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Chapter 10

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Chapter 10

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  1. Chapter 10 • 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. 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

  7. 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

  8. 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

  9. 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

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

  11. 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

  12. 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

  13. MODEL OF NEURAL AND HYPERTROPHIC FACTORS

  14. 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

  15. 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

  16. 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

  17. 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

  18. 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

  19. 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

  20. 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

  21. 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

  22. 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)

  23. 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

  24. Muscle Soreness:Exercise-Induced Muscle Cramps • EAMC type 1: muscle overload/fatigue • Excite muscle spindle, inhibit Golgi tendon organ  abnormal a-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

  25. 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