fast twitch muscles
Slow twitch muscles of highly trained
endurance athletes tend to be larger than
nontrained individuals
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2
Cardiovascular Adaptations
Myocardial hypertrophy increase in
size
Increase in end diastolic volumes
Eccentric hypertrophy increase in size of left
ventricular cavity
Concentric hypertrophy increase thickening of
wall
Reversibility principle return to normal size with
detraining
Negative effects of hypertrophy with disease
(hypertension may lead to failure)
Cardiovascular Adaptations
Increase in plasma volume 12-20% increases
within 3-6 training sessions
Increase of plasma albumin (protein = water
retention)
Enhances circulatory reserve
improves end diastolic volume/ venous return
Improves stroke volume
Improves oxygen delivery
Improved temperature regulation
Returns to normal levels within 1 week after training
ceases (reversibility)
Cardiovascular Adaptations
Heart rate
Decreased resting HR
Decreased HR in submaximal exercise
Exercise training increases
parasympathetic activity (exercise is not as
stressful)
Decrease in HR also a response of
improved stroke volume and cardiac output
Cardiovascular Adaptations
Increased stroke volume at rest and
during exercise.
Four contributing factors:
1. Increase in left ventricular volume
2. Reduced cardiovascular stiffness
3. Increased diastolic filling times
4. Improved intrinsic cardiac contractile
function
Cardiovascular adaptations
Increased maximum cardiac output
How does this affect VO2 and VO2 max?
HR max decreases with training, but cardiac
output still increases; How?
There is a training induced reduction in
submaximal cardiac output:
1. More effective blood flow
2. Enhanced ability of trained muscles to
generate ATP aerobically at a lower PO2
Cardiovascular adaptations
Increased a-vO2 difference (arteriole-
venous difference)
- Improved extraction of O2 from blood
What are possible factor for greater O2
extraction?
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3
Cardiovascular adaptations
Improvement in blood flow and distribution
Dependent on a number of factors:
Training specificity reliance on type I(slow twtich)
muscle fibers versus type II (fast twitch)
Improvements of O2 delivery, extraction, and use
Increased vasculature to specific muscles trained
At submaximal exercise levels/ lower cardiac
output = no change or lower muscle blood flow)
blood flow is improved to slow twitch muscle fibers
and the expense of delivery to fast twitch
Cardiovascular responses
Aerobic training responses related to blood
flow during maximal exercise
1. increased skeletal muscle flow
a) Increased cardiac output
b) Improved distribution of blood flow from nonactive
areas (renal/ splanchnic flow reduction)
c) Enlargement of arteries and veins, increased
capillarization of muscle by 10% per gram of muscle.
2. Increased coronary blood flow
a) Improved vascularization and capillarization of
coronary arteries
b) Improved control of vascular resistance and blood
distribution
Cardiovascular Responses
Reduction of blood pressure
Both systolic and diastolic
Reasons why?
Increased vasculature capillaries in
muscles
Blunted SNS response (PSNS override)
Exercise is not as stressful
Improved HR contractility
Pulmonary Adaptations
Aerobic training response
Maximal exercise
Ventilation improves by increasing rate and
tidal volume
Improved VO
2
consumption
Improved CO
2
removal via alveolar ventilation
Pulmonary adaptations
Submaximal exercise
Reduces ventilatory equivalent of oxygen
Body is more efficient so need is lower
Decreased total exercise oxygen cost related to breathing
1. reduces fatiguing effect during exercise on muscles
used in ventilation
2. oxygen that was used for ventilatory muscles can now
be used for active skeletal muscles
Principles of specificity this reduction is seen only if the
mode or specificity of muscles trained remains the same
in aerobic training.
Pulmonary adaptations
Improved ventilatory endurance
Reduce fatigue of inspiratory muscles in
prolonged, high intensity exercise
Improved force production on ventilatory
muscles (more efficient)
These adaptations benefit exercise by:
1. reducing overall exercise energy demands
due to less respiratory work
2. Reduction in lactate buildup with prolonged
exercise
3. Improved metabolism of ventilatory muscles
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Blood Lactate Response
Reduction of blood lactate
concentrations
1. decreased rate of lactate formation
2. increased lactate clearance during
exercise
3. combined effects of increased lactate
clearance and lactate removal
Other Aerobic Training
Adaptations
Body composition reduction in body fat
Improved thermoregulation improved sweating,
improved blood plasma volumes
Improved performance improved VO
2
max,
improved muscular strength and endurance
Improved psychological state
Reduction of stress/ anxiety
Decrease in mild to moderate depression
Reduction in neuroticism (negative emotional states)
Improved mood, self esteem, and self concept