Adaptations to Resistance Training

1. Adaptations to Resistance Training Physiological Aspects of Human Performance

2. Terminology • 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.

3. Effects of Resistance Training

4. Effects onNeuromuscular Systems • Fiber Hypertrophy versus Fiber Hyperplasia • Muscle Atrophy • Fiber Type Alteration • Neural Control • Biochemical • Muscle Cells • Capillary Supply • Muscle Hypertrophy

5. Neural Control • Initial increase in expression of strength due to improved neural control of muscle contraction.

6. Neural Control • 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).

7. Biochemical Changes • Equivocal increases in concentration of muscle creatine, phosphocreatine, ATP, and glycogen. • Enzyme activity of ATP-PC (creatinephospho-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.

8. Muscle Cells • 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.

9. Capillary Supply • 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).

10. Muscle Hypertrophy • Transient hypertrophy: tissue edema • Chronic hypertrophy: structural changes

11. Muscle Hypertrophy • 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.

12. Fiber Hypertrophy versusFiber Hyperplasia Increased number of individual fibers • muscle fibers split longitudinally • observed in animals with intense training • cross-sectional studies in humans 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

13. Fiber Type Alteration • 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

14. Connective Tissue and Bone • 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.

15. Muscle Atrophy • Immobility causes decrease in muscle size (use it or lose it) • Atrophy primarily affects ST muscle fiber types

16. Effect on Cardiovascular System

17. Resting Heart Rate • Short-term resistive training studies show no change or smallinsignificantchanges of about 5 to 12% in resting Heart Rate. • Changes attributed to decreased sympathetic and increased parasympathetic drive to heart.

18. Resting Blood Pressure • 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.

19. Central Effects • 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.

20. Central Effects • 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.

21. Serum Lipids • 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.

22. Muscular Soreness 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. 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.

23. Muscle Soreness • 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 creatinekinase and myoglobin.

24. Muscular Soreness

25. Muscle Soreness • 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.

26. Muscle Soreness • Physiological purpose of inflammatory process is to rid cells of damaged tissue & prepare the tissue for repair. • Edema and chemical substances (PGE2) 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.

27. Muscle Soreness • 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.

28. Illustration References • McArdle, William D., Frank I. Katch, and Victor L. Katch. 2000. Essentials of Exercise Physiology 2nd ed. Image Collection. Lippincott Williams & Wilkins. • Plowman, Sharon A. and Denise L. Smith. 1998. Digital Image Archive for Exercise Physiology. Allyn & Bacon.