1. Adaptations to Resistance Training

2. Resistance Training: Introduction Resistance training yields substantial strength gains via neuromuscular changes Important for overall fitness and health Critical for athletic training programs

3. 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 –Learn to produce true maximal movement 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

4. Mechanisms of Muscle Strength Gain Hypertrophy versus atrophy –  Muscle size   muscle strength –  Muscle size   muscle strength –But association more complex than that Strength gains result from –  Muscle size –Altered neural control

5. Figure 10.1a

6. Figure 10.1b

7. Figure 10.1c

8. Mechanisms of Muscle Strength Gain: Neural Control Strength gain cannot occur without neural adaptations via plasticity –Strength gain can occur without hypertrophy –Property of motor system, not just muscle Motor unit recruitment, stimulation frequency, other neural factors essential

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

10. 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

11. Mechanisms of Muscle Strength Gain: Motor Unit Rate Coding Limited evidence suggests rate coding increases with resistance training, especially rapid movement, ballistic-type training

12. 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

13. 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 –Fiber hypertrophy, fiber hyperplasia, or both

14. 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

15. Mechanisms of Muscle Strength Gain: Fiber Hypertrophy More myofibrils More actin, myosin filaments More sarcoplasm More connective tissue

16. 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

17. Mechanisms of Muscle Strength Gain: Fiber Hyperplasia Humans –Most hypertrophy due to fiber hypertrophy –Fiber hyperplasia also contributes –Fiber hypertrophy versus fiber hyperplasia may depend on resistance training intensity/load –Higher intensity  (type II) fiber hypertrophy Fiber hyperplasia may only occur in certain individuals under certain conditions

18. Mechanisms of Muscle Strength Gain: Fiber Hyperplasia Can occur through fiber splitting Also occurs through satellite cells –Myogenic stem cells –Involved in skeletal muscle regeneration –Activated by stretch, injury –After activation, cells proliferate, migrate, fuse

19. MODEL OF NEURAL AND HYPERTROPHIC FACTORS

20. 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

21. 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

22. 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 –  Neuromuscular activity (Reversible) effects on types I and II fibers –Cross-sectional area  cell contents degenerate –Type I affected more than type II

23. 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

24. 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

25. 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

26. 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

27. 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

28. 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

29. 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

30. 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

31. Figure 10.10

32. 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

33. 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)

34. 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

35. 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

36. 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