Transcript 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
Outline
 Principles of Training
Overload
Specificity
 Research Designs to
Study Training
 Endurance Training
and VO2 Max
Training Programs and
Changes in VO2 Max
 VO2 Max: Cardiac
Output and the
Arteriovenous O2
Difference
Stroke Volume
Arteriovenous O2
Difference
 Detraining and VO2
Max
 Endurance Training:
Effects on
Performance and
Homeostasis
Biochemical Adaptations
and the Oxygen Deficit
Biochemical Adaptations
and the Plasma Glucose
Concentration
Biochemical Adaptations
and Blood pH
Biochemical Adaptations
and Lactate Removal
 Endurance Training:
Links Between Muscle
and Systemic
Physiology
Peripheral Feedback
Central Command
 Physiological Effects
of Strength Training
 Physiological
Mechanisms Causing
Increased Strength
Neural Factors
Muscular Enlargement
Concurrent Strength and
Endurance Training
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Introduction
Chapter 13
Exercise: A Challenge to Homeostasis
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Figure 13.1
Principles of Training
Chapter 13
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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Endurance Training and VO2 Max
Chapter 13
A Closer Look 13.1
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
Endurance Training and VO2 Max
Chapter 13
A Closer Look 13.2
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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Detraining and VO2 Max
Chapter 13
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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Chapter 13
Detraining and VO2 Max
Detraining and Changes in VO2 Max and
Cardiovascular Variables
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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
A Closer Look 13.3
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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Biochemical Adaptations and Blood pH
Chapter 13
Biochemical Adaptations and Blood pH
• Lactate production during exercise
LDH
pyruvate + NADH
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
to maintain the pH of the blood
d. an increase in lactate removal
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Exercise and Resistance to Infection
Chapter 13
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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Physiological Effects of Strength Training
Chapter 13
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
– High-resistance (2–10 RM) training
 Gains in strength
– Low-resistance training (20+ RM)
 Gains in endurance
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Physiological Effects of Strength Training
Chapter 13
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
– Important for activities of daily living, balance, and
reduced risk of falls
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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
Physiological Mechanisms Causing Increased Strength
Neural and Muscular 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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Chapter 13
Study Questions
1.
Define the following principles of training: overload and
specificity.
2.
Give one example each of a cross-sectional study and a
longitudinal study.
3.
What are the typical VO2 max values for young men and
women? Cardiac patients?
4.
Given the formula for VO2 max using heart rate, stroke
volume, and the a-vO2 difference, which variable is most
important in explaining the differences in VO2 max in
different populations? Give a quantitative example.
5.
Describe how the increase in VO2 max comes about for the
sedentary subject who undertakes an endurance training
program.
6.
Explain the importance of preload, afterload, and
contractility in the increase of the maximal stroke volume
that occurs with endurance training.
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Chapter 13
Study Questions
7.
What are the most important changes in muscle structure
that are responsible for the increase in the maximal a-vO2
difference that occurs with endurance training?
8.
What causes the VO2 max to decrease following termination
of an endurance training program?
9.
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 increase utilization of FFA and sparing of blood
glucose and muscle glycogen
c. a reduction in lactate and H+ formation that helps to
maintain the pH of the blood
d. an increase in lactate removal
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Chapter 13
Study Questions
10. Define central command and peripheral feedback and
explain how changes in muscle as a result of endurance
training can be responsible for the lower heart rate,
ventilation, and catecholamine response to a submaximal
exercise bout.
11. In short-term training programs, what neural factors may be
responsible for the increase in strength?
12. Contrast hyperplasia with hypertrophy, and explain the role
of each in the increase in muscle size that occurs with longterm strength training.
13. Does strength training interfere with the physiological
effects of endurance training?
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