Muscles another action potential. It spreads to the surrounding

Musclesare a crucial aspect of the human body. They produce movement, stabilizejoints, generate heat, and maintain posture and body position. Skeletal musclesare voluntary in that they can be stimulated by conscious control. Skeletalmuscles are responsible for movement of the body and are activated by variousprocesses including action potentials and cross bridge cycling.

Excitation-contraction coupling produces movement through these processes.            An action potential must occur for the muscle to move.The action potential travels down the motor neuron until it reaches theterminal end. Once there, it stimulates the opening of voltage-gated calciumchannels. The calcium ions then enter the axon terminal from the sarcoplasmicreticulum and move down their gradient. The presence of calcium causesacetylcholine to be released from synaptic vesicles into the synaptic cleft byexocytosis. It then binds to nicotinic receptors on the sarcolemma, whichcauses the receptors to open their ion channels.

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Sodium ions flow into themuscle fiber and potassium ions flow out, creating an end plate potential bydepolarization in the membrane. The ion channels close when the enzyme acetylcholinesteraseremoves the acetylcholine from the receptor.            The end plate potential can create another actionpotential.

It spreads to the surrounding membrane and opens ion channels,causing more depolarization as sodium ions enter. An action potential isgenerated when the membrane voltage reaches threshold. The action potentialcontinues to spread out from the source and causes further depolarization andion channel opening along the membrane. Once sodium ion channels close,potassium ion channels open, releasing potassium into the extracellular fluid.The charge inside the membrane becomes more negative, repolarizing thesarcolemma.             The action potential also causes cross bridge cycling tooccur.

The action potential travels down the T tubules of the sarcolemma,causing the tubule proteins to change shape. Calcium ion release channels inthe sarcoplasmic reticulum are opened, causing calcium ions to enter thecytosol. Once there, the calcium ions bind to troponin, changing its shape. Thechanged troponin moves the tropomyosin, preventing it from blocking the myosinbinding sites on the thin filaments. The myosin of the thick filaments forms across bridge by attaching its heads to the binding sites on the actin of thethin filaments. The ADP and P? on the myosin head are then released, causing thehead to pivot and bend and pull the thin filament towards the M line. The crossbridge breaks after ATP attaches to the myosin head, causing it to detach fromthe actin. The ATP is then hydrolyzed which readies the myosin head for thenext cross bridge.

            There are many steps involved in muscle contraction andif even one does not work, a contraction will not occur. One possibledisruption would be the blocking of calcium ion voltage-gated channels. Calciumions entering the axon terminal is a critical and early step inexcitation-contraction coupling.

Without it, acetylcholine would not bereleased to bind to the receptors. Blocking those nicotinic receptors wouldalso prevent contraction as the ion channels would remain closed andimpermeable to sodium and potassium ions. One other way to prevent contractionwould be if acetylcholinesterase was over-stimulated. The removal ofacetylcholine from the receptors or reducing the amount able to bind in thefirst place would close the ion channels early or hinder them from openingentirely. If the movement of sodium and potassium ions is stopped, there willnot be enough to cause depolarization or an end plate potential, haltingcontraction.            There are some disorders that can cause issues withmuscle contraction. One such disorder is myasthenia gravis, or MG.

MG ischaracterized by skeletal muscle weakness and is caused by antibodies thatattack the nicotinic acetylcholine receptors. This prevents the acetylcholinefrom binding and opening the ion channels, therefore halting contraction. Whilethere is no definitive cure for MG, it can be controlled. Some people with MGhave large thymus glands that likely give instructions for producing theantibodies. The thymus gland can be removed, and this may reduce symptoms.Anticholinesterase and immunosuppressant medications may also help by slowingthe removal of acetylcholine from the synaptic cleft, leaving it more time forattachment, and by reducing the production of antibodies, respectively.