Chapter 13:

The Physiology of Training

Effect on VO2 MAX, Performance, Homeostasis and Strength
EXERCISE PHYSIOLOGY Theory and Application to Fitness and Performance, 5th edition Scott K. Powers & Edward T. Howley
Presentation revised and updated by

TK Koesterer, Ph.D., ATC Humboldt State University

(c) 2004 The McGraw-Hill Companies, Inc. All rights reserved.

Objectives
Explain the basic principles of training: overload and specificity Contrast cross-sectional with longitudinal research studies 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 State the VO2 MAX values for various sedentary, active and athletic populations State the formula VO2 MAX using HR, SV and a-v O2 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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Objectives
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 Define preload, afterload, and contractility, and discuss the role of each in the increase in the maximal SV that occurs with endurance training Describe the changes in muscle structure that are responsible for the increase in the maximal a-v O2 difference with endurance training Describe the underlying causes for the decrease in VO2 MAX that occurs with cessation of endurance training
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Objectives
Describe how the capillary and mitochondrial changes that occur in muscle as a result of an endurance training program are related to the following: a lower O2 deficit, and 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 Discuss how changes in central command and peripheral feedback following an endurance training program can lower the HR, ventilation, and catecholamine responses to a submaximal exercise bout Contrast the role of neural adaptation with hypertorphy in the increase in strength that occurs with resistance training
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Exercise A Challenge to Homeostasis

Fig 13.1
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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 the muscle fibers involved Type of exercise Reversibility Gains are lost when overload is removed
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Research Designs to Study Training

Cross-sectional Longitudinal studies studies Examine groups Examine groups of before and after differing physical training activity at one time Record changes Record differences over time in the between groups 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 15% (average) - 40% (strenuous or prolonged training) Greater increase in highly deconditioned or diseased subjects Genetic predisposition Accounts for 40%-66% VO2max
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Calculation of VO2max
Product of maximal cardiac output (Q) and arteriovenous difference (a-vO2)

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

Improvements in VO2max 50% due to SV 50% due to a-vO2 Differences in VO2max in normal subjects Due to differences in SVmax
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Stroke Volume and Increased VO2max

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 (c) 2004 The McGraw-Hill Companies, Inc. All rights reserved.

Factors Increasing Stroke Volume

Fig 13.2
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a-vO2 Difference and Increased VO2max

Improved ability of the muscle to extract oxygen from the blood Muscle blood flow Capillary density Mitochondial number Increased a-vO2 difference accounts for 50% of increased VO2max

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Factors Causing Increased VO2max

Fig 13.3
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Detraining and VO2max

Decrease in VO2max with cessation of training SVmax maximal a-vO2 difference Opposite of training effect
Fig 13.4

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Endurance Training Effects on Performance

Improved performance following endurance training Structural and biochemical changes in muscle Mitochondrial number Enzyme activity Capillary density

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Structural and Biochemical Adaptations to Endurance Training

Mitochondrial number Oxidative enzymes Krebs cycle (citrate synthase) Fatty acid (-oxidation) cycle Electron transport chain NADH shuttling system Change in type of LDH Adaptations quickly lost with detraining
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Detraining Changes in Mitochondria

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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Training/Detraining Mitochondrial Changes

Fig 13.5
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Effect Intensity and Duration on Mitochondrial Enzymes

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 IIb)

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Changes in CS Activity Due to Different Training Programs

Fig 13.6
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Mitochondrial Number and ADP Concentration on VO2

[ADP] stimulates mitochondrial ATP production Increased mitochondrial number following training Lower [ADP] needed to increase ATP production and VO2

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Mitochondrial Number and ADP Concentration on VO2

Fig 13.7

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Biochemical Adaptations and Oxygen Deficit

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 Results in less lactic acid formation and less PC depletion

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Effects of Endurance Training on O2 Deficit

Fig 13.8
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Biochemical Changes and FFA Oxidation

Increased mitochondrial number and capillary density Increased capacity to transport FFA from plasma to cytoplasm to mitochondria Increased enzymes of -oxidation Increased rate of acetyl CoA formation Increased FFA oxidation Spares muscle glycogen and blood glucose
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FFA Oxidation and Glucose-Sparing

Fig 13.9
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Blood Lactate Concentration

Balance between lactate production and removal Lactate production during exercise NADH, pyruvate, and LDH in the cytoplasm
pyruvate + NADH LDH lactate + NAD

Blood pH affected by blood lactate concentration

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Mitochondrial and Biochemical Adaptations and Blood pH

Fig 13.10
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Blood Lactate Concentration

Fig 13.11
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Biochemical Adaptations and Lactate Removal

Fig 13.13
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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
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One Leg Training Study

Fig 13.14

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Peripheral Control of Cardiorespiratory Responses

Fig 13.15
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Central Control of Cardiorespiratory Responses

Fig 13.16
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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) Long-term strength training
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Neural and Muscular Adaptations to Resistance Training

Fig 13.17
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