Transcript Chapter 13

Chapter 13:
The Physiology of Training
Effect on VO2 MAX, Performance,
Homeostasis and Strength
EXERCISE PHYSIOLOGY
Theory and Application to Fitness and Performance, 5th edition
Scott K. Powers & Edward T. Howley
Presentation revised and updated by
TK Koesterer, Ph.D., ATC
Humboldt State University
Objectives
• Explain the basic principles of training: overload and
specificity
• Contrast cross-sectional with longitudinal research
studies
• Indicate the typical change in VO2 MAX with endurance
training programs, and the effect of the initial
(pretraining) value on the magnitude of the increase
• State the VO2 MAX values for various sedentary, active
and athletic populations
• State the formula VO2 MAX using HR, SV and a-v O2
difference; indicate which of the variables is most
important in explaining the wide range of VO2 MAX
values in the population
Objectives
• Discuss, using the variables identified in objective 5,
how the increase in VO2 MAX comes about for the
sedentary subject who participates in an endurance
training program
• Define preload, afterload, and contractility, and
discuss the role of each in the increase in the
maximal SV that occurs with endurance training
• Describe the changes in muscle structure that are
responsible for the increase in the maximal a-v O2
difference with endurance training
• Describe the underlying causes for the decrease in
VO2 MAX that occurs with cessation of endurance
training
Objectives
• Describe how the capillary and mitochondrial changes
that occur in muscle as a result of an endurance training
program are related to the following: a lower O2 deficit,
and increased utilization of FFA and a sparing of blood
glucose and muscle glycogen, a reduction in lactate and
H+ formation, and an increase in lactate removal
• Discuss how changes in “central command” and
“peripheral feedback” following an endurance training
program can lower the HR, ventilation, and
catecholamine responses to a submaximal exercise bout
• Contrast the role of neural adaptation with hypertorphy in
the increase in strength that occurs with resistance
training
Exercise
A Challenge to Homeostasis
Fig 13.1
Principles of Training
• Overload
– Training effect occurs when a system is
exercised at a level beyond which it is
normally accustomed
• Specificity
– Training effect is specific to the muscle
fibers involved
– Type of exercise
• Reversibility
– Gains are lost when overload is removed
Research Designs to
Study Training
• Cross-sectional
studies
– Examine groups of
differing physical
activity at one time
– Record differences
between groups
• Longitudinal studies
– Examine groups
before and after
training
– Record changes
over time in the
groups
Endurance Training and VO2max
• Training to increase VO2max
– Large muscle groups, dynamic activity
– 20-60 min, 3-5 times/week, 50-85% VO2max
• Expected increases in VO2max
– 15% (average) - 40% (strenuous or prolonged
training)
– Greater increase in highly deconditioned or
diseased subjects
• Genetic predisposition
– Accounts for 40%-66% VO2max
Calculation of VO2max
• Product of maximal cardiac output (Q) and
arteriovenous difference (a-vO2)
VO2max = HRmax x SVmax x (a-vO2)max
• Improvements in VO2max
– 50% due to  SV
– 50% due to  a-vO2
• Differences in VO2max in normal subjects
– Due to differences in SVmax
Stroke Volume
and Increased VO2max
• Increased SVmax
–  Preload (EDV)
•  Plasma volume
•  Venous return
•  Ventricular volume
–  Afterload (TPR)
•  Arterial constriction
•  Maximal muscle blood flow with no
change in mean arterial pressure
–  Contractility
Factors Increasing Stroke Volume
Fig 13.2
a-vO2 Difference and Increased
VO2max
• Improved ability of the muscle to extract
oxygen from the blood
–  Muscle blood flow
–  Capillary density
–  Mitochondial number
• Increased a-vO2 difference accounts for 50%
of increased VO2max
Factors Causing Increased VO2max
Fig 13.3
Detraining and VO2max
• Decrease in VO2max
with cessation of
training
–  SVmax
–  maximal a-vO2
difference
• Opposite of training
effect
Fig 13.4
Endurance Training
Effects on Performance
• Improved performance following endurance
training
• Structural and biochemical changes in
muscle
–  Mitochondrial number
•  Enzyme activity
–  Capillary density
Structural and Biochemical
Adaptations to Endurance Training
•  Mitochondrial number
•  Oxidative enzymes
– Krebs cycle (citrate synthase)
– Fatty acid (-oxidation) cycle
– Electron transport chain
•  NADH shuttling system
• Change in type of LDH
• Adaptations quickly lost with detraining
Detraining
Changes in Mitochondria
• About 50% of the increase in mitochondrial
content was lost after one week of detraining
• All of the adaptations were lost after five
weeks of detraining
• It took four weeks of retraining to regain the
adaptations lost in the first week of detraining
Training/Detraining
Mitochondrial Changes
Fig 13.5
Effect Intensity and Duration on
Mitochondrial Enzymes
• Citrate synthase (CS)
– Marker of mitochondrial oxidative capacity
– Light to moderate exercise training
• Increased CS in high oxidative fibers
(Type I and IIa)
– Strenuous exercise training
• Increased CS in low oxidative fibers
(Type IIb)
Changes in
CS Activity
Due to
Different
Training
Programs
Fig 13.6
Mitochondrial Number and
ADP Concentration on VO2
• [ADP] stimulates mitochondrial ATP
production
• Increased mitochondrial number following
training
– Lower [ADP] needed to increase ATP
production and VO2
Mitochondrial
Number and
ADP
Concentration
on VO2
Fig 13.7
Biochemical Adaptations
and Oxygen Deficit
• Oxygen deficit is lower following training
– Same VO2 at lower [ADP]
– Energy requirement can be met by
oxidative ATP production at the onset of
exercise
• Results in less lactic acid formation and less
PC depletion
Effects of Endurance Training
on O2 Deficit
Fig 13.8
Biochemical Changes
and FFA Oxidation
• Increased mitochondrial number and capillary
density
– Increased capacity to transport FFA from
plasma to cytoplasm to mitochondria
• Increased enzymes of -oxidation
– Increased rate of acetyl CoA formation
• Increased FFA oxidation
– Spares muscle glycogen and blood
glucose
FFA Oxidation and
Glucose-Sparing
Fig 13.9
Blood Lactate Concentration
• Balance between lactate production and
removal
• Lactate production during exercise
– NADH, pyruvate, and LDH in the
cytoplasm
pyruvate + NADH
LDH
lactate + NAD
• Blood pH affected by blood lactate
concentration
Mitochondrial and Biochemical
Adaptations and Blood pH
Fig 13.10
Blood Lactate Concentration
Fig 13.11
Biochemical Adaptations
and Lactate Removal
Fig 13.13
Links Between Muscle and
Systemic Physiology
• Biochemical adaptations to training influence
the physiological response to exercise
– Sympathetic nervous system ( E/NE)
– Cardiorespiratory system ( HR, 
ventilation)
• Due to:
– Reduction in “feedback” from muscle
chemoreceptors
– Reduced number of motor units recruited
• Demonstrated in one leg training studies
One Leg Training Study
Fig 13.14
Peripheral Control of
Cardiorespiratory Responses
Fig 13.15
Central Control of
Cardiorespiratory Responses
Fig 13.16
Physiological Effects of
Strength Training
• Strength training results in increased muscle
size and strength
• Neural factors
– Increased ability to activate motor units
– Strength gains in initial 8-20 weeks
• Muscular enlargement
– Mainly due enlargement of fibers
(hypertrophy)
– Long-term strength training
Neural and Muscular Adaptations
to Resistance Training
Fig 13.17