The myosin and actin sliding filament theory of muscle contraction: Summary of Biochemical Events of Muscle Contraction: 1. Nerve impulse arrives at neuromuscular junction (neuron to muscle cell communication). 2. Acetylcholine (ACh) is released from motor neuron and diffuses across to the motor end plate. 3. ACh binds with nicotinic receptors at the motor end plate (a specialized portion of sarcolemma). Receptors are linked to ligand gated ion channels, allowing Na+ influx (plus a little bit of K+ efflux), resulting in the depolarization of the muscle cell membrane. This results in a motor end plate potential, which becomes an action potential (AP) in muscle cells. 4. The impulse (AP) is spread very quickly through out the cell by the transverse (T) tubules. Located on the T-tubules are the dihydropyridine (DHP) receptors that are mechanically linked to the lateral sacs (terminal cisternae) of the sarcoplasmic reticulum (SR). When triggered by the change in membrane potential (AP) traveling down the t-tubules, the DHP receptors mechanically opens gates on the SR. This then causes the SR to release the Ca2+ it has stored there into the cytosol (sarcoplasm) of the skeletal muscle. 5. The increase in [Ca2+]i binds to the regulatory protein troponin, causing it to change shape and move. 6. The movement of troponin then moves tropomyosin away from covering the active site on actin, thus exposing the myosin binding site on actin. 7. Due to the strong affinity between them, the myosin head binds to the actin (crossbridge). 8. Crossbridge formation stimulates ATPase activity, and allows the power stroke to occur. The power stroke is the pulling of actin toward the M line by the pivoting of the myosin head. The myosin head is going from a high E state to a low E state during the power stroke (PE converted to KE). 9. If more ATP is available, then the crossbridge is broken and myosin releases actin. This allows for the repositioning of the myosin head into the high energy state. 10. Then, if the nerve impulse is still present, steps 7 through 9 will be repeated. This muscle contraction will continue until: 1) the impulse stops or 2) fatigue occurs. If Nerve Impulse Stops: 1. Ca2+ will be pumped back into SR (re-sequestered) by active transport (Ca2+ATPase). 2. Without the increased [Ca2+]i, troponin is no longer bound to Ca2+ and the tropomyosin then moves back over to cover the binding sites on actin. Thus crossbridges formation cannot occur. 3. When all the myosin heads detach, actin slides back to its original position and the muscle relaxes. Muscle fatigue is associated with the build-up of lactic acid due to anaerobic metabolism of glucose The production of lactic acid allows glycolysis to continue for short periods in the absence of oxygen but eventually lactic acid build- up inhibits enzymes of glycolysis Lactic acid build-up produces an “oxygen debt” Lactic acid must be removed from muscle by aerobic metabolism after strenuous activity ceases. [Sources: Nichols University and SDmirmar A&P lecture notes, and BraneGane educational videos]. youtube/playlist?list=PLMbjNMpW9bsqqyFb2ot7h8HZjJS0cqg8n
Posted on: Wed, 21 Jan 2015 20:45:05 +0000
Recently Viewed Topics
© 2015