Lec26
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The document discusses several topics related to muscle contraction, including: 1. Excitation-contraction coupling, where an action potential causes the release of calcium ions, triggering muscle contraction. 2. Neuromuscular transmission, where a nerve impulse causes the release of acetylcholine at the neuromuscular junction, generating an action potential in the muscle fiber. 3. The sliding filament theory which explains how calcium ions allow the overlapping of actin and myosin filaments, causing sarcomeres to shorten and generate force.
Lec26
- 1. Excitation contraction couplingTransmission of action potential along transverse tubules (T tubules)T tubules action potentials caused release of Ca ions inside the muscle fiber.Ca ions caused contractionOverall process called Excitation Contraction Coupling
- 2. Neuromuscular transmissionAction Potential through motor nerve fiberAxon TerminalOpening of Voltage gated Calcium channelsEntry of Calcium ions from Extracellular fluidOpening of vesicles & release of AchThe 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 cleftPassage of AchPostsynaptic membraneBinding of Ach with Receptor and formation of Ach-Receptor complexOpening of the ligand gated sodium channels & entry of sodium ions from ECFDevelopment of end plate potentialMuscle FiberGeneration of Action PotentialExcitation contracting couplingMuscular contraction
- 6. Neuromuscular Transmission Nerve impulse reaches end of axonCa channels openRelease of Ach into synaptic cleftDiffusion of Ach across the cleftAttachment of Ach to ach receptors on sarcolemmaOpening of Na channels which initiates depolarization of sarcolemma Development of end plate potentialGeneration of action potentialThe action potential causes the release of Ca ion from the terminal cisternaeMuscular contraction
- 7. Generation of Action potentialResting sarcolemma is polarizedOutside 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 sarcolemmaIon gates open (Na rushes into cell and K rushes out of cellCells interior becomes less negativeDepolarization Generation of Action potential
- 9. DepolarizationLoss of state of polarityLoss of negative membrane potentialsNerve stimulus is strong enoughAction potential is generated from neuromuscular junction across the sarcolemma in all directionsAction potential separates over cell surfaceGeneration 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 proceedsThe influx of Ca ion, triggering the exposure of binding sites on actinThe Action potential brings about the release of Ca ion from the terminal cisternaeCa ion binds to the troponin, causing change in conformation of the troponin tropomyosin complexThis conformation changes exposes the binding site on actin
- 13. Sliding Filament The binding of myosin to actinMyosin head bind to actin site and forming cross bridgeMovement of thin filamentRelease of ADP and PiThe myosin cross bridge pulls the thin filament inward toward the centre of sarcomere
- 14. Sliding Filament Disconnecting Myocin head from ActinATP binds to the myosin head disconnecting from actinRepositioning of the myosin headThe release of myosin head trigger the hydrolysis of ATP molecule into ADP and PiEnergy is transferred from ATP to the myosin head Removal of Ca ion Ca ion transported back into the sarcoplasmic reticulumTroponin - tropomyosin complex covers the binding sites on Actin
- 17. CONTRACTIONISOTONIC CONTRACTIONS CAUSES THE MUSCLE LENGTH TO CHANGE AND THE LOAD TO MOVEUSED INWALKINGMOVING ANY PART OF THE BODY
- 18. CONTRACTIONS
- 19. CONTRACTIONSISOMETRIC CONTRACTIONSTENSION BUILDS TO THE MUSCLE’SCAPACITY, BUT THE MUSCLENEITHER SHORTENS OR LENGTHENS. USED INSTANDINGSITTING
- 20. CONTRACTIONS
- 21. MUSCLE TWITCHA single rapid contraction in response of muscle to a stimulusMuscle fiber contracts and then relaxes Strong twitchWeak TwitchDepends on the number of motor units activated
- 22. MUSCLE CONTRACTIONTHERE ARE THREE PHASES:LATENT PERIODPERIOD OF CONTRACTIONPERIOD OF RELAXATION
- 23. LATENT PERIODFirst few seconds following stimulationIncrease in muscle tensionCa releaseCross bridgeNo shortening of muscles
- 24. PERIOD OF CONTRACTIONCross bridges are activeSarcomere shorten
- 25. PERIOD OF RELAXATIONRe entry of Ca to Sarcoplasmic ReticulumMuscle tension decreases to zeroCross bridge endsMuscle returns to original length
- 26. GRADED MUSCLE RESPONSESVariations in the degree of muscle contractionThree ways muscle contraction are gradedDegree of muscle stretchBy changing the strength of the stimulusBy changing the frequency (speed) of stimulationSummationTetanus
- 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 stimulatedUnstretched (Overly contracted , results weak contraction) Overlapping of thin filamentsOverstretched (Too stretched, weak contraction results) Thin filaments are pulled to the end of thick filamentsModerately 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)