Presentation on theme: "Physiological Aspects of Human Performance. Adaptation refers to how the body adjusts to repeated (chronic) stress. Disinhibition: reducing the inhibition."— Presentation transcript:
Adaptation refers to how the body adjusts to repeated (chronic) stress. Disinhibition: reducing the inhibition of muscle action by reflex protective mechanisms. Size Principle: motor neurons with low threshold, slow twitch velocity, and small diameter are recruited first, with progressively larger and higher threshold neuron recruitment as more force is required. Synchronization: simultaneously recruiting motor units.
Effects of Resistance Training On the Neuromuscular Systems NeuralMuscularOn Other SystemsSkeletalCardiovascular
Neural Control Biochemical Muscle Cells Capillary Supply Muscle Hypertrophy Fiber Hypertrophy versus Fiber Hyperplasia Muscle Atrophy Fiber Type Alteration
Initial increase in expression of strength due to improved neural control of muscle contraction.
Increased neural activation of the muscle by recruiting more motor units and/or activating higher threshold motor units first to enhance the rate of force development (alter the Size Principle). More efficient recruitment pattern. Improved synchronization of motor units. Neural reflex facilitation and reduced autogenic inhibition of motor neurons (inhibit GTOs).
Equivocal increases in concentration of muscle creatine, phosphocreatine, ATP, and glycogen. Enzyme activity of ATP-PC (creatine phospho-kinase, myokinase) increased with isokinetic training. Little or no change in activity of ATP-PC enzymes with resistance training. Increase or no change in glycolytic enzyme activities by resistance training. Small but significant increases in aerobic enzyme activities in high volume-short rest.
Myoglobin content in muscles following strength training may decrease. Mitochondrial density has been shown to decrease with resistance training because of dilution effects of muscle fiber hypertrophy.
Increase number of capillaries in a muscle helps support metabolism and contributes to total muscle size. Improved capillarization has been observed with resistance training by body builders but decreased in power and weight lifters. Increase of capillaries linked to intensity and volume of resistance training. Time course of changes in capillary density slow (more than 12 weeks).
Muscle enlargement is generally paralleled by increased muscle strength. Increased muscle strength is NOT always paralleled by gains in muscle size. Increase in fiber area of both ST and FT muscle fibers. FT fiber area appears to increase to greater extent than ST fiber area.
Increased size of individual fibers due to: * more myofibrils * new actin & myosin myofilaments added to periphery of myofibrils * more sarcoplasm * more connective tissue surrounding fiber Increased number of individual fibers * muscle fibers split longitudinally * observed in animals with intense training * cross-sectional studies in humans
Neither speed (anaerobic) nor endurance (aerobic) training could alter basic fiber type in early studies Only motor neuron cross innervation could alter fiber types Specific training improves specific (O or G) metabolic capacities
Supporting ligaments, tendons and fascia strengthen as muscle strength increases. Connective tissue proliferates around individual muscle fibers, this thickens and strengthens muscle’s connective tissue harness. Bone mineral content increases more slowly, over 6- to 12-month period.
Immobility causes decrease in muscle size (use it or lose it) Atrophy primarily affects ST muscle fiber types
Cardiovascular System Heart RateBlood PressureCentral EffectsSerum Lipids
Short-term resistive training studies show no change or small insignificant changes of about 5 to 12% in resting Heart Rate. Changes attributed to decreased sympathetic and increased parasympathetic drive to heart.
Training effects of regular resistive training on resting blood pressure are inconsistent. Some short-term studies have shown increases in SBP as a result of high- intensity training. Most studies of resistive training show either no difference or decreases in systolic or diastolic blood pressures.
Chronic resistance training alters cardiac dimensions: concentric hypertrophy. Increased posterior left ventricular and intraventricular septum wall thickness. Little or no change in left ventricle chamber.
Left ventricular concentric hypertrophy resulting from resistive training can be accompanied by strengthened myocardium and increased stroke volume at rest and during exercise. Stroke volume is not significantly increased when it is related to body surface area or lean body mass.
The effect of resistance training on the lipid profile are inconsistent. Short-term training studies are also inconclusive. Both positive effects and no effect have been shown in serum lipids as a result of resistive training. Volume of training appears to be a primary factor affecting serum lipids.
Acute muscular soreness occurs during and immediately following the exercise period. Muscular contraction causes ischemia. Because of ischemia, metabolic waste products accumulate and stimulate pain. Delayed onset muscular soreness in days following strenuous unaccustomed physical activity. Intensity of muscle discomfort increases in hours after activity, reaching a peak 24-48 hours. Generally resolved within a week.
Greater soreness results from exercise involving repeated strain during active lengthening than concentric and isometric actions. Cell damage markers: Calcium leaks from SR into cell Serum levels creatine kinase and myoglobin.
Excessive mechanical forces disrupt structural components in muscle fibers, connective tissue, extrasarcoplasmic cytoskeleton, and sarcolemma. Tissue injury initiates inflammatory reaction in damaged muscle. Elements of inflammatory process include increased blood flow and tissue permeability.
Physiological purpose of inflammatory process is to rid cells of damaged tissue & prepare the tissue for repair. Edema and chemical substances (PGE 2 ) stimulate muscle afferents & increase sensitivity of pain receptors. Inflammatory reaction causes secondary chemical reaction through formation of oxygen radicals, proteases, and phospholipids and nitric oxide. This is initiated early in the injury process, but full manifestation is 1-3 days following stress begin DOMS.
Inflammation is followed by healing phase and formation of protective proteins. There are increases in growth factors, collagen, and fibronectin fragments, enzyme inhibitors, oxygen scavengers, and remodeling collagenase. This process heals the tissue and prevents further incidence of DOMS during subsequent exercise sessions.
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