Dr.

Mustafa Qamar

The Physiology of Training: Effect

on VO2 Max, Performance,
Homeostasis, and Strength

revivephysio.net
 Introduction

Exercise: A Challenge to Homeostasis

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 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,
8% isometric)
▪ Reversibility
▪ Gains are lost when overload is removed
 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.
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 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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 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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 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

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 Endurance Training and VO2 Max

Range of VO2 Max Values in the Population

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 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.
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 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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 VO2 Max: Cardiac Output and the Arteriovenous Difference

Changes in VO2 Max with Training

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 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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 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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 VO2 Max: Cardiac Output and the Arteriovenous Difference

Factors Increasing Stroke Volume

Figure 13.2
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 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
▪ a-vO2 difference
▪ Higher stroke volume linked to:
▪ Higher blood volume and red cell volume
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 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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 VO2 Max: Cardiac Output and the Arteriovenous Difference

Factors Causing Increased VO2 Max

Figure 13.3
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 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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 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

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 VO2 Max

Detraining and Changes in VO2 Max and

Cardiovascular Variables

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 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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 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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 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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 Endurance Training: Effects on Performance and Homeostasis

Time Course of Training/Detraining

Mitochondrial Changes

Figure 13.5
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 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 higher-intensity,
longer-duration training
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 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
▪ High-resistance (2–10 RM) training
• Gains in strength
▪ Low-resistance training
• Gains in endurance
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 Physiological Effects of Strength Training

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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 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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 Physiological Mechanisms Causing Increased Strength

Neural and Muscular Adaptations

to Resistance Training

Figure 13.17
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 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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 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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 Physiological Mechanisms Causing Increased Strength

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

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▪ Linear and undulating
programs
• Variations in
volume/intensity over
time
▪ More effective than
non-periodized training
for improving strength
and endurance
 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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 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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