Download Chapter 13

Scott K. Powers • Edward T. Howley
Theory and Application to Fitness and Performance
SEVENTH EDITION
Chapter
The Physiology of Training: Effect
on VO2 Max, Performance,
Homeostasis, and Strength
Presentation prepared by:
Brian B. Parr, Ph.D.
University of South Carolina Aiken
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Chapter 13
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.
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Chapter 13
Objectives
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.
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.
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Chapter 13
Objectives
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. a lower O2
deficit
b. an
increased utilization of FFA and a sparing of
blood glucose and muscle glycogen
c. a
reduction in lactate and H+ formation
d.
an increase in lactate removal
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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Chapter 13
Exercise: A Challenge to
Homeostasis
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Introduction
Figure 13.1
Chapter 13
Principles of Training
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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Chapter 13
Principles of Training
In Summary
 The principle of overload states that for a training
effect to occur, a system or tissue must be
challenged with an intensity, duration, or frequency
of exercise to which it is unaccustomed. Over time
the tissue or system adapts to this load. The
reversibility principle is a corollary to the overload
principle.
 The principle of specificity indicates that the training
effect is limited to the muscle fibers involved in the
activity. In addition, the muscle fiber adapts
specifically to the type of activity: mitochondrial and
capillary adaptations to endurance training, and
contractile protein adaptations to resistive weight
training.
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Chapter 13
Research Designs to Study Training
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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Chapter 13
Research Designs to Study Training
In Summary
 Cross-sectional training studies
contrast the physiological responses of
groups differing in habitual physical
activity (e.g., sedentary individuals
versus runners).
 Longitudinal training studies examine
the changes taking place over the
course of a training program.
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Chapter 13
Endurance Training and VO2 Max
Endurance Training and VO2 Max
• Training to increase VO2 max
– Large muscle groups, dynamic activity
– 20–60 min, 3–5 times/week, 50–85% VO2 max
• Expected increases in VO2 max
– Average = 15%
– 2–3% in those with high initial VO2 max
• Requires intensity of 95–100% VO2 max
– 30–50% in those with low initial VO2 max
• Training intensity of 40–70% VO2 max
• Genetic predisposition
– Accounts for 40%–66% VO2 max
– Prerequisite for VO2 max of 60–80 ml•kg–1•min–1
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Chapter 13
Endurance Training and VO2 Max
Range of VO2 Max Values in
the Population
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Chapter 13
Endurance Training and VO2 Max
The HERITAGE Family Study
• Designed to study the role of genotype in cardiovascular,
metabolic, and hormonal responses to exercise and
training
• Some results:
– Heritability of VO2 max is ~50%
• Maternal contribution is ~30%
– Large variation in change in VO2 max with training
• Average improvement 15–20%
• Ranged from slight decrease to 1 L/min increase
• Heritability of change in VO2 max is 47%
– Difference genes for sedentary VO2 max and change
in VO2 max with training
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Chapter 13
Endurance Training and VO2 Max
In Summary
 Endurance training programs that increase VO2 max involve a
large muscle mass in dynamic activity for twenty to sixty
minutes per session, three to five times per week, at an
intensity of 50% to 85% VO2 max.
 Although VO2 max increases an average of about 15% as a
result of an endurance training program, the largest increases
are associated with deconditioned or patient populations
having very low pretraining VO2 max values.
 Genetic predisposition accounts for 40% to 60% of one’s VO2
max value. Very strenuous and/or prolonged training can
increase VO2 max in normal sedentary individuals by more than
40%.
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Chapter 13
VO2 Max: Cardiac Output and the Arteriovenous Difference
Calculation of VO2 Max
• Product of maximal cardiac output and
arteriovenous difference
VO2 max = HR max x SV max x (a-vO2) max
• Differences in VO2 max in different
populations
– Primarily due to differences in SV max
• Improvements in VO2 max
– 50% due to SV
– 50% due to a-vO2
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Chapter 13
VO2 Max: Cardiac Output and the Arteriovenous Difference
Differences in VO2 Max Values
Among Populations
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Chapter 13
VO2 Max: Cardiac Output and the Arteriovenous Difference
Changes in VO2 Max with
Training
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Chapter 13
VO2 Max: Cardiac Output and the Arteriovenous Difference
In Summary
 In young sedentary subjects, approximately
50% of the increase in VO2 max due to
training is related to an increase in maximal
stroke volume (maximal heart rate remains
the same), and 50% is due to an increase in
the a-vO2 difference.
 The large differences in VO2 max in the
normal population (2 versus 6 liters/min) are
due to differences in maximal stroke volume.
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Chapter 13
VO2 Max: Cardiac Output and the Arteriovenous Difference
Stroke Volume
• Increased maximal stroke volume
–  Preload (EDV)
•  Plasma volume
•  Venous return
•  Ventricular volume
–  Afterload (TPR)
•  Arterial constriction
•  Maximal muscle blood flow with no change in
mean arterial pressure
–  Contractility
• Changes occur rapidly
– 11% increase in plasma volume with six days of
training
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Chapter 13
VO2 Max: Cardiac Output and the Arteriovenous Difference
Factors Increasing Stroke
Volume
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Figure 13.2
Chapter 13
Endurance Training and VO2 Max
Why Do Some Individuals Have High VO2 Max
Values Without Training?
• Some individuals have very high VO2 max values with no history of
training
– VO2 max = 65.3 ml•kg–1•min–1
– Compared to 46.3 ml•kg–1•min–1 in sedentary with low VO2 max
• Higher VO2 max due to:
– Higher maximal cardiac output, stroke volume, and lower total
peripheral resistance
– No difference in a-vO2 difference or maximal
heart rate
• Higher stroke volume linked to:
– Higher blood volume and red cell volume
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Chapter 13
VO2 Max: Cardiac Output and the Arteriovenous Difference
Arteriovenous O2 Difference
• a-vO2 max
–  Muscle blood flow
•  SNS vasoconstriction
– Improved ability of the muscle to extract
oxygen from the blood
•  Capillary density
•  Mitochondial number
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Chapter 13
VO2 Max: Cardiac Output and the Arteriovenous Difference
Factors Causing Increased VO2
Max
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Figure 13.3
Chapter 13
VO2 Max: Cardiac Output and the Arteriovenous Difference
In Summary
 The training-induced increase in maximal
stroke volume is due to both an increase in
preload and a decrease in afterload.
a. The increased preload is primarily due
to an increase in end diastolic ventricular
volume and
the associated increase in
plasma volume.
 b. The decreased afterload is due to a decrease in
the arteriolar constriction in the trained
muscles, increasing maximal muscle blood flow
with no change in the mean arterial blood
pressure.
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Chapter 13
VO2 Max: Cardiac Output and the Arteriovenous Difference
In Summary
 In young sedentary subjects, 50% of the increase in
VO2 max is due to an increase in the systemic a-vO2
difference. The increased a-vO2 difference is due to
an increase in the capillary density of the trained
muscles that is needed to accept the increase in
maximal muscle blood flow. The greater capillary
density allows for a sufficiently slow red blood cell
transit time through the muscle, providing enough
time for oxygen diffusion, which is facilitated by the
increase in the number of mitochondria.
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Chapter 13
Detraining and VO2 Max
Detraining and VO2 Max
• Decrease in VO2 max with cessation of
training
–  SV max
• Rapid loss of plasma volume
–  Maximal a-vO2 difference
•  Mitochondria
•  Oxidative capacity of muscle
–  Type IIa fibers and  type IIx fibers
– Initial decrease (12 days) due to  SV max
– Later decrease due to  a-vO2 max
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Detraining and ChangesDetraining
in VO
and VO Max
2
Max and Cardiovascular
Variables
Chapter 13
2
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Figure 13.4
Chapter 13
Detraining and VO2 Max
In Summary
 The decrease in VO2 max with cessation
of training is due to both a decrease in
maximal stroke volume and a decrease
in oxygen extraction, the reverse of
what happens with training.
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Chapter 13
Endurance Training: Effects on Performance and Homeostasis
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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Chapter 13
Endurance Training: Effects on Performance and Homeostasis
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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Chapter 13
Endurance Training: Effects on Performance and Homeostasis
Changes in Oxidative Enzymes
with Training
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Chapter 13
Endurance Training: Effects on Performance and Homeostasis
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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Chapter 13
Endurance Training: Effects on Performance and Homeostasis
Time Course of Training/Detraining
Mitochondrial Changes
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Figure 13.5
Chapter 13
Endurance Training: Effects on Performance and Homeostasis
Role of Exercise Intensity and Duration on
Mitochondrial Adaptations
• Citrate synthase (CS)
– Marker of mitochondrial oxidative capacity
• Effect of exercise intensity
– 55%, 65%, or 75% VO2 max
– Increased CS in oxidative (IIa) fibers with all training
intensities
• Effect of exercise duration
– 30, 60, or 90 minutes
– No difference between durations on CS activity in
IIa fibers
– Increase in CS activity in IIx fibers with higherintensity, longer-duration training
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Chapter 13
Endurance Training: Effects on Performance and Homeostasis
Changes in Citrate Synthase Activity
with Exercise
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Figure 13.6
Chapter 13
Endurance Training: Effects on Performance and Homeostasis
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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Chapter 13
Endurance Training: Effects on Performance and Homeostasis
Mitochondrial Number and ADP
Concentration Needed to Increase VO2
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Figure 13.7
Chapter 13
Endurance Training: Effects on Performance and Homeostasis
Endurance Training Reduces the
O2 Deficit
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Figure 13.8
Chapter 13
Endurance Training: Effects on Performance and Homeostasis
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
– Increased fatty acid binding protein and fatty acid translocase
• Transport of FFA from the cytoplasm to the mitochondria
– Increased mitochondrial number
• Higher levels of CPT I and FAT
• 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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Chapter 13
Endurance Training: Effects on Performance and Homeostasis
Effect of Mitochondria and Capillaries on
Free-Fatty Acid and Glucose Utilization
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Figure 13.9
Chapter 13
Endurance Training: Effects on Performance and Homeostasis
In Summary
 The combination of the increase in the density of capillaries
and the number of mitochondria per muscle fiber increases the
capacity to transport FFA from the plasma  cytoplasm 
mitochondria.
 The increase in the enzymes of the fatty acid cycle increases
the rate of formation of acetyl-CoA from FFA for oxidation in the
Krebs cycle. This increase in fat oxidation in endurance-trained
muscle spares both muscle glycogen and plasma glucose, the
latter being a focal point of homeostatic regulatory
mechanisms. These points are summarized in Figure 13.9.
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Chapter 13
Biochemical Adaptations and Blood pH
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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Chapter 13
Biochemical Adaptations and Blood pH
Mitochondrial and Biochemical
Adaptations and Blood pH
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Figure 13.10
Chapter 13
Biochemical Adaptations and Blood pH
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
• Redistribution of blood flow to liver and
kidney
– Increased lactate removal
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Chapter 13
Biochemical Adaptations and Blood pH
Redistribution of Blood Flow and
Lactate Removal
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Figure 13.13
Chapter 13
Biochemical Adaptations and Blood pH
In Summary
 Mitochondrial adaptations to endurance training
include an increase in the enzymes involved in
oxidative metabolism: Krebs cycle, fatty-acid (oxidation) cycle, and the electron transport chain.
 Those mitochondrial adaptations result in the
following:

a. a smaller O2 deficit due to a more rapid
increase in oxygen uptake at the onset of work
 b. an increase in fat metabolism that spares muscle
glycogen and blood glucose
 c. a reduction in lactate and H+ formation that helps
maintain the pH of the blood
 d. an increase in lactate removal
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to
Chapter 13
Exercise and Resistance to Infection
A Closer Look 13.4
Exercise and Resistance to Infection
• J-shaped relationship between amount and intensity of exercise
and risk of URTI
• Marathon run alters immune system
– Elevated neutrophils, reduced lymphocytes and natural killer
cells
– Decreases in NK and T-cell function
– Decreases in nasal neutrophil activity
– Decreases in nasal and salivary IgA concentrations
– Increases in pro-inflammatory cytokines
• “Open window” hypothesis
– Immune suppression following marathon increases risk of
infection
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Chapter 13
Exercise and Resistance to Infection
J-Shaped Relationship Between
Exercise and URTI
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Figure 13.11
Chapter 13
Exercise and Resistance to Infection
The “Open Window” Theory
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Figure 13.12
Chapter 13
Endurance Training: Links Between Muscle and Systemic Physiology
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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Chapter 13
Endurance Training: Links Between Muscle and Systemic Physiology
Lack of
Transfer
of
Training
Effect
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Figure 13.14
Chapter 13
Endurance Training: Links Between Muscle and Systemic Physiology
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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Chapter 13
Endurance Training: Links Between Muscle and Systemic Physiology
Peripheral Control of Heart Rate,
Ventilation, and Blood Flow
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Figure 13.15
Chapter 13
Endurance Training: Links Between Muscle and Systemic Physiology
Central Control of
Cardiorespiratory Responses
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Figure 13.16
Chapter 13
Endurance Training: Links Between Muscle and Systemic Physiology
In Summary
 The biochemical changes in muscle due to
endurance training influence the
physiological responses to exercise. The
reduction in “feedback” from
chemoreceptors in the trained muscle and a
reduction in the need to recruit motor units
to accomplish a work task results in reduced
sympathetic nervous system, heart rate, and
ventilation responses in submaximal
exercise.
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Chapter 13
Physiological Effects of Strength Training
Physiological Effects of Strength
Training
• Muscular strength
– Maximal force a muscle or muscle group can
generate
• 1 repetition maximum (1-RM)
• Muscular endurance
– Ability to make repeated contractions against a
submaximal load
• Strength training
– Percent gain inversely proportional to initial
strength
• Genetic limitation
to gains in strength
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Chapter 13
Physiological Effects of Strength Training
A Closer Look 13.5
Aging, Strength, and Training
• Decline in strength after age 50
– Loss of muscle mass (sarcopenia)
• Loss of both type I and II fibers
• Atrophy of type II fibers
• Loss of intramuscular fat and connective tissue
– Loss of motor units
– Reorganization of motor units
• Progressive resistance training
– Causes muscle hypertrophy and strength
gains
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Chapter 13
Physiological Mechanisms Causing Increased Strength
Physiological Mechanisms
Causing Increased Strength
• Strength training results in increased
muscle size and strength
• Initial 8–20 weeks
– Neural adaptations
• Long-term training (20+ weeks)
– Muscle hypertrophy
– High-intensity training can result in
hypertrophy with 10 sessions
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Chapter 13
Neural
andMechanisms
Muscular
Physiological
Causing Increased Strength
Adaptations
to Resistance Training
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Figure 13.17
Chapter 13
Physiological Mechanisms Causing Increased Strength
Neural Factors
• Early gains in strength
– Initial 8–20 weeks
• Adaptations
– Improved ability to recruit motor units
– Learning
– Coordination
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Chapter 13
Physiological Mechanisms Causing Increased Strength
Muscular Enlargement
• Hypertrophy
– Enlargement of both type I and II fibers
• Low-intensity (high RM), high-volume training
results in smaller type II fibers
• Heavy resistance (low RM) results in larger type II
fibers
– No increase in capillary density
• Hyperplasia
– Increase in muscle fiber number
– Mainly seen in long-term strength training
• Not as much evidence as muscle hypertrophy
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Chapter 13
Physiological Mechanisms Causing Increased Strength
The Winning Edge 13.1
Periodization of Strength Training
• Traditional training programs
– Variations in intensity (RM), sets, and repetitions
• Periodization
– Also includes variation of:
• Rest periods, type of exercise, number of training
sessions, and training volume
– Develop workouts to achieve optimal gains in:
• Strength, power, motor performance, and/or hypertrophy
– Linear and undulating programs
• Variations in volume/intensity over time
– More effective than non-periodized training for improving
strength and endurance
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Chapter 13
Physiological Mechanisms Causing Increased Strength
Concurrent Strength and
Endurance Training
• Potential for interference of adaptations
– Endurance training increases mitochondial
protein
– Strength training increases contractile
protein
– Depends on intensity, volume, and
frequency of training
• Studies show conflicting results
– Depends on intensity, volume, and
frequency of training
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Chapter 13
Physiological Mechanisms Causing Increased Strength
In Summary
 Increases in strength due to short-term (eight
to twenty weeks) training are the results of
neural adaptations, while gains in strength in
long-term training programs are due to an
increase in the size of the muscle.
 There is evidence both for and against the
proposition that the physiological effects of
strength training interfere with the
physiological effects of endurance training.
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