Adaptations to Resistance Training

Resistance Training: IntroductionResistance Training: Introduction

• Resistance training yields substantial strength gains via neuromuscular changes

• Important for overall fitness and health

• Critical for athletic training programs

Resistance Training: Resistance Training: Gains in Muscular FitnessGains 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 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

Figure 10.1Figure 10.1aa

Mechanisms of Muscle Strength Gain:Mechanisms of Muscle Strength Gain:Neural ControlNeural 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:Mechanisms of Muscle Strength Gain:Motor Unit Recruitment 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:Mechanisms of Muscle Strength Gain:Motor Unit Recruitment 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:Mechanisms of Muscle Strength Gain:Muscle HypertrophyMuscle 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:Mechanisms of Muscle Strength Gain:Fiber HypertrophyFiber Hypertrophy

• More myofibrils

• More actin, myosin filaments

• More sarcoplasm

• More connective tissue

Mechanisms of Muscle Strength Gain:Mechanisms of Muscle Strength Gain:Fiber HyperplasiaFiber 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:Mechanisms of Muscle Strength Gain:Neural Activation + HypertrophyNeural 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

MODEL OF NEURAL AND HYPERTROPHIC FACTORS

Mechanisms of Muscle Strength Gain:Mechanisms of Muscle Strength Gain:Atrophy and InactivityAtrophy and Inactivity

• Reduction or cessation of activity major change in muscle structure and function

• Limb immobilization studies

• Detraining studies

Mechanisms of Muscle Strength Gain:Mechanisms of Muscle Strength Gain:Fiber Type AlterationsFiber 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

Muscle SorenessMuscle 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:Muscle Soreness:Acute Muscle SorenessAcute 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:Muscle Soreness:DOMSDOMS

• 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:Muscle Soreness:DOMS Structural DamageDOMS 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:Muscle Soreness:DOMS and PerformanceDOMS 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

Muscle Soreness:Muscle Soreness:DOMS and PerformanceDOMS 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:Muscle Soreness:Reducing DOMSReducing 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:Muscle Soreness:Exercise-Induced Muscle CrampsExercise-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:Muscle Soreness:Exercise-Induced Muscle CrampsExercise-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

Muscle Soreness:Muscle Soreness:Exercise-Induced Muscle CrampsExercise-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