1. Chapter 13 The Physiology of Training: Effect on VO2 max, Performance, Homeostasis, and Strength
EXERCISE PHYSIOLOGY
Theory and Application to Fitness and Performance, 6th edition
Scott K. Powers & Edward T. Howley

2. Exercise: A Challenge to Homeostasis
Figure 13.1

3. 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

4. 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

5. 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

6. Range of VO2max Values in the Population
Table 13.1

7. Product of maximal cardiac output and arteriovenous difference
Calculation of VO2max
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

9. 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

10. Factors Increasing Stroke Volume
Figure 13.2

11. 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

12. Factors Causing Increased VO2max
Figure 13.3

13. 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

14. Detraining and Changes in VO2max and Cardiovascular Variables
Figure 13.4

15. 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

16. 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

17. Changes in Oxidative Enzymes With Training
Table 13.4

18. Time Course of Training/Detraining Mitochondrial Changes
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

19. Time Course of Training/Detraining Mitochondrial Changes
Figure 13.5

20. 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

21. Changes in Citrate Synthase Activity With Exercise
Figure 13.6

22. 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

23. Mitochondrial Number and ADP Concentration Needed to Increase VO2
Figure 13.7

24. Endurance Training Reduces the O2 Deficit
Figure 13.8

25. 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

26. Effect of Mitochondria and Capillaries on Free-Fatty Acid and Glucose Utilization
Figure 13.9

27. Biochemical Adaptations and Blood pH
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 + NAD
LDH
M4  M3H  M2H2  MH3  H4

28. Mitochondrial and Biochemical Adaptations and Blood pH
Figure 13.10

29. Biochemical Adaptations and 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

30. Biochemical Adaptations and Lactate Removal
Figure 13.12

31. J-Shaped Relationship Between Exercise and URTI
Figure 13.11

32. 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

33. Lack of Transfer of Training Effect
Figure 13.13

34. 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

35. Peripheral Control of Heart Rate, Ventilation, and Blood Flow
Figure 13.14

36. Central Control of Cardiorespiratory Responses
Figure 13.15

37. 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

38. Neural and Muscular Adaptations to Resistance Training
Figure 13.16

39. 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