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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
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 ,[object Object]
 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
Exciting Contraction Coupling
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
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)
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
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
Generation of Action Potential
Generation of Action Potential
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
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
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
Sliding-Filament Mechanism
Sliding-Filament Mechanism
CONTRACTION ISOTONIC CONTRACTIONS CAUSES  THE MUSCLE LENGTH TO  CHANGE AND THE LOAD TO MOVE USED IN WALKING MOVING ANY PART OF THE BODY
CONTRACTIONS
CONTRACTIONS ISOMETRIC CONTRACTIONS TENSION BUILDS TO THE MUSCLE’S CAPACITY, BUT THE MUSCLE NEITHER SHORTENS OR LENGTHENS.  USED IN STANDING SITTING
CONTRACTIONS
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
MUSCLE CONTRACTION THERE ARE THREE PHASES: LATENT PERIOD PERIOD OF CONTRACTION PERIOD OF RELAXATION
LATENT PERIOD First few seconds following stimulation Increase in muscle tension Ca release Cross bridge No shortening of muscles
PERIOD OF CONTRACTION Cross bridges are active Sarcomere shorten
PERIOD OF RELAXATION Re entry of Ca to Sarcoplasmic Reticulum Muscle tension decreases to zero Cross bridge ends Muscle returns to original length
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
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

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Lec26

  • 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.
  • 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
  • 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
  • 17. CONTRACTION ISOTONIC CONTRACTIONS CAUSES THE MUSCLE LENGTH TO CHANGE AND THE LOAD TO MOVE USED IN WALKING MOVING ANY PART OF THE BODY
  • 19. CONTRACTIONS ISOMETRIC CONTRACTIONS TENSION BUILDS TO THE MUSCLE’S CAPACITY, BUT THE MUSCLE NEITHER SHORTENS OR LENGTHENS. USED IN STANDING SITTING
  • 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)