C H A P T E R 3

1. C H A P T E R 3 NEUROMUSCULAR ADAPTATIONS TO RESISTANCE TRAINING

2. w Note changes in the muscle structure and in the neural mechanisms controlling the muscle that occur during resistance training. (continued) Learning Objectives w Learn the differences among the terms muscular strength, power, and endurance. w Examine how strength is gained through resistance training.

3. Learning Objectives w Learn what causes muscle soreness and how to prevent it. w Discover how to design and tailor a resistance training program to the specific needs of an individual. w Find out if there are strength training differences between women and men and between younger and older persons.

4. Defining Muscular Performance Strength—the maximal force a muscle or muscle group can generate. Power—the product of strength and the speed of movement. Muscular endurance—the capacity to sustain repeated muscle actions.

5. w The one-repetition maximum (1RM) is a functional test that is often used to measure strength; it is the maximum weight that can be lifted once. Evaluating Strength

6. Power w The functional application of strength and speed w The key component of many athletic performances. w Power = (force x distance)/time, or work/time, or force x velocity w If two individuals can lift the same amount of weight, but one can lift it faster, she is generating more power.

7. Muscular Endurance w Can be evaluated by noting the number of repetitions you can perform at a given percentage of your 1RM w Is increased through gains in muscular strength w Is increased through changes in local muscular metabolic and circulatory capacity

8. Dramatic effects of strength training Resistance training programs can produce a 25% to 100% improvement in strength within 3 to 6 months, irrespective of age or gender.

9. Results of Resistance Training on Muscle Strength in Males w Alterations of neural control of trained muscle. w Increased muscle size (hypertrophy).

10. Neural Adaptations w Synchronization and recruitment of additional motor units • Decreased neural inhibition; e.g., decreased GTO effects w Decreased co-activation of antagonist muscles w Increased rate coding (increased firing frequency of active motor units) Muscle Hypertrophy w Fiber hypertrophy w Fiber hyperplasia (??? – probably not) Mechanisms of Gains in Muscle Strength

11. Muscle Size wHypertrophy refers to increases in muscle size. wAtrophy refers to decreases in muscle size. • Although muscle strength involves more than just muscle size, in general strength is directly related to the cross-sectional area of the muscle or muscle group (specific force, e.g., kg force/cm2).

12. Muscle Size

13. A significant body of literature now shows: Resistance training can benefit almost everyone, regardless of his or her sex, age, level of athletic involvement, or sport.

14. Selecting the Appropriate Resistance Strength—few reps and high resistance (6RM) Muscular endurance—many reps and low resistance (20RM) Power—several sets of few reps and moderate resistance; emphasize speed of movement Muscle size—more than 3 sets of 6RM to 12RM loads; short rest periods

15. Muscle Hypertrophy Transient—pumping up of muscle during a single exercise bout due to “squeezing” of fluid from the blood plasma into the interstitial spaces of the muscle because of high muscle pressures. Chronic—increase of muscle size after long-term resistance training due to changes in muscle fiber number (fiber hyperplasia) or muscle fiber size (fiber hypertrophy).

16. Muscle Fiber Hypertrophy w The numbers of myofibrils and thick and thin filaments increase, so there are more cross-bridges in the cross-section of muscle, and hence, greater strength. wProtein turnover is continuous in the muscle; during hypertrophy, muscle protein synthesis increases more than proteindegradation during the post-exercise period. wTestosterone plays a role in promoting muscle growth. w Training at higher intensities, i.e., performing lower reps with higher loads, appears to cause greater fiber hypertrophy than training at lower intensities.

17. Fiber Hypertrophy A,B – Former weight lifter C,D – Distance runner E,F – Sprinter Muscle Biopsy

18. FIBER HYPERTROPHY AFTER TRAINING

19. Muscle Fiber Hyperplasia w Muscle fibers may split with intense weight training. w Each half may then increase in size. w Hyperplasia has been shown to occur in some experimental animal models; it has not been clearly demonstrated in human subjects. Quail and chicken: hanging a weight on the wing – hypertrophy of the latissimus muscles Cat: pulling a lever to obtain food (not as clear) – hypertrophy of the wrist flexor muscles

20. RESISTANCE TRAINING IN CATS

21. SPLITTING MUSCLE FIBER

22. “Double-Muscled” Animals Genetically engineered mouse that does not produce myostatin, which turns off muscle development in the fetus and inhibits muscle growth after birth.

23. “Double-Muscled” Humans? Do heavily muscled humans have the genetic mutation that suppresses myostatin production?

24. Science and Strength Training Is genetic engineering the new frontier for development of super strength? Although anabolic steroids, human growth hormone, and other pharmacological interventions are effective, altering genes may be the most dramatic intervention in the near future.

25. Science and Strength Training From Shah et. al. Amer J Physiol 279:E715,2000

26. Science and Strength Training Muscle Loading/Contraction ( immediately post exercise) PKB/Akt eIF2B regulation ? mTOR eIF4A S6K1 4E-BP1 eIF4G eIF4E eIF4E rpS6 • Translation of 5’TOP containing mRNAs?? – eIF2B-epsilon over expression

27. Science and Strength Training Fluckey JD et al.Am J Physiol Endocrinol Metab, In press, 2006.

28. Science and Strength Training

29. Science and Strength Training

30. STRENGTH CHANGES IN WOMEN Strength trained for 20 weeks; then no training for 30-32 weeks; then retrained for 6 weeks

31. CHANGES IN MAJOR FIBER TYPES

32. This study demonstrated: • Dramatic strength gains with resistance training • Relatively small losses of strength during a period of reduced training • Rapid recovery of strength with retraining • Hypertrophy of all three fiber types, but greater enlargement of fast twitch fibers

33. Effects of Muscular Inactivity w Muscular atrophy (decrease in muscle size) w Decrease in muscle protein synthesis and/or an increase in protein degradation w Rapid strength loss

34. Models of Muscular Inactivity • Human: • Casting • Bed rest • Animal • Hindlimb suspension • Casting • Denervation These models are particularly useful for studying the effects of 0 gravity (space flight) on muscles.

35. Are Muscle Fiber Type Alterations Possible? Type FTb (IIb) fibers are converted to type FTa (IIa) with resistance training. There is recent evidence that some conversion from ST to FTa may occur with a combination of resistance training and short-interval speed work..

36. Acute Muscle Soreness w Probably results froman accumulation of water (edema) or waste products in the muscles (e.g., lactic acid) w Usually disappears within minutes after exercise, with no lasting effects This may be experienced, for example, after a hard bout of uphill running, stair climbing, or other concentric exercise.

37. Delayed-Onset Muscle Soreness (DOMS) w Results primarily from eccentric contractions w Is associated with damage or injury to muscle fibers w Probably is caused by inflammation in the damaged muscles w May be due to edema (associated with the inflammation) in the muscle compartment w Is felt 12 to 48 hours after a strenuous bout of exercise, and may last up to a week First paper to use the acronym, “DOMS” - Armstrong, RB. Med Sci Sports Exerc 16: 529, 1984

38. Muscle before and immediately after running a marathon Myofibrils (sarcomeres) Disrupted sarcomeres Mitochondria

39. Muscle Fibers Immediately after a Marathon

40. Exercise-induced muscle injury Inflammation 2 days after downhill running Normal Inflamed

41. Satellite Cells Satellite cells are “adult stem cells” that are available to maintain a relatively constant nucleus to muscle mass ratio. Bischoff, The Satellite Cell, Myology, 1994

42. SATELLITE CELL RESPONSE TO INJURY

43. Armstrong’s Sequence of Events in DOMS 1. Structural damage to muscle fibers from high forces 2. Impaired calcium homeostasis resulting in necrosis 3. Inflammation: macrophage invasion of the damaged tissue 4. Accumulation of irritants that stimulate nociceptors within muscle

44. Muscle Injury and Performance w Injury causes a reduction in the force-generating capacity of muscles due to 1. physical disruption of the muscle, 2. failure in the excitation-contraction coupling process, and 3. loss of contractile protein w Maximal force-generating capacity returns after weeks w Muscle glycogen synthesis is impaired

45. Reducing Muscle Injury w Reduce eccentric component of muscle action during early training w Start training at a low intensity, increasing gradually or w Begin with a high-intensity, exhaustive bout of eccentric-action exercise to cause much soreness initially, but decrease future pain Over-the-counter anti-inflammatory drugs (e.g., aspirin) have not been shown to be effective in alleviating DOMS, although there is some disagreement on this issue.

46. Exercise-Induced Muscle Cramps wMay be due to fluid or electrolyte imbalances and/or sustained alpha-motoneuron activity from increased muscle spindle activity and/or decreased Golgi tendon organ activity. w Rest, passive stretching, and holding the muscle in the stretched position can be effective treatments w Proper conditioning, stretching, and nutrition are possible prevention strategies.

48. Prolonged nature of the strength loss 3 sets of 15 eccentric contractions done by the elbow flexors Soreness Howell et al., J Physiol 464:183, 1993

49. Crouse and co-workers

50. DECREASE IN STRENGTH AFTER INJURY