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Chapter 13
The Physiology of Training:
Effect on VO2 max, Performance,
Homeostasis, and Strength
EXERCISE PHYSIOLOGY
Theory and Application to Fitness and Performance, 6th edition
Scott K. Powers & Edward T. Howley
Presentation revised and updated by
Brian B. Parr, Ph.D.
University of South Carolina Aiken
© 2007 McGraw-Hill Higher Education. All Rights Reserved.
Objectives
1. Explain the basic principles of training: overload and specificity.
2. Contrast cross-sectional with longitudinal research studies.
3. 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.
4. State the typical VO2 max values for various sedentary, active,
and athletic populations,
5. State the formula for VO2 max using heart rate, stroke volume,
and the a-vO2 difference; indicate which of the variables is most
important in explaining the wide range of VO2 max values in the
population.
6. 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.
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Objectives
7. Define preload, afterload, and contractility, and discuss the role
of each in the increase in the maximal stroke volume that
occurs with endurance training.
8. Describe the changes in muscle structure that are responsible
for the increase in the maximal a-vO2 difference with
endurance training.
9. Describe the underlying causes for the decrease in VO2 max
that occurs with cessation of endurance training.
10. Describe how the capillary and mitochondrial changes that
occur in muscle as a result of an endurance training program
are related to the following adaptations to submaximal
exercise: a lower O2 deficit, an 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.
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Objectives
11. Discuss how changes in “central command” and “peripheral
feedback” following an endurance training program can lower
the heart rate, ventilation, and catecholamine responses to a
submaximal exercise bout.
12. Contrast the role of neural adaptations with hypertrophy in the
increase in strength that occurs with resistance training.
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Exercise: A Challenge to Homeostasis
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Figure 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:
•
•
•
•
Muscle fibers involved
Energy system involved (aerobic vs. anaerobic)
Velocity of contraction
Type of contraction (eccentric, concentric, isometric)
 Reversibility
– Gains are lost when overload is removed
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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
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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
– Average = 15%
– 2-3% in those with high initial VO2max
– 30–50% in those with low initial VO2max
 Genetic predisposition
– Accounts for 40%-66% VO2max
– Prerequisite for VO2max of 60–80 ml•kg-1•min-1
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Range of VO2max Values in the Population
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Table 13.1
Calculation of VO2max
 Product of maximal cardiac output and arteriovenous
difference
VO2max = HRmax x SVmax x (a-vO2)max
 Differences in VO2max in different populations
– Due to differences in SVmax
 Improvements in VO2max
– 50% due to SV
– 50% due to a-vO2
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Increased VO2max With Training
 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
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Factors Increasing Stroke Volume
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Figure 13.2
Increased VO2max With Training
 a-vO2max
–  Muscle blood flow
•  SNS vasoconstriction
– Improved ability of the muscle to extract oxygen
from the blood
•  Capillary density
•  Mitochondial number
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Factors Causing Increased VO2max
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Figure 13.3
Detraining and VO2max
 Decrease in VO2max with cessation of training
–  SVmax
• Rapid loss of plasma volume
–  Maximal a-vO2 difference
•  Mitochondria
•  Oxidative capacity of muscle
-  Type IIa fibers and  type IIx fibers
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Detraining and Changes in VO2max and
Cardiovascular Variables
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Figure 13.4
Effects of Endurance Training on
Performance
 Maintenance of homeostasis
– More rapid transition from rest to steady-state
– Reduced reliance on glycogen stores
– Cardiovascular and thermoregulatory adaptations
 Neural and hormonal adaptations
– Initial changes in performance
 Structural and biochemical changes in muscle
–  Mitochondrial number
–  Capillary density
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Structural and Biochemical Adaptations to
Endurance Training
 Increased capillary density
 Increased number of mitochondria
 Increase in oxidative enzymes
– Krebs cycle (citrate synthase)
– Fatty acid (-oxidation) cycle
– Electron transport chain
 Increased NADH shuttling system
– NADH from cytoplasm to mitochondria
 Change in type of LDH
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Changes in Oxidative Enzymes With
Training
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Table 13.4
Time Course of Training/Detraining
Mitochondrial Changes
 Training
– Mitochondria double with five weeks of training
 Detraining
– 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
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Time Course of Training/Detraining
Mitochondrial Changes
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Figure 13.5
Effect Intensity and Duration on
Mitochondrial Adaptations
 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 IIx
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Changes in Citrate Synthase Activity With
Exercise
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Figure 13.6
Biochemical Adaptations and the Oxygen
Deficit
 [ADP] stimulates mitochondrial ATP production
 Increased mitochondrial number following training
– Lower [ADP] needed to increase ATP production
and VO2
 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
• Faster rise in VO2 curve and steady-state is reached
earlier
 Results in less lactic acid formation and less PC
depletion
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Mitochondrial Number and ADP
Concentration Needed to Increase VO2
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Figure 13.7
Endurance Training Reduces the
O2 Deficit
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Figure 13.8
Biochemical Adaptations and the Plasma
Glucose Concentration
 Increased utilization of fat and sparing of plasma
glucose and muscle glycogen
 Transport of FFA into the muscle
– Increased capillary density
• Slower blood flow and greater FFA uptake
 Transport of FFA from the cytoplasm to the
mitochondria
– Increased mitochondrial number and carnitine
transferase
 Mitochondrial oxidation of FFA
– Increased enzymes of -oxidation
• Increased rate of acetyl-CoA formation
• High citrate level inhibits PFK and glycolysis
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Effect of Mitochondria and Capillaries on
Free-Fatty Acid and Glucose Utilization
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Figure 13.9
Biochemical Adaptations and Blood pH
 Lactate production during exercise
pyruvate + NADH
LDH
lactate + NAD
– Increased mitochondrial number
• Less carbohydrate utilization = less pyruvate formed
– Increased NADH shuttles
• Less NADH available for lactic acid formation
– Change in LDH type
M4  M3H  M2H2  MH3  H4
• Heart form (H4) has lower affinity for pyruvate = less lactic
acid formation
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Mitochondrial and Biochemical
Adaptations and Blood pH
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Figure 13.10
Biochemical Adaptations and Lactate
Removal
 Lactate removal
– By nonworking muscle, liver, and kidneys
– Gluconeogenesis in liver
 Increased capillary density
– Muscle can extract same O2 with lower blood flow
– More blood flow to liver and kidney
• Increased lactate removal
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Biochemical Adaptations and Lactate
Removal
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Figure 13.12
J-Shaped Relationship Between Exercise
and URTI
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Figure 13.11
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
– Lack of transfer of training effect to untrained leg
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Lack of
Transfer
of
Training
Effect
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Figure 13.13
Peripheral and Central Control of
Cardiorespiratory Responses
 Peripheral feedback from working muscles
– Group III and group IV nerve fibers
• Responsive to tension, temperature, and chemical
changes
• Feed into cardiovascular control center
 Central Command
– Motor cortex, cerebellum, basal ganglia
• Recruitment of muscle fibers
• Stimulates cardiorespiratory control center
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Peripheral Control of Heart Rate,
Ventilation, and Blood Flow
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Figure 13.14
Central Control of Cardiorespiratory
Responses
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Figure 13.15
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
– May be due to increased number of fibers
• Hyperplasia
– Long-term strength training
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Neural and Muscular Adaptations
to Resistance Training
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Figure 13.16
Training to Improve Muscular Strength
 Traditional training programs
– Variations in intensity, sets, and repetitions
 Periodization
– Volume and intensity of training varied over time
– More effective than non-periodized training for
improving strength and endurance
 Concurrent strength and endurance training
– Adaptations may or may not interfere with each
other
• Depends on intensity, volume, and frequency of training
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