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Chapter 13 The Physiology of Training: Effect on VO 2 max, Performance, Homeostasis, and Strength

Chapter 13 The Physiology of Training: Effect on VO 2 max, Performance, Homeostasis, and Strength. EXERCISE PHYSIOLOGY Theory and Application to Fitness and Performance, 6th edition Scott K. Powers & Edward T. Howley. Presentation revised and updated by Brian B. Parr, Ph.D.

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Chapter 13 The Physiology of Training: Effect on VO 2 max, Performance, Homeostasis, and Strength

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  1. Chapter 13The 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 Presentation revised and updated by Brian B. Parr, Ph.D. University of South Carolina Aiken © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  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. • 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. © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  3. Objectives • 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. • 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 lower O2 deficit, an 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. © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  4. Objectives • 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. © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  5. Exercise: A Challenge to Homeostasis Figure 13.1 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  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: • 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  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 • 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  9. Range of VO2max Values in the Population Table 13.1 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  10. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  11. © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  12. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  13. Factors Increasing Stroke Volume Figure 13.2 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  14. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  15. Factors Causing Increased VO2max Figure 13.3 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  16. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  17. Detraining and Changes in VO2max and Cardiovascular Variables Figure 13.4 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  18. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  19. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  20. Changes in Oxidative Enzymes With Training Table 13.4 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  21. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  22. Time Course of Training/Detraining Mitochondrial Changes Figure 13.5 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  23. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  24. Changes in Citrate Synthase Activity With Exercise Figure 13.6 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  25. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  26. Mitochondrial Number and ADP Concentration Needed to Increase VO2 Figure 13.7 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  27. Endurance Training Reduces the O2 Deficit Figure 13.8 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  28. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  29. Effect of Mitochondria and Capillaries on Free-Fatty Acid and Glucose Utilization Figure 13.9 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  30. LDH pyruvate + NADH lactate + NAD 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 M4 M3H  M2H2  MH3  H4 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  31. Mitochondrial and Biochemical Adaptations and Blood pH Figure 13.10 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  32. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  33. Biochemical Adaptations and Lactate Removal Figure 13.12 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  34. J-Shaped Relationship Between Exercise and URTI Figure 13.11 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  35. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  36. Lack of Transfer of Training Effect Figure 13.13 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  37. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  38. Peripheral Control of Heart Rate, Ventilation, and Blood Flow Figure 13.14 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  39. Central Control of Cardiorespiratory Responses Figure 13.15 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  40. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  41. Neural and Muscular Adaptations to Resistance Training Figure 13.16 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

  42. 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 © 2007 McGraw-Hill Higher Education. All Rights Reserved.

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