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Chapter 10. Adaptations to Resistance Training. Chapter 10 Overview. Resistance training: gains in muscular fitness Mechanisms of muscle strength gain Muscle soreness Resistance training for special populations. Resistance Training: Introduction.
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Chapter 10 • Adaptations to Resistance Training
Chapter 10 Overview • Resistance training: gains in muscular fitness • Mechanisms of muscle strength gain • Muscle soreness • Resistance training for special populations
Resistance Training: Introduction • Resistance training yields substantial strength gains via neuromuscular changes • Important for overall fitness and health • Critical for athletic training programs
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
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
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
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
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
Mechanisms of Muscle Strength Gain:Motor Unit Rate Coding • Limited evidence suggests rate coding increases with resistance training, especially rapid movement, ballistic-type training
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
Mechanisms of Muscle Strength Gain:Other Neural Factors • Coactivation of agonists, antagonists • Normally antagonists oppose agonist force • Reduced coactivation may strength gain • Morphology of neuromuscular junction
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
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
Mechanisms of Muscle Strength Gain:Fiber Hypertrophy • More myofibrils • More actin, myosin filaments • More sarcoplasm • More connective tissue
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
Muscle Soreness:Sequence of Events in DOMS 1. High tension in muscle structural damage to muscle, cell membrane 2. Membrane damage disturbs Ca2+ homeostasis in injured fiber • Inhibits cellular respiration • Activates enzymes that degrade Z-disks (continued)
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
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
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