1. 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

2. 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

3. 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

4. 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

5. Exercise A Challenge to Homeostasis
Fig 13.1

6. 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

7. 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

8. 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

9. Calculation of VO2max VO2max = HRmax x SVmax x (a-vO2)max
Product of maximal cardiac output (Q) and arteriovenous difference (a-vO2)
Improvements in VO2max
50% due to  SV
50% due to  a-vO2
Differences in VO2max in normal subjects
Due to differences in SVmax
VO2max = HRmax x SVmax x (a-vO2)max

10. 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

11. Factors Increasing Stroke Volume
Fig 13.2

12. 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

13. Factors Causing Increased VO2max
Fig 13.3

14. Detraining and VO2max Decrease in VO2max with cessation of training
 SVmax
 maximal a-vO2 difference
Opposite of training effect
Fig 13.4

15. Endurance Training Effects on Performance
Improved performance following endurance training
Structural and biochemical changes in muscle
 Mitochondrial number
 Enzyme activity
 Capillary density

16. 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

17. 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

18. Training/Detraining Mitochondrial Changes
Fig 13.5

19. 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)

20. Changes in CS Activity Due to Different Training Programs
Fig 13.6

21. 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

22. Mitochondrial Number and ADP Concentration on VO2
Fig 13.7

23. 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

24. Effects of Endurance Training on O2 Deficit
Fig 13.8

25. 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

26. FFA Oxidation and Glucose-Sparing
Fig 13.9

27. Blood Lactate Concentration
Balance between lactate production and removal
Lactate production during exercise
NADH, pyruvate, and LDH in the cytoplasm
Blood pH affected by blood lactate concentration
pyruvate + NADH
lactate + NAD
LDH

28. Mitochondrial and Biochemical Adaptations and Blood pH
Fig 13.10

29. Blood Lactate Concentration
Fig 13.11

30. Biochemical Adaptations and Lactate Removal
Fig 13.13

31. 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

32. One Leg Training Study
Fig 13.14

33. Peripheral Control of Cardiorespiratory Responses
Fig 13.15

34. Central Control of Cardiorespiratory Responses
Fig 13.16

35. 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

36. Neural and Muscular Adaptations to Resistance Training
Fig 13.17