1. Adaptations to Resistance Training

2. 1. If you had a choice of research project in this class what would it be and why? 2. What would you describe as resistance training?

3. 1. What is the difference between hypertrophy and atrophy? 2. Give a real life example of how each could take place.

4. 1. Find someone in the room and arm wrestle them. Come to me with the winners.

5. Make two columns on your paper. I want you to make a column with 20 vocab words from ch 9 and 10. A column with the definitions next to it. Cut them out and place them in the envelope with your name too!

6. 1. What is autogenic inhibition? What does it have to do with muscles? 2. How could this have related to arm wrestling yesterday?

7. 1. What is DOMS? When does it usually take place? What causes it?

8. 15 multiple Choice Questions 10 True/False Questions 3 Short answer Questions 2 Essay Questions with a choice between the two Answers must be on a separate sheet.

9. 1. What are two ways you can reduce DOMS? 2. How is DOMS and acute muscle soreness different?

10. 1. We are going to watch a clip about how THE ROCK got in shape. After you have watched the clip tell me if this would work for building muscle why/why not?clip

11. 1. What is the difference between hypertrophy and hyperplasia? 2. Do they both effect strength? Explain.

12. Resistance Training: Gains in Muscular Fitness After 3 to 6 months of resistance training –25 to 100% strength gain –Learn to more effectively produce force Strength gains similar as a percent of initial strength –Young men experience greatest absolute gains versus young women, older men, children –Due to incredible muscle plasticity

13. Mechanisms of Muscle Strength Gain Hypertrophy –  Muscle size   muscle strength –  Muscle size   muscle strength Strength gains result from –  Muscle size –Altered neural control Atrophy –Loss of muscle size due to inactivity

14. Figure 10.1c

15. Mechanisms of Muscle Strength Gain: Neural Control Strength gain cannot occur without neural adaptations via plasticity –Strength gain can occur without hypertrophy Motor unit recruitment, stimulation frequency, other neural factors essential

16. Mechanisms of Muscle Strength Gain: Motor Unit Recruitment Normally motor units recruited asynchronously Synchronous recruitment  strength gains –May produce more forceful contraction –Improves rate of force development –  Capability to exert steady forces Resistance training  synchronous recruitment

17. Mechanisms of Muscle Strength Gain: Motor Unit Recruitment Strength gains may also result from greater motor unit recruitment –  Neural drive during maximal contraction –  Frequency of neural discharge (rate coding) –  Inhibitory impulses Likely that some combination of improved motor unit synchronization and motor unit recruitment  strength gains

18. Mechanisms of Muscle Strength Gain: Autogenic Inhibition Normal intrinsic inhibitory mechanisms –Golgi tendon organs –Inhibit muscle contraction if tendon tension too high –Prevent damage to bones and tendons Training can  inhibitory impulses –Muscle can generate more force –May also explain superhuman feats of strength

19. Mechanisms of Muscle Strength Gain: Muscle Hypertrophy Hypertrophy: increase in muscle size Transient hypertrophy (after exercise bout) –Due to edema formation from plasma fluid –Disappears within hours Chronic hypertrophy (long term) –Reflects actual structural change in muscle

20. Mechanisms of Muscle Strength Gain: Chronic Muscle Hypertrophy Maximized by –High-velocity eccentric training –Disrupts sarcomere Z-lines (protein remodeling) Concentric training may limit muscle hypertrophy, strength gains More myofibrils More actin, myosin filaments More sarcoplasm More connective tissue

21. Mechanisms of Muscle Strength Gain: Fiber Hypertrophy Resistance training   protein synthesis –Muscle protein content always changing –During exercise: synthesis , degradation  –After exercise: synthesis , degradation  Testosterone facilitates fiber hypertrophy –Natural anabolic steroid hormone –Synthetic anabolic steroids  large increases in muscle mass

22. Mechanisms of Muscle Strength Gain: Fiber Hyperplasia Cats –Intense strength training  fiber splitting –Each half grows to size of parent fiber Chickens, mice, rats –Intense strength training  only fiber hypertrophy –But difference may be due to training regimen

23. Figure 10.3

24. Figure 10.4

25. Figure 10.5

26. Mechanisms of Muscle Strength Gain: Neural Activation + Hypertrophy Short-term  in muscle strength –Substantial  in 1RM –Due to  voluntary neural activation –Neural factors critical in first 8 to 10 weeks Long-term  in muscle strength –Associated with significant fiber hypertrophy –Net  protein synthesis takes time to occur –Hypertrophy major factor after first 10 weeks

27. Mechanisms of Muscle Strength Gain: Atrophy and Inactivity Reduction or cessation of activity  major change in muscle structure and function Limb immobilization studies Detraining studies

28. Mechanisms of Muscle Strength Gain: Immobilization Major changes after 6 h –Lack of muscle use  reduced rate of protein synthesis –Initiates process of muscle atrophy First week: strength loss of 3 to 4% per day –  Size/atrophy (Reversible) effects on types I and II fibers –Type I affected more than type II

29. Mechanisms of Muscle Strength Gain: Detraining Leads to  in 1RM –Strength losses can be regained (~6 weeks) –New 1RM matches or exceeds old 1RM Once training goal met, maintenance resistance program prevents detraining –Maintain strength and 1RM –Reduce training frequency

30. Figure 10.6a

31. Mechanisms of Muscle Strength Gain: Fiber Type Alterations Training regimen may not outright change fiber type, but –Type II fibers become more oxidative with aerobic training –Type I fibers become more anaerobic with anaerobic training Fiber type conversion possible under certain conditions –Cross-innervation –Chronic low-frequency stimulation –High-intensity treadmill or resistance training

32. Mechanisms of Muscle Strength Gain: Fiber Type Alterations Type IIx  type IIa transition common 20 weeks of heavy resistance training program showed –Static strength, cross-sectional area  –Percent type IIx , percent type IIa  Other studies show type I  type IIa with high-intensity resistance work + short- interval speed work

33. Muscle Soreness From exhaustive or high-intensity exercise, especially the first time performing a new exercise Can be felt anytime –Acute soreness during, immediately after exercise –Delayed-onset soreness one to two days later

34. Muscle Soreness: Acute Muscle Soreness During, immediately after exercise bout –Accumulation of metabolic by-products (H + ) –Tissue edema (plasma fluid into interstitial space) –Edema  acute muscle swelling Disappears within minutes to hours

35. Muscle Soreness: DOMS DOMS: delayed-onset muscle soreness –1 to 2 days after exercise bout –Type 1 muscle strain –Ranges from stiffness to severe, restrictive pain Major cause: eccentric contractions –Example: Level run pain < downhill run pain –Not caused by  blood lactate concentrations

36. Muscle Soreness: DOMS Structural Damage Indicated by muscle enzymes in blood –Suggests structural damage to muscle membrane –Concentrations  2 to 10 times after heavy training –Index of degree of muscle breakdown Onset of muscle soreness parallels onset of  muscle enzymes in blood

37. Muscle Soreness: DOMS Structural Damage Sarcomere Z-disks: anchoring points of contact for contractile proteins –Transmit force when muscle fibers contract –Z-disk, myofilament damage after eccentric work Physical muscle damage  DOMS pain –Fiber damage and blood enzyme changes may occur without causing pain –Muscle damage also precipitates muscle hypertrophy

38. Figure 10.8

39. Figure 10.9a

40. Figure 10.9b

41. Muscle Soreness: DOMS and Inflammation White blood cells defend body against foreign materials and pathogens –White blood cell count  as soreness  –Connection between inflammation and soreness? Muscle damage  inflammation  pain –Damaged muscle cells attract neutrophils –Neutrophils release attractant chemicals, radicals –Released substances stimulate pain nerves –Macrophages remove cell debris

42. Muscle Soreness: Sequence of Events in DOMS 1. High tension in muscle  structural damage to muscle, cell membrane 2. Membrane damage disturbs Ca 2+ homeostasis in injured fiber –Inhibits cellular respiration –Activates enzymes that degrade Z-disks (continued)

43. Muscle Soreness: Sequence of Events in DOMS (continued) 3. After few hours, circulating neutrophils  4. Products of macrophage activity, intracellular contents accumulate –Histamine, kinins, K + –Stimulate pain in free nerve endings –Worse with eccentric exercise

44. Muscle Soreness: Sequence of Events in DOMS Damage to muscle fiber, plasmalemma sets up chain of events –Release of intracellular proteins –Increase in muscle protein turnover Damage and repair processes involve buildup of intra- and extracellular molecules Precise causes of skeletal muscle damage and repair still poorly understood

45. Muscle Soreness: DOMS and Performance DOMS   muscle force generation Loss of strength from three factors –Physical disruption of muscle (see figures 10.8, 10.9) –Failure in excitation-contraction coupling (appears to be most important) –Loss of contractile protein

46. Figure 10.10

47. Muscle Soreness: DOMS and Performance Muscle damage   glycogen resynthesis Slows/stops as muscle repairs itself Limits fuel-storage capacity of muscle Other long-term effects of DOMS: weakness, ultrastructural damage, 3-ME excretion

48. Figure 10.11

49. Muscle Soreness: Reducing DOMS Must reduce DOMS for effective training Three strategies to reduce DOMS –Minimize eccentric work early in training –Start with low intensity and gradually increase –Or start with high-intensity, exhaustive training (soreness bad at first, much less later on)

50. Muscle Soreness: Exercise-Induced Muscle Cramps Frustrating to athletes –Occur even in highly fit athletes –Occur during competition, after, or at rest Frustrating to researchers –Multiple unknown causes –Little information on treatment and prevention EAMCs versus nocturnal cramps

51. Muscle Soreness: Exercise-Induced Muscle Cramps EAMC type 1: muscle overload/fatigue –Excite muscle spindle, inhibit Golgi tendon organ  abnormal  -motor neuron control –Localized to overworked muscle –Risks: age, poor stretching, history, high intensity EAMC type 2: electrolyte deficits –Excessive sweating  Na +, Cl - disturbances –To account for ion loss, fluid shifts –Neuromuscular junction becomes hyperexcitable

52. Muscle Soreness: Exercise-Induced Muscle Cramps Treatment depends on type of cramp Fatigue-related cramps –Rest –Passive stretching Electrolyte-related (heat) cramps –Prompt ingestion of high-salt solution, fluids –Massage –Ice

53. Resistance Training for Special Populations: Women Have same ability to develop strength Women’s peak 1RM < men’s peak 1RM Differences due to muscle size, hormones Same techniques appropriate for both sexes

54. Resistance Training for Special Populations: Age Children and adolescents –Myth: resistance training unsafe due to growth plate, hormonal changes –Truth: safe with proper safeguards –Children can gain both strength and muscle mass Elderly –Helps restore age-related loss of muscle mass –Improves quality of life and health –Helps prevent falls

55. Resistance Training for Sport Training beyond basic strength, power, and endurance needs of the sport not worth it Training costs valuable time Training results should be tested with sport- specific performance metric