© 2007 McGraw-Hill Higher Education. All Rights Reserved. Presentation revised and updated by Brian...

© 2007 McGraw-Hill Higher Education. All Rights Reserved.

Presentation revised and updated by

Brian B. Parr, Ph.D.University of South Carolina Aiken

Chapter 13The Physiology of Training:

Effect on VO2 max, Performance, Homeostasis, and Strength

EXERCISE PHYSIOLOGYTheory and Application to Fitness and Performance, 6th edition

Scott K. Powers & Edward T. Howley


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.


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.


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.


Exercise: A Challenge to Homeostasis

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


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

– 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


Range of VO2max Values in the Population

Table 13.1


Product of maximal cardiac output and arteriovenous difference

Differences in VO2max in different populations

– Due to differences in SVmax

Improvements in VO2max

– 50% due to SV

– 50% due to a-vO2

VO2max = HRmax x SVmax x (a-vO2)max

Calculation of VO2max


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


Factors Increasing Stroke Volume

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


Factors Causing Increased VO2max

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


Detraining and Changes in VO2max and Cardiovascular Variables

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


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


Changes in Oxidative Enzymes With Training

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


Time Course of Training/Detraining Mitochondrial Changes

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


Changes in Citrate Synthase Activity With Exercise

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


Mitochondrial Number and ADP Concentration Needed to Increase VO2

Figure 13.7


Endurance Training Reduces the O2 Deficit

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


Effect of Mitochondria and Capillaries on Free-Fatty Acid and Glucose Utilization

Figure 13.9


Lactate production during exercise

– Increased mitochondrial number• Less carbohydrate utilization = less pyruvate formed

– Increased NADH shuttles• Less NADH available for lactic acid formation

– Change in LDH type

• Heart form (H4) has lower affinity for pyruvate = less lactic acid formation

pyruvate + NADH lactate + NADLDH

Biochemical Adaptations and Blood pH

M4 M3H M2H2 MH3 H4


Mitochondrial and Biochemical Adaptations and Blood pH

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


Biochemical Adaptations and Lactate Removal

Figure 13.12


J-Shaped Relationship Between Exercise and URTI

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


Lack of Transfer of Training Effect

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


Peripheral Control of Heart Rate, Ventilation, and Blood Flow

Figure 13.14


Central Control of Cardiorespiratory Responses

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


Neural and Muscular Adaptations to Resistance Training

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

© 2007 McGraw-Hill Higher Education. All Rights Reserved. Presentation revised and updated by Brian...

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Transcript of © 2007 McGraw-Hill Higher Education. All Rights Reserved. Presentation revised and updated by Brian...