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Chapter 13
The 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
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Exercise: A Challenge to Homeostasis
Figure 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:• 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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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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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
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Range of VO2max Values in the Population
Table 13.1
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• 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
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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
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Factors Increasing Stroke Volume
Figure 13.2
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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
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Factors Causing Increased VO2max
Figure 13.3
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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
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Detraining and Changes in VO2max and Cardiovascular Variables
Figure 13.4
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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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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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Changes in Oxidative Enzymes With Training
Table 13.4
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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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Time Course of Training/Detraining Mitochondrial Changes
Figure 13.5
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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
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Changes in Citrate Synthase Activity With Exercise
Figure 13.6
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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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Mitochondrial Number and ADP Concentration Needed to Increase VO2
Figure 13.7
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Endurance Training Reduces the O2 Deficit
Figure 13.8
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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
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Effect of Mitochondria and Capillaries on Free-Fatty Acid and Glucose Utilization
Figure 13.9
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• 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
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Mitochondrial and Biochemical Adaptations and Blood pH
Figure 13.10
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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
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Biochemical Adaptations and Lactate Removal
Figure 13.12
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J-Shaped Relationship Between Exercise and URTI
Figure 13.11
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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– Lack of transfer of training effect to untrained leg
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Lack of Transfer
of Training Effect
Figure 13.13
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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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Peripheral Control of Heart Rate, Ventilation, and Blood Flow
Figure 13.14
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Central Control of Cardiorespiratory Responses
Figure 13.15
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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– May be due to increased number of fibers
• Hyperplasia– Long-term strength training
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Neural and Muscular Adaptations to Resistance Training
Figure 13.16
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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