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Lec26

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Transcript

  • 1. Excitation contraction coupling
    Transmission of action potential along transverse tubules (T tubules)
    T tubules action potentials caused release of Ca ions inside the muscle fiber.
    Ca ions caused contraction
    Overall process called Excitation Contraction Coupling
  • 2. Neuromuscular transmission
    Action Potential through motor nerve fiber
    Axon Terminal
    Opening of Voltage gated Calcium channels

    Entry of Calcium ions from Extracellular fluid

    Opening of vesicles & release of Ach
    • The function of neuromuscular junction is to transmit the impulses from the nerve to the muscle.
    • 3. When the impulses are transmitted from nerve to the muscle, a series of events occur in the neuromuscular junction:
    Release of acetylcholine
    Action of acetylcholine
    Binding with receptors
    Miniature end plate potential
    Destruction of acetylcholine
    Synaptic cleft
    Passage of Ach
    Postsynaptic membrane
    Binding of Ach with Receptor and formation of
    Ach-Receptor complex

    Opening of the ligand gated sodium channels
    & entry of sodium ions from ECF

    Development of end plate potential
    Muscle Fiber
    Generation of Action Potential

    Excitation contracting coupling

    Muscular contraction
  • 4. Exciting Contraction Coupling
  • 5.
  • 6. Neuromuscular Transmission
    Nerve impulse reaches end of axon
    Ca channels open
    Release of Ach into synaptic cleft
    Diffusion of Ach across the cleft
    Attachment of Ach to ach receptors on sarcolemma
    Opening of Na channels which initiates depolarization of sarcolemma
    Development of end plate potential
    Generation of action potential
    The action potential causes the release of Ca ion from the terminal cisternae
    Muscular contraction
  • 7. Generation of Action potential
    Resting sarcolemma is polarized
    Outside the cell is positive (predominant extracellular ion is Na)
    Inside the cell is negative (predominant intracellular ion is K)
  • 8. Stimulation Ach binding to Ach receptors on sarcolemma
    Ion gates open (Na rushes into cell and K rushes out of cell
    Cells interior becomes less negative
    Depolarization
    Generation of Action potential
  • 9. Depolarization
    Loss of state of polarity
    Loss of negative membrane potentials
    Nerve stimulus is strong enough
    Action potential is generated from neuromuscular junction across the sarcolemma in all directions
    Action potential separates over cell surface
    Generation of Action potential
  • 10. Generation of Action Potential
  • 11. Generation of Action Potential
  • 12. Sliding Filament
    Explains the relationship between thick and thin filaments as contraction proceeds
    The influx of Ca ion, triggering the exposure of binding sites on actin
    The Action potential brings about the release of Ca ion from the terminal cisternae
    Ca ion binds to the troponin, causing change in conformation of the troponin tropomyosin complex
    This conformation changes exposes the binding site on actin
  • 13. Sliding Filament
    The binding of myosin to actin
    Myosin head bind to actin site and forming cross bridge
    Movement of thin filament
    Release of ADP and Pi
    The myosin cross bridge pulls the thin filament inward toward the centre of sarcomere
  • 14. Sliding Filament
    Disconnecting Myocin head from Actin
    ATP binds to the myosin head disconnecting from actin
    Repositioning of the myosin head
    The release of myosin head trigger the hydrolysis of ATP molecule into ADP and Pi
    Energy is transferred from ATP to the myosin head
    Removal of Ca ion
    Ca ion transported back into the sarcoplasmic reticulum
    Troponin - tropomyosin complex covers the binding sites on Actin
  • 15. Sliding-Filament Mechanism
  • 16. Sliding-Filament Mechanism
  • 17. CONTRACTION
    ISOTONIC CONTRACTIONS CAUSES
    THE MUSCLE LENGTH TO CHANGE AND THE LOAD TO MOVE
    USED IN
    WALKING
    MOVING ANY PART OF THE BODY
  • 18. CONTRACTIONS
  • 19. CONTRACTIONS
    ISOMETRIC CONTRACTIONS
    TENSION BUILDS TO THE MUSCLE’S
    CAPACITY, BUT THE MUSCLE
    NEITHER SHORTENS OR LENGTHENS.
    USED IN
    STANDING
    SITTING
  • 20. CONTRACTIONS
  • 21. MUSCLE TWITCH
    A single rapid contraction in response of muscle to a stimulus
    Muscle fiber contracts and then relaxes
    Strong twitch
    Weak Twitch
    Depends on the number of motor units activated
  • 22. MUSCLE CONTRACTION
    THERE ARE THREE PHASES:
    LATENT PERIOD
    PERIOD OF CONTRACTION
    PERIOD OF RELAXATION
  • 23. LATENT PERIOD
    First few seconds following stimulation
    Increase in muscle tension
    Ca release
    Cross bridge
    No shortening of muscles
  • 24. PERIOD OF CONTRACTION
    Cross bridges are active
    Sarcomere shorten
  • 25. PERIOD OF RELAXATION
    Re entry of Ca to Sarcoplasmic Reticulum
    Muscle tension decreases to zero
    Cross bridge ends
    Muscle returns to original length
  • 26. GRADED MUSCLE RESPONSES
    Variations in the degree of muscle contraction
    Three ways muscle contraction are graded
    Degree of muscle stretch
    By changing the strength of the stimulus
    By changing the frequency (speed) of stimulation
    Summation
    Tetanus
  • 27. Degree of muscle stretch (The Effect of Sarcomere Length on Tension)
    Amount of tension (force) generated by the muscle depends on length of muscle before it was stimulated
    Unstretched (Overly contracted , results weak contraction)
    Overlapping of thin filaments
    Overstretched (Too stretched, weak contraction results)
    Thin filaments are pulled to the end of thick filaments
    Moderately stretched (Optimum resting length produces greatest force when muscle contracts
    Moderate overlapping produces maximum contraction developed when optimum overlap of thick and thin filaments
  • 28. Degree of muscle stretch (The Effect of Sarcomere Length on Tension)