1. The Physiology of Training: Effect on VO2 Max, Performance, Homeostasis, and Strength

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 typical VO2 max values for various sedentary, active, and athletic populations.
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.

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 stroke volume that occurs with endurance training.
Describe the changes in muscle structure that are responsible for the increase in the maximal a-vO2 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 adaptations to submaximal exercise: a. a lower O2 deficit b. an increased utilization of FFA and a sparing of blood glucose and muscle glycogen c. a reduction in lactate and H+ formation d. an increase in lactate removal
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.
Contrast the role of neural adaptations with hypertrophy in the increase in strength that occurs with resistance training.

5. Outline Principles of Training Detraining and VO2 Max
Overload
Specificity
Research Designs to Study Training
Endurance Training and VO2 Max
Training Programs and Changes in VO2 Max
VO2 Max: Cardiac Output and the Arteriovenous O2 Difference
Stroke Volume
Arteriovenous O2 Difference
Detraining and VO2 Max
Endurance Training: Effects on Performance and Homeostasis
Biochemical Adaptations and the Oxygen Deficit
Biochemical Adaptations and the Plasma Glucose Concentration
Biochemical Adaptations and Blood pH
Biochemical Adaptations and Lactate Removal
Endurance Training: Links Between Muscle and Systemic Physiology
Peripheral Feedback
Central Command
Physiological Effects of Strength Training
Physiological Mechanisms Causing Increased Strength
Neural Factors
Muscular Enlargement
Concurrent Strength and Endurance Training

6. Exercise: A Challenge to Homeostasis
Introduction
Exercise: A Challenge to Homeostasis
Figure 13.1

7. 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

8. Principles of Training
In Summary
The principle of overload states that for a training effect to occur, a system or tissue must be challenged with an intensity, duration, or frequency of exercise to which it is unaccustomed. Over time the tissue or system adapts to this load. The reversibility principle is a corollary to the overload principle.
The principle of specificity indicates that the training effect is limited to the muscle fibers involved in the activity. In addition, the muscle fiber adapts specifically to the type of activity: mitochondrial and capillary adaptations to endurance training, and contractile protein adaptations to resistive weight training.

9. 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

10. Research Designs to Study Training
In Summary
Cross-sectional training studies contrast the physiological responses of groups differing in habitual physical activity (e.g., sedentary individuals versus runners).
Longitudinal training studies examine the changes taking place over the course of a training program.

11. Endurance Training and VO2 Max
Training to increase VO2 max
Large muscle groups, dynamic activity
20–60 min, 3–5 times/week, 50–85% VO2 max
Expected increases in VO2 max
Average = 15%
2–3% in those with high initial VO2 max
Requires intensity of 95–100% VO2 max
30–50% in those with low initial VO2 max
Training intensity of 40–70% VO2 max
Genetic predisposition
Accounts for 40%–66% VO2 max
Prerequisite for VO2 max of 60–80 ml•kg–1•min–1

12. Range of VO2 Max Values in the Population
Endurance Training and VO2 Max
Range of VO2 Max Values in the Population

13. A Closer Look 13.1 The HERITAGE Family Study
Endurance Training and VO2 Max
A Closer Look 13.1 The HERITAGE Family Study
Designed to study the role of genotype in cardiovascular, metabolic, and hormonal responses to exercise and training
Some results:
Heritability of VO2 max is ~50%
Maternal contribution is ~30%
Large variation in change in VO2 max with training
Average improvement 15–20%
Ranged from slight decrease to 1 L/min increase
Heritability of change in VO2 max is 47%
Difference genes for sedentary VO2 max and change in VO2 max with training

14. Endurance Training and VO2 Max
In Summary
Endurance training programs that increase VO2 max involve a large muscle mass in dynamic activity for twenty to sixty minutes per session, three to five times per week, at an intensity of 50% to 85% VO2 max.
Although VO2 max increases an average of about 15% as a result of an endurance training program, the largest increases are associated with deconditioned or patient populations having very low pretraining VO2 max values.
Genetic predisposition accounts for 40% to 60% of one’s VO2 max value. Very strenuous and/or prolonged training can increase VO2 max in normal sedentary individuals by more than 40%.

15. VO2 Max: Cardiac Output and the Arteriovenous Difference
Calculation of VO2 Max
Product of maximal cardiac output and arteriovenous difference
Differences in VO2 max in different populations
Primarily due to differences in SV max
Improvements in VO2 max
50% due to SV
50% due to a-vO2
VO2 max = HR max x SV max x (a-vO2) max

16. Differences in VO2 Max Values Among Populations
VO2 Max: Cardiac Output and the Arteriovenous Difference
Differences in VO2 Max Values Among Populations

17. Changes in VO2 Max with Training
VO2 Max: Cardiac Output and the Arteriovenous Difference
Changes in VO2 Max with Training

18. VO2 Max: Cardiac Output and the Arteriovenous Difference
In Summary
In young sedentary subjects, approximately 50% of the increase in VO2 max due to training is related to an increase in maximal stroke volume (maximal heart rate remains the same), and 50% is due to an increase in the a-vO2 difference.
The large differences in VO2 max in the normal population (2 versus 6 liters/min) are due to differences in maximal stroke volume.

19. Stroke Volume Increased maximal stroke volume  Preload (EDV)
VO2 Max: Cardiac Output and the Arteriovenous Difference
Stroke Volume
Increased maximal stroke volume
 Preload (EDV)
 Plasma volume
 Venous return
 Ventricular volume
 Afterload (TPR)
 Arterial constriction
 Maximal muscle blood flow with no change in mean arterial pressure
 Contractility
Changes occur rapidly
11% increase in plasma volume with six days of training

20. Factors Increasing Stroke Volume
VO2 Max: Cardiac Output and the Arteriovenous Difference
Factors Increasing Stroke Volume
Figure 13.2

21. Endurance Training and VO2 Max
A Closer Look 13.2 Why Do Some Individuals Have High VO2 Max Values Without Training?
Some individuals have very high VO2 max values with no history of training
VO2 max = 65.3 ml•kg–1•min–1
Compared to 46.3 ml•kg–1•min–1 in sedentary with low VO2 max
Higher VO2 max due to:
Higher maximal cardiac output, stroke volume, and lower total peripheral resistance
No difference in a-vO2 difference or maximal heart rate
Higher stroke volume linked to:
Higher blood volume and red cell volume

22. Arteriovenous O2 Difference
VO2 Max: Cardiac Output and the Arteriovenous Difference
Arteriovenous O2 Difference
a-vO2 max
 Muscle blood flow
 SNS vasoconstriction
Improved ability of the muscle to extract oxygen from the blood
 Capillary density
 Mitochondial number

23. Factors Causing Increased VO2 Max
VO2 Max: Cardiac Output and the Arteriovenous Difference
Factors Causing Increased VO2 Max
Figure 13.3

24. VO2 Max: Cardiac Output and the Arteriovenous Difference
In Summary
The training-induced increase in maximal stroke volume is due to both an increase in preload and a decrease in afterload a. The increased preload is primarily due to an increase in end diastolic ventricular volume and the associated increase in plasma volume. b. The decreased afterload is due to a decrease in the arteriolar constriction in the trained muscles, increasing maximal muscle blood flow with no change in the mean arterial blood pressure.

25. VO2 Max: Cardiac Output and the Arteriovenous Difference
In Summary
In young sedentary subjects, 50% of the increase in VO2 max is due to an increase in the systemic a-vO2 difference. The increased a-vO2 difference is due to an increase in the capillary density of the trained muscles that is needed to accept the increase in maximal muscle blood flow. The greater capillary density allows for a sufficiently slow red blood cell transit time through the muscle, providing enough time for oxygen diffusion, which is facilitated by the increase in the number of mitochondria.

26. Detraining and VO2 Max Decrease in VO2 max with cessation of training
 SV max
Rapid loss of plasma volume
 Maximal a-vO2 difference
 Mitochondria
 Oxidative capacity of muscle
 Type IIa fibers and  type IIx fibers
Initial decrease (12 days) due to  SV max
Later decrease due to  a-vO2 max

27. Detraining and Changes in VO2 Max and Cardiovascular Variables
Detraining and VO2 Max
Detraining and Changes in VO2 Max and Cardiovascular Variables
Figure 13.4

28. Detraining and VO2 Max
In Summary
The decrease in VO2 max with cessation of training is due to both a decrease in maximal stroke volume and a decrease in oxygen extraction, the reverse of what happens with training.

29. Effects of Endurance Training on Performance
Endurance Training: Effects on Performance and Homeostasis
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

30. Structural and Biochemical Adaptations to Endurance Training
Endurance Training: Effects on Performance and Homeostasis
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

31. Changes in Oxidative Enzymes with Training
Endurance Training: Effects on Performance and Homeostasis
Changes in Oxidative Enzymes with Training

32. Time Course of Training/Detraining Mitochondrial Changes
Endurance Training: Effects on Performance and Homeostasis
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

33. Time Course of Training/Detraining Mitochondrial Changes
Endurance Training: Effects on Performance and Homeostasis
Time Course of Training/Detraining Mitochondrial Changes
Figure 13.5

34. Endurance Training: Effects on Performance and Homeostasis
A Closer Look 13.3 Role of Exercise Intensity and Duration on Mitochondrial Adaptations
Citrate synthase (CS)
Marker of mitochondrial oxidative capacity
Effect of exercise intensity
55%, 65%, or 75% VO2 max
Increased CS in oxidative (IIa) fibers with all training intensities
Effect of exercise duration
30, 60, or 90 minutes
No difference between durations on CS activity in IIa fibers
Increase in CS activity in IIx fibers with higher-intensity, longer-duration training

35. Changes in Citrate Synthase Activity with Exercise
Endurance Training: Effects on Performance and Homeostasis
Changes in Citrate Synthase Activity with Exercise
Figure 13.6

36. Biochemical Adaptations and the Oxygen Deficit
Endurance Training: Effects on Performance and Homeostasis
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

37. Mitochondrial Number and ADP Concentration Needed to Increase VO2
Endurance Training: Effects on Performance and Homeostasis
Mitochondrial Number and ADP Concentration Needed to Increase VO2
Figure 13.7

38. Endurance Training Reduces the O2 Deficit
Endurance Training: Effects on Performance and Homeostasis
Endurance Training Reduces the O2 Deficit
Figure 13.8

39. Biochemical Adaptations and the Plasma Glucose Concentration
Endurance Training: Effects on Performance and Homeostasis
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
Increased fatty acid binding protein and fatty acid translocase
Transport of FFA from the cytoplasm to the mitochondria
Increased mitochondrial number
Higher levels of CPT I and FAT
Mitochondrial oxidation of FFA
Increased enzymes of -oxidation
Increased rate of acetyl-CoA formation
High citrate level inhibits PFK and glycolysis

40. Endurance Training: Effects on Performance and Homeostasis
Effect of Mitochondria and Capillaries on Free-Fatty Acid and Glucose Utilization
Figure 13.9

41. Endurance Training: Effects on Performance and Homeostasis
In Summary
The combination of the increase in the density of capillaries and the number of mitochondria per muscle fiber increases the capacity to transport FFA from the plasma  cytoplasm  mitochondria.
The increase in the enzymes of the fatty acid cycle increases the rate of formation of acetyl-CoA from FFA for oxidation in the Krebs cycle. This increase in fat oxidation in endurance-trained muscle spares both muscle glycogen and plasma glucose, the latter being a focal point of homeostatic regulatory mechanisms. These points are summarized in Figure 13.9.

42. 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

43. Mitochondrial and Biochemical Adaptations and Blood pH
Figure 13.10

44. Biochemical Adaptations and Lactate Removal
Biochemical Adaptations and Blood pH
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
Redistribution of blood flow to liver and kidney
Increased lactate removal

45. Redistribution of Blood Flow and Lactate Removal
Biochemical Adaptations and Blood pH
Redistribution of Blood Flow and Lactate Removal
Figure 13.13

46. Biochemical Adaptations and Blood pH
In Summary
Mitochondrial adaptations to endurance training include an increase in the enzymes involved in oxidative metabolism: Krebs cycle, fatty-acid (-oxidation) cycle, and the electron transport chain.
Those mitochondrial adaptations result in the following: a. a smaller O2 deficit due to a more rapid increase in oxygen uptake at the onset of work b. an increase in fat metabolism that spares muscle glycogen and blood glucose c. a reduction in lactate and H+ formation that helps to maintain the pH of the blood d. an increase in lactate removal

47. A Closer Look 13.4 Exercise and Resistance to Infection
J-shaped relationship between amount and intensity of exercise and risk of URTI
Marathon run alters immune system
Elevated neutrophils, reduced lymphocytes and natural killer cells
Decreases in NK and T-cell function
Decreases in nasal neutrophil activity
Decreases in nasal and salivary IgA concentrations
Increases in pro-inflammatory cytokines
“Open window” hypothesis
Immune suppression following marathon increases risk of infection

48. J-Shaped Relationship Between Exercise and URTI
Exercise and Resistance to Infection
J-Shaped Relationship Between Exercise and URTI
Figure 13.11

49. The “Open Window” Theory
Exercise and Resistance to Infection
The “Open Window” Theory
Figure 13.12

50. Links Between Muscle and Systemic Physiology
Endurance Training: Links Between Muscle and Systemic Physiology
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

51. Lack of Transfer of Training Effect
Endurance Training: Links Between Muscle and Systemic Physiology
Lack of Transfer of Training Effect
Figure 13.14

52. Peripheral and Central Control of Cardiorespiratory Responses
Endurance Training: Links Between Muscle and Systemic Physiology
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

53. Peripheral Control of Heart Rate, Ventilation, and Blood Flow
Endurance Training: Links Between Muscle and Systemic Physiology
Peripheral Control of Heart Rate, Ventilation, and Blood Flow
Figure 13.15

54. Central Control of Cardiorespiratory Responses
Endurance Training: Links Between Muscle and Systemic Physiology
Central Control of Cardiorespiratory Responses
Figure 13.16

55. Endurance Training: Links Between Muscle and Systemic Physiology
In Summary
The biochemical changes in muscle due to endurance training influence the physiological responses to exercise. The reduction in “feedback” from chemoreceptors in the trained muscle and a reduction in the need to recruit motor units to accomplish a work task results in reduced sympathetic nervous system, heart rate, and ventilation responses in submaximal exercise.

56. Physiological Effects of Strength Training
Muscular strength
Maximal force a muscle or muscle group can generate
1 repetition maximum (1-RM)
Muscular endurance
Ability to make repeated contractions against a submaximal load
Strength training
Percent gain inversely proportional to initial strength
Genetic limitation to gains in strength
High-resistance (2–10 RM) training
Gains in strength
Low-resistance training (20+ RM)
Gains in endurance

57. A Closer Look 13.5 Aging, Strength, and Training
Physiological Effects of Strength Training
A Closer Look 13.5 Aging, Strength, and Training
Decline in strength after age 50
Loss of muscle mass (sarcopenia)
Loss of both type I and II fibers
Atrophy of type II fibers
Loss of intramuscular fat and connective tissue
Loss of motor units
Reorganization of motor units
Progressive resistance training
Causes muscle hypertrophy and strength gains
Important for activities of daily living, balance, and reduced risk of falls

58. Physiological Mechanisms Causing Increased Strength
Strength training results in increased muscle size and strength
Initial 8–20 weeks
Neural adaptations
Long-term training (20+ weeks)
Muscle hypertrophy
High-intensity training can result in hypertrophy with 10 sessions

59. Neural and Muscular Adaptations to Resistance Training
Physiological Mechanisms Causing Increased Strength
Neural and Muscular Adaptations to Resistance Training
Figure 13.17

60. Neural Factors Early gains in strength Initial 8–20 weeks Adaptations
Physiological Mechanisms Causing Increased Strength
Neural Factors
Early gains in strength
Initial 8–20 weeks
Adaptations
Improved ability to recruit motor units
Learning
Coordination

61. Muscular Enlargement Hypertrophy
Physiological Mechanisms Causing Increased Strength
Muscular Enlargement
Hypertrophy
Enlargement of both type I and II fibers
Low-intensity (high RM), high-volume training results in smaller type II fibers
Heavy resistance (low RM) results in larger type II fibers
No increase in capillary density
Hyperplasia
Increase in muscle fiber number
Mainly seen in long-term strength training
Not as much evidence as muscle hypertrophy

62. The Winning Edge 13.1 Periodization of Strength Training
Physiological Mechanisms Causing Increased Strength
The Winning Edge 13.1 Periodization of Strength Training
Traditional training programs
Variations in intensity (RM), sets, and repetitions
Periodization
Also includes variation of:
Rest periods, type of exercise, number of training sessions, and training volume
Develop workouts to achieve optimal gains in:
Strength, power, motor performance, and/or hypertrophy
Linear and undulating programs
Variations in volume/intensity over time
More effective than non-periodized training for improving strength and endurance

63. Concurrent Strength and Endurance Training
Physiological Mechanisms Causing Increased Strength
Concurrent Strength and Endurance Training
Potential for interference of adaptations
Endurance training increases mitochondial protein
Strength training increases contractile protein
Depends on intensity, volume, and frequency of training
Studies show conflicting results

64. Physiological Mechanisms Causing Increased Strength
In Summary
Increases in strength due to short-term (eight to twenty weeks) training are the results of neural adaptations, while gains in strength in long-term training programs are due to an increase in the size of the muscle.
There is evidence both for and against the proposition that the physiological effects of strength training interfere with the physiological effects of endurance training.

65. Study Questions
Define the following principles of training: overload and specificity.
Give one example each of a cross-sectional study and a longitudinal study.
What are the typical VO2 max values for young men and women? Cardiac patients?
Given the formula for VO2 max using heart rate, stroke volume, and the a-vO2 difference, which variable is most important in explaining the differences in VO2 max in different populations? Give a quantitative example.
Describe how the increase in VO2 max comes about for the sedentary subject who undertakes an endurance training program.
Explain the importance of preload, afterload, and contractility in the increase of the maximal stroke volume that occurs with endurance training.

66. Study Questions
What are the most important changes in muscle structure that are responsible for the increase in the maximal a-vO2 difference that occurs with endurance training?
What causes the VO2 max to decrease following termination of an endurance training program?
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. a lower O2 deficit b. an increase utilization of FFA and sparing of blood glucose and muscle glycogen c. a reduction in lactate and H+ formation that helps to maintain the pH of the blood d. an increase in lactate removal

67. Study Questions
Define central command and peripheral feedback and explain how changes in muscle as a result of endurance training can be responsible for the lower heart rate, ventilation, and catecholamine response to a submaximal exercise bout.
In short-term training programs, what neural factors may be responsible for the increase in strength?
Contrast hyperplasia with hypertrophy, and explain the role of each in the increase in muscle size that occurs with long-term strength training.
Does strength training interfere with the physiological effects of endurance training?