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1020 Immunology

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Kinesiology & Health Science
KINE 1020
Angelo Belcastro

Muscle Health and Fitness January 8, 14 MSK Disorders- WHO classifications • Muscle Structure/ Function • Transient and reversal decrease in muscle function. Muscle fatigue – mins/hrs • Functional/Physical Activity Limitation • Injury or damage and associated pain leading to impaired movement- days to years • Restrictions • Injury leading to chronic disability, degeneration and loss of muscle (muscles diseases) – ongoing Understanding Factors Impacting Muscle Health and Fitness I Muscle Structure/ Function: II Functional/Physical Activity III Restrictions: Chronic Muscle Fatigue Limitations: Pain/Muscle Conditions Soreness Definitions and - Muscle Diseases Characteristics: - Aging: functional -Functional limitations limitations and muscle -structural limitations loss due to sarcopenia -metabolic limitations Many causes; central and peripheral mechanisms FATIGUE • Skeletal Muscle Fatigue: a condition in which there is a loss in the capacity for developing force and/or velocity of muscle resulting from muscle activity under a demand/load which is reversible by rest • IS IT GOOD OR BAD? • Causes of fatigue (regulation vs. failure) o Prevents one from over working muscle which can lead to injury (fail-safe mechanism) o OR, it is the muscle’s inability to meet demands of the body o Calcium and /or metabolic hypothesis • Sites of fatigue (many) o Central – peripheral MSD 1 Components of Central Fatigue 1. Planning of voluntary movements (motivation) 2. Motor cortex and supraspinal outputs (afferent/efferent signals) 3. Upper motor neurons 4. Lower motor neurons • Central fatigue not a contributor when doing intensities of 30-60% because brain still sends the same pattern of mV • Rather ability to coordinate muscle movements is lost, decreasing function or force generated Components of Peripheral Fatigue (no issues in MSD I) 5. Neuromuscular junction (sends signals from alpha motor neuron , acetylcholine moves across junction to muscle fiber stimulating muscle, running along sarcolemma running down T-tubule stimulate sarcoplasmic reticulum releasing Ca) 6. Sarcolemma, T-tubule, and sarcoplasmic Reticulum (Ca hypothesis) 7. Metabolic systems (metabolic hypothesis) 8. Actin-myosin interaction Hypothesis 1. Ca hypothesis 2. Metabolic hypothesis 3. Breakdown and degradative hypothesis Peripheral Fatigue Site: Impact on Neuromuscular Junction (NMJ) • NMJ (minimal electrophysiological evidence) • No biochemical evidence that NMJ blockage is a problem Impact on Sarcolemma and T-tubule System • Sarcolemma and T-tubule • The quality if the action potentials are changed • Sarcolemma • Fatigue at the sarcolemma site is associated with a change in membrane potential o Resting membrane potential is becoming more positive; with exercise (increased excitability) altered ion movements (leaky membrane) o Due to higher positive nature, it become more excitably, and ions move more readily back and forth (potassium, calcium) • T-Tubule • Size/strength of action potential become smaller (decrease in amplitude) o Therefore electrical signals are not sufficient to activate ion channels in t-tubule system to release calcium Impact on Sarcoplasmic Reticulum (Ca movement) • Calcium release is cyclical – release and uptake • Cause for muscle relaxation • Force decreasing due to Ca going being uptaken by SR • A reduction in the amount of calcium being released from the SR due to: o Depressed Ca release channel protein (ryanodine receptor RyR)  RyR protein loses function and become less effective  Not as much Ca is coming out of SR at every action potential  Strength of action potential has also been decreased ontop of the protein being less effective  END result: less Ca being released o More Ca stuck or staying in SR o A reduction in the amount of calcium being returned (uptake) by SR calcium pump protein  The longer the Ca stays out in the proximity of actin and myosin, the longer it takes for the muscle to relax  Decreases activity of SR Ca ATPase pump (SERCA) Sequences of Changes in SR 1. Depressed Ca release from SR 2. The calcium remaining in the SR is more difficult to release – increased Ca staying in SR 3. Decrease Ca return to SR – relaxat
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