BIOD27H3 Lecture 17: BGYB30H3 Lecture 17 Notes Control of Body Movement-Nov 5

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BGYB30H3 Lecture 17 Notes
-the sliding filament model is the mechanism of force generation in the muscle
-muscles shorten when they contract
-actin and myosin slide past each other during contraction, causing cross-bridge cycling
-cross bridge cycling requires energy from ATP to cause contraction and allows tension without
movement
-at rest, thick and thin filaments in the myofibril overlap slightly
-when muscle contracts, Z disks move towards each other
-thin filament slides over thick filaments towards the M-line in the center
-sarcomere, H band, and I bands shorten during contraction while the A band remains the
same
-rigor state involves no ADP/ATP occupying 2nd binding site while myosin heads bind to G-actin
-when ATP binds to myosin, affinity for actin decreases and actin is released from the binding
site
-in the second stage myosin hydrolyzes ATP to form ADP and Pi but the molecules remain
bonded to myosin head in order for it to move and bind to next actin molecule near the M-line
-the newly formed bridge between myosin and another actin molecule is weak because
troponin partially blocks the myosin binding site
-myosin head is full of potential energy, which is the state most muscles are found in
-power stroke is the third stage where calcium binds to troponin to cause tropomyosin to open
the binding site
-the newly formed bridge becomes strong and Pi is released from the myosin head
-myosin head swings towards the M-line and actin filament slides toward the M-line
-in the fourth stage, myosin releases ADP, which marks the end of the power stroke
-the rigor state is brief because of ATP supply
-in resting state, troponin prevents binding of myosin to actin
-increased calcium, due to depolarization of muscle, causes calcium to bind to troponin and pull
tropomyosin away from the myosin binding site (completing the power stroke)
-acetylcholine initiates action potential in motor end plate of muscle fibre
-action potential going down t-tubules causes calcium release from sarcoplasmic reticulum
-a muscle twitch involves acetylcholine released from the somatic motor neuron and generating
an action potential in the motor end plate
-acetylcholine causes monovalent nicotinic receptors to allow sodium and potassium flux
-action potential goes down the t-tubules to trigger calcium release from the sarcoplasmic
reticulum
-calcium binding with troponin exposes the binding site to start cross bridge cycle
-muscle only has a certain amount of ATP to generate 8 twitches
-back up ATP comes from phosphocreatin
-phosphocreatin has high energy Pi bonds that transfer energy to ADP to form ATP
-creatine kinase causes the transfer of a phosphate group
-latent period is the time taken for an action potential from the motor end plate to cause a
muscle contraction
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Document Summary

The sliding filament model is the mechanism of force generation in the muscle. Actin and myosin slide past each other during contraction, causing cross-bridge cycling. Cross bridge cycling requires energy from atp to cause contraction and allows tension without movement. At rest, thick and thin filaments in the myofibril overlap slightly. When muscle contracts, z disks move towards each other. Thin filament slides over thick filaments towards the m-line in the center. Sarcomere, h band, and i bands shorten during contraction while the a band remains the same. Rigor state involves no adp/atp occupying 2nd binding site while myosin heads bind to g-actin. When atp binds to myosin, affinity for actin decreases and actin is released from the binding site. In the second stage myosin hydrolyzes atp to form adp and pi but the molecules remain bonded to myosin head in order for it to move and bind to next actin molecule near the m-line.

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