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MECHANISM OF MUSCLE CONTRACTION

MECHANISM OF MUSCLE CONTRACTION. Ginus Partadiredja The Department of Physiology UGM, Yogyakarta. Muscle = neuron  excited chemically, electrically, mechanically to produce action potentials Muscle  neuron  contractile mechanism activated by action potentials. Skeletal muscle:

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MECHANISM OF MUSCLE CONTRACTION

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  1. MECHANISM OF MUSCLE CONTRACTION Ginus Partadiredja The Department of Physiology UGM, Yogyakarta

  2. Muscle = neuron  excited chemically, electrically, mechanically to produce action potentials • Muscle  neuron  contractile mechanism activated by action potentials

  3. Skeletal muscle: • cross-striations • does not contract without innervation • lacks anatomic & functional connections between fibers • voluntary control • Cardiac muscle: • cross-striations • functionally syncytial • contracts rhythmically in the absence of external innervation • contains pacemaker • Smooth muscle: • Lacks cross-striations • functionally syncytial • contains pacemaker

  4. Skeletal muscle  muscle fibers  myofibrils • Muscle fiber: multinucleated, long, cylindrical, single cell surrounded by sarcolemma (cell membrane)

  5. Skeletal muscle  muscle fibers  myofibrils  filaments

  6. Hexagonal pattern

  7. Filaments = contractile proteins: • Myosin II (thick filament) • Actin • Tropomyosin • Troponin: - Troponin I thin filament • - Troponin T • - Troponin C

  8. Thick filaments  A bands Thin filaments  I bands

  9. Myosin  2 globular heads & long tail • Head of myosin contains actin-binding site & catalytic site that hydrolize ATP

  10. Thin filaments  two chains of actin • Tropomyosin in the groove of actin • Troponin: T binds other troponin to tropomyosin • I inhibits the interaction of myosin & actin • C contains the binding sites for Ca+2

  11. Sarcotubular system = T system + sarcoplasmic reticulum • T system of tubules + adjacent terminal cisternae = triad • T system  rapid transmission of action potentials from the cell membrane to the fibrils

  12. The resting membrane potential of muscle = -90 mV • The action potential = 2 – 4 ms • The speed along the muscle = 5 m/s • The absolute refractory period = 1 – 3 ms • The distribution of ions  nerve cells • Depolarization = Na+ influx • Repolarization = K+ efflux • Depolarization starts at motor end plate  transmitted along the fiber  contractile response

  13. Sequence of events during transmission from the motor nerve  the muscles = transmission in synapses between neurons

  14. Sequence of Events in Contraction and Relaxation of Skeletal Muscle Steps in Contraction: 1. Discharge of motor neuron  end of motor neuron  Ca+2 enters the endings

  15. 2. Release of transmitter (acetylcholine) at motor end-plate 3. Binding of acetylcholine to nicotinic acetylcholine receptors (concentrated at the tops of the junctional folds)

  16. Junctional folds

  17. Increased Na+ and K+ conductance in end-plate membrane • Generation of end-plate potential • Generation of action potential in muscle fibers

  18. 7. Inward spread of depolarization along T tubules  excitation – contraction coupling 8. Release of Ca+2 from terminal cisterns of sarcoplasmic reticulum and diffusion to thick and thin filaments

  19. 9. Binding of Ca+2 to troponin C, uncovering myosin-binding sites on actin (at resting, troponin I is tightly bound to actin and tropomyosin covers the sites where myosin heads bind to actin) • ATP is then split  ADP + Pi  contraction

  20. 10. Formation of cross-linkages between actin and myosin and sliding of thin on thick filaments, producing movement

  21. Steps in Relaxation: • Ca+2 pumped back into sarcoplasmic reticulum  diffuses into the terminal cisterns, ready to be released by next action potential • Release of Ca+2 from troponin • Cessation of interaction between actin and myosin

  22. Muscular Contraction • The width of A bands is constant • Z lines move closer

  23. Production of ATP in Muscle Fibers (Tortora & Derrickson, 2006) • 3 ways of ATP production: • From creatine phosphate • Anaerobic cellular respiration (ATP-producing reactions not requiring oxygen) • Aerobic cellular respiration (ATP-producing reactions requiring oxygen, in mitochondria)

  24. Creatine Phosphate • Creatine: small amino acid-like molecule formed in liver, kidneys, pancreas  transported to msucles • Relaxed muscles  creatine phosphate 3-4x > ATP • Relaxation: ATP + creatine  creatine phosphate + ADP (by creatine kinase) • Contraction: creatine phosphate + ADP  ATP + creatine (by creatine kinase) • For  15 seconds contraction (100-m dash)

  25. 2. Anaerobic Cellular Respiration • Creatine phosphate is depleted then: • Glucose (from blood or from the breakdown of glycogen in muscles)  glycolysis  2 pyruvic acid + 2 ATP (produces 4 ATP but net gain of 2 ATP) • Pyruvic acid  mitochondria, aerobic respiration  ATP • No oxygen (anaerobic) in cytosol: 80% Pyruvic acid  lactic acid  blood (becomes acid)  liver  convert back into glucose • For 30 - 40 seconds activity (400-m race)

  26. 3. Aerobic Cellular Respiration • Sources of ATP: pyruvic acid, fatty acid (breakdown of triglycerides; yields > 100 ATP), amino acids (breakdown of proteins) • Sufficient oxygen: Pyruvic acid  mitochondria  oxydized  ATP + CO2 + H2O + heat • Slower than glycolysis, but yields 36 ATP • Sources of oxygen: hemoglobin & myoglobin • For > 10 minutes activity (marathon race)

  27. Energy Sources (Ganong, 2005) ATP + H2O  ADP + H3PO4 + 7.3 kcal Phosphorylcreatine + ADP ↔ Creatine + ATP Rest & light exercise: FFA  CO2 + H2O + ATP Increased intensity of exercise Glucose + 2 ATP (or glycogen + 1 ATP)  2 Lactic acid + 4 ATP (anaerobic) Glucose + 2 ATP (or glycogen + 1 ATP)  6CO2 + 6H2O + 40ATP (aerobic)

  28. 100-m dash (10 seconds)  85% of energy is derived anaerobically • 2-mile race (10 minutes)  20% of energy is derived anaerobically • long-distance race (60 minutes)  5% of energy is derived anaerobically

  29. Muscle fatigue: The inability of muscle to maintain force of contraction after prolonged activity, caused by: • Inadequate release of Ca+2 from sarcoplasmic reticulum • Depletion of creatine phosphate • ATP levels = resting levels • Insufficient oxygen • Depletion of glycogen • Buildup of lactic acid & ADP • Failure of action potentials in releasing ACh

  30. Oxygen Consumption after Exercise • Oxygen debt  added oxygen, over and above the resting oxygen consumption, taken into the body after exercise • Convert lactic acid  glycogen stores in liver (small amount) • Resynthesize creatine phosphate & ATP • Replace the oxygen removed from myoglobin • Much of lactic acid  pyruvic acid for ATP production (heart, liver, kidneys, skeletal muscles) • Better term: recovery oxygen uptake ( chemical reactions, heart & muscles still working, recovery processes)

  31. Types of Contraction Isotonic (A) and isometric (B) contraction

  32. Types of Contraction • Isometric (“same length”) contraction: Contraction occurs without an appreciable decrease in the length of the whole muscle  do not work (work = force x distance)

  33. Isotonic (“same tension”) contraction: Contraction against a constant load  do work

  34. Isotonic contraction Cause more damage

  35. Muscle twitch: brief contraction followed by relaxation of all muscle fibers in a motor unit caused by a single action potential in its motor neuron • “Fast” muscle fibers: fine movements (7.5 ms) • “Slow” muscle fibers: gross movements (100 ms)

  36. Summation of Contractions • No refractory period such as in neuronsin muscle fibers • Repeated stimulation  summation of contractions • Tetanus (tetanic contraction)  continuous contraction: • Fused (complete) tetanus • Unfused (incomplete) tetanus

  37. Types of Muscle Fibers

  38. Disorders and Abnormalities • Myasthenia gravis: skeletal muscles are weak and tire easily; caused by autoantibodies  destroying nicotinic acetylcholine receptors • Lambert-Eaton syndrome: muscle weakness; caused by antibodies against Ca+2 channels in the nerve endings • Denervation hypersensitivity • Contracture: No relaxation due to the inhibition of Ca+2 transport into the reticulum

  39. Disorders and Abnormalities • Hypotonia: decreased or lost muscle tone • Flaccid paralysis  loss of muscle tone, loss/ reduction of tendon reflexes, atrophy, degeneration of muscles (disorders of nervous system; electrolytes imbalances (Na+, Ca+2, Mg+2) • Hypertonia: increased muscle tone • Spastic paralysis  increased muscle tone, tendon reflexes, pathological reflexes (Babinski sign) • Rigidity  increased muscle tone, not reflexes (tetanus)

  40. Disorders and Abnormalities • Muscular dystrophy: progressive weakness of skeletal muscle  caused by mutations in genes for muscle proteins • Duchene’s muscular dystrophy  dystrophin protein is absent from muscle; X-linked; fatal by 30 y/o • Metabolic myopathies (e.g. McArdle’s syndrome)  mutations in genes of enzymes involved in carbohydrates, fats, and proteins, metabolism • Myotonia  muscle relaxation is prolonged after contraction; abnormal genes in chromosomes 7, 17, or 19, which produce abnormalities of Na+ or Cl- channels

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