Muscular Strength: Training Muscles to Become Stronger

Learning outcomes Explain the physiological mechanisms of muscle strength gain Describe the physiological processes involved in delayed onset muscle soreness and strategies to avoid the occurrence of DOMS Discuss resistance training principles 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

Assessing Muscular Strength Cable tensiometry Dynamometry One-repetition maximum (1-RM) Computer-assisted, electromechanical, and isokinetic methods Isokinetic dynamometer Resistance-training equipment categories

Assessment Considerations Standardize pretesting instructions Uniformity of warm-up Adequate practice Standardize testing protocol Body position Joint angles Reps Scoring criteria Score relative to body size

Sex Differences in Muscular Strength Similar ability to develop strength Women’s peak 1RM < men’s peak 1RM Absolute muscle strength Males 30% higher on lower-body, 50% higher on upper-body lifts Differences due to muscle size, hormones Same techniques appropriate for both sexes

Sex Differences in Muscular Strength Relative Strength Differences

Types of Contractions Static muscle contraction Isometric Dynamic muscle action Concentric action Muscle shortens Eccentric action Muscle lengthens

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

Figure 10.4

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

Figure 10.5

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

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)