CHAPTER 10 Adaptations to Resistance Training Resistance Training

CHAPTER 10 Adaptations to Resistance Training

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 – But association more complex than that • Strength gains result from – Muscle size – Altered neural control

Figure 10. 1 a

Figure 10. 1 b

Figure 10. 1 c

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: 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 • 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

MODEL OF NEURAL AND HYPERTROPHIC FACTORS

Mechanisms of Muscle Strength Gain: Neural Activation + Hypertrophy • Short-term in muscle strength – Substantial in 1 RM – 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 1 RM – Strength losses can be regained (~6 weeks) – New 1 RM matches or exceeds old 1 RM • Once training goal met, maintenance resistance program prevents detraining – Maintain strength and 1 RM – 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 IIa with high-intensity resistance work + shortinterval 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 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

Figure 10. 10

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

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)

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

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

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