1. Aerobic Conditioning u Muscle Adaptations

2. Key Points u 1. Muscle adapts to become a more effective energy provider. u An improved capacity for oxygen extraction from the blood supply. u An altered cellular control of energy metabolism.

3. Key Points u Improvements in maximal cardiac output and other adaptations not related to biochemical changes in the muscles.

4. Key Points u 2. Training adaptations are induced specifically in the muscles actively used in the exercise. u These adaptations are sustained by continued activity and lost following inactivity.

5. Key Points u Intensity and duration are important factors influencing muscle adaptations.

6. Key Points u 3. Muscle adaptations enhances performance in competitive sport. u Adaptations developed in non-athletic populations by routine activity are important in promoting healthier living.

7. Aerobic Conditioning u The ability to sustain an exercise task such as running or cycling requires that the energy utilization within the active muscle (i.e., the rate of ATP breakdown) is fully matched by energy supply processes (i.e., ATP resynthesis).

8. Aerobic Conditioning u If the energy demand is not met, muscle fatigue ensues.

9. Aerobic Conditioning u Extended duration activity is driven by aerobic metabolism, i.e., the consumption of oxygen to drive the oxidation of CHO and fatty acids.

10. Aerobic Conditioning u The mitochondria within the muscle fibers respond to chemical signals produced during the contractions by using the energy derived through oxygen consumption to resynthesize ATP from ADP + P (the products of ATP breakdown).

11. Aerobic Conditioning u This process requires a sufficient delivery of oxygen to the active muscle fibers and an adequate fuel supply within the cell to support oxygen consumption.

12. Aerobic Conditioning u These fuels include CHO and fatty acids supplied from within the cell or from the circulation.

13. Aerobic Conditioning u Oxygen must be derived from an adequate blood flow and must defuse from the red blood cells in the capillaries to the mitochondria in the muscle fibers.

14. Aerobic Conditioning u Thus, disruption in energy provision could occur if fuel supplies within the muscle fibers are exhausted and/or if the circulation does not provide an adequate supply of fuels or oxygen.

15. Aerobic Conditioning u Participation in endurance types of exercise training causes muscular adaptations that influence these processes controlling energy provision.

16. Aerobic Conditioning u Such training adaptations serve to redesign muscle and lead to an improved capacity for oxygen exchange between capillary and tissue, and to an improved control of metabolism within the muscle fibers.

17. Aerobic Conditioning u Both factors provide a better foundation for improved physical performance.

18. Muscle Design Muscle Fiber Type: u Type I = SLO u Type IIa = FTO u Type IIb = FTG

19. Classification of Muscle Fibers u Characteristic Type IType II a TypeII b u Oxidative capacity HighMod. HighLow u Glycolytic capacity LowHighHighest u Contractile speed SlowFastFast u Fatigue resistant HighModerateLow u Motor unit strength LowHighHigh

20. Characteristics of Muscle Fiber Types  CharacteristicST FT a FT b u Fibers per motor neuron10-180 300-800300-800 u Motor neuron sizeSmall LargeLarge u Nerve conduction velocitySlow FastFast u Contraction speed (ms)110 5050 u Type of myosin ATPaseSlow FastFast u Sarcoplasmic Ret. Dev.Low HighHigh

21. Muscle Fibers u While there are meaningful adaptations in skeletal muscle fibers induced by exercise training, training does not seem to cause marked shifts between slow and fast fiber type distributions.

22. Muscle Fibers u Thus the very high proportion of type I fibers (e.g., 70-90%) observed in the muscles of elite endurance athletes is probably a genetic endowment rather than an adaptation to training.

23. Mitochondria u One fundamental biochemical adaptation induced by exercise is an increase in the mitochondrial content throughout the trained muscle fibers.

24. Mitochondria u This greater mitochondrial content increases the capacity for aerobic energy provision from both fatty acid and CHO oxidation and can be found in both slow and fast twitch fibers when they are prompted to adapt by the exercise program.

25. Mitochondria u It is also likely that the increase in mitochondrial content improves the control of energy metabolism, influences the muscle fibers to oxidize more fatty acids and less glycogen, and improves muscle performance.

26. Muscle Capillary Density u Exercise training increases the number of capillaries surrounding individual muscle fibers.

27. Muscle Capillary Density Increased capillary density improves the O 2 exchange between capillary and fiber by: u presenting a greater surface area for the diffusion of oxygen, u by shortening the average distance required for oxygen to diffuse into the muscle, u and/or by increasing the length of time for diffusion to occur.

28. Muscle Capillary Density u Increased capillary density contributes to the increased O 2 extraction. u This accounts, in part, for the increase in VO 2max that is observed in endurance trained individuals.

29. Blood Flow Capacity u The blood flow capacity of normal skeletal muscle is exceptionally high. u Cardiac output could not increase sufficiently to perfuse all the blood vessels in our muscle mass, if they were to maximally dilate.

30. Blood Flow Capacity u Even during intense exercise requiring VO 2max, this limitation of cardiac output means that only a fraction of an individual’s entire muscle mass can be active, and then it functions only at a fraction of its blood flow capacity.

31. Blood Flow Capacity u Nevertheless, there is evidence that the peak flow capacity of muscle is increased by endurance training, but the value of this adaptation in muscles in unclear.

32. Blood Flow Capacity Important adaptations to training: u Optimal utilization of the flow delivered to the muscle. u Exchange of nutrients between capillaries and fibers.

33. Blood Flow Capacity u This places importance on the vasomotor control of the arterial supply/resistance vessels and on diffusion exchange properties of vessels surrounding the muscle fibers.

34. Metabolism u The increase in mitochondrial content of trained muscles should have a number of metabolic effects that serve to improve performance, at least during prolonged exercise.

35. Metabolism u First, the increase in mitochondria should make it possible for a greater rate of fatty acid oxidation after training, even when the circulating fatty acid concentration available to the muscle is not elevated.

36. Metabolism u Second, an increase in mitochondrial content of a muscle fiber alters the biochemical signals controlling energy metabolism during submaximal exercise.

37. Metabolism u In effect, when compared to the untrained state, the signals within trained muscle fibers that accelerate metabolism during exercise are attenuated, thereby reducing the rate of CHO breakdown and probably contributing to the sparing of muscle glycogen observed in trained subjects.

38. Metabolism u Thus, the biochemical adaptations in muscle help provide the foundation for metabolic changes favorable to endurance performance in trained subjects.

39. Training Stimulus u At present, the underlying mechanisms responsible for inducing the training adaptations in muscle are not known.

40. Training Stimulus u However, it is clear that the muscles must be recruited during the exercise task in order to adapt to the training program.

41. Training Stimulus u Those muscles (or fibers within a muscle) not involved in the exercise task do not adapt.

42. Training Stimulus u Thus, the critical stimulus for adaptation is something very specific to the active fibers and not likely to be some generalized factor circulating in the blood that influences all muscles.

43. Training Stimulus u Further, for a given exercise program, training must be performed for a sufficient duration of days or weeks to allow the muscle-specific biochemical adaptations to reach steady-state.

44. Training Stimulus u For example, muscle mitochondrial content appears to reach a steady-state after approximately 4-5 weeks of training.

45. Training Stimulus u The magnitude of the training-induced increase in mitochondrial content is also influenced by the duration of the daily exercise bout.

46. Training Stimulus u Longer exercise bouts generally produce greater increases in mitochondrial content.

47. Training Stimulus u Further, exercise intensity interacts with the duration of the exercise bout to make the initial minutes of exercise even more effective in establishing a stimulus for adaptation.

48. Training Stimulus u The peak adaptation in mitochondrial content seems to occur with shorter durations of exercise as the intensity of each training bout is increased.

49. Training Stimulus u The benefit of very prolonged training sessions in enhancing performance may be related to adaptations in cardiovascular function, fluid balance, substrate availability, or other factors not directly related to muscle-specific adaptations.

50. Training Stimulus u At least part of the beneficial effect of increasing exercise intensity on training-induced adaptations in muscles can be attributed to the effect of intensity on muscle recruitment.

51. Training Stimulus u Once peak performance (e.g., force development and/or power output) is obtained from an involved set of muscle fibers, a greater power output is achieved by recruitment of additional muscle fibers.

52. Training Stimulus u This is illustrated by the marked adaptation that becomes apparent in the low-oxidative fibers as they are recruited to meet the demands of the more intense exercise task.

53. Short-term Training u Not all of the improvement in exercise performance that accompanies training can be accounted for by long-term biochemical adaptations.

54. Short-term Training u For example, even within days of beginning an exercise program, there is evidence for an improvement in the performance of muscle and in metabolism.

55. Short-term Training u The brief training time causes an initial shift in neuromuscular and/or cardiovascular control that improves muscle fiber utilization, metabolism, and blood flow distribution.

56. Short-term Training u This is an example of the complexity of changes and the variety of training durations required to achieve particular adaptations that occur in the transition from a relatively inactive condition to an optimally trained state.

57. Short-term Training u All the improvement in exercise performance after training cannot be attributed solely to the muscle adaptations developed in this summary.

58. Short-term Training u Other changes (e.g., neuromuscular, cardiovascular, and endocrine) can be instrumental in contributing to enhanced exercise performance after training for many weeks or months.

59. Detraining u Just as meaningful adaptations are induced by physical activity, they are gradually lost in persons who become inactive.

60. Detraining u The extent and time course of regression are not known for many variables and are likely related to the exact process under consideration.

61. Detraining u For example, roughly 50% of the increased muscle mitochondrial content induced by training can be lost within 1 week of detraining.

62. Detraining u A return to training will recover the muscle adaptations; however, the time required to reestablish the steady-state trained condition can take longer than the detraining interval.

63. Summary u While the adaptations to an endurance type of training are very complex and multifaceted, change within the active muscles are probably fundamental to the metabolic and functional alterations that support the enhanced endurance performance observed after training.

64. Summary u The adaptations that involve remodeling of the muscle (e.g., enhanced mitochondrial content and increased capillary density) are influenced by the duration and intensity of daily exercise, require an extended training period to achieve a steady-state adaptations, and are lost with inactivity.