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Muscles
are a crucial aspect of the human body. They produce movement, stabilize
joints, generate heat, and maintain posture and body position. Skeletal muscles
are voluntary in that they can be stimulated by conscious control. Skeletal
muscles are responsible for movement of the body and are activated by various
processes 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 the
terminal end. Once there, it stimulates the opening of voltage-gated calcium
channels. The calcium ions then enter the axon terminal from the sarcoplasmic
reticulum and move down their gradient. The presence of calcium causes
acetylcholine to be released from synaptic vesicles into the synaptic cleft by
exocytosis. It then binds to nicotinic receptors on the sarcolemma, which
causes the receptors to open their ion channels. Sodium ions flow into the
muscle fiber and potassium ions flow out, creating an end plate potential by
depolarization in the membrane. The ion channels close when the enzyme acetylcholinesterase
removes the acetylcholine from the receptor.

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            The end plate potential can create another action
potential. It spreads to the surrounding membrane and opens ion channels,
causing more depolarization as sodium ions enter. An action potential is
generated when the membrane voltage reaches threshold. The action potential
continues to spread out from the source and causes further depolarization and
ion 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 the
sarcolemma.

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

            There are many steps involved in muscle contraction and
if even one does not work, a contraction will not occur. One possible
disruption would be the blocking of calcium ion voltage-gated channels. Calcium
ions entering the axon terminal is a critical and early step in
excitation-contraction coupling. Without it, acetylcholine would not be
released to bind to the receptors. Blocking those nicotinic receptors would
also prevent contraction as the ion channels would remain closed and
impermeable to sodium and potassium ions. One other way to prevent contraction
would be if acetylcholinesterase was over-stimulated. The removal of
acetylcholine from the receptors or reducing the amount able to bind in the
first place would close the ion channels early or hinder them from opening
entirely. If the movement of sodium and potassium ions is stopped, there will
not be enough to cause depolarization or an end plate potential, halting
contraction.

            There are some disorders that can cause issues with
muscle contraction. One such disorder is myasthenia gravis, or MG. MG is
characterized by skeletal muscle weakness and is caused by antibodies that
attack the nicotinic acetylcholine receptors. This prevents the acetylcholine
from binding and opening the ion channels, therefore halting contraction. While
there is no definitive cure for MG, it can be controlled. Some people with MG
have large thymus glands that likely give instructions for producing the
antibodies. The thymus gland can be removed, and this may reduce symptoms.
Anticholinesterase and immunosuppressant medications may also help by slowing
the removal of acetylcholine from the synaptic cleft, leaving it more time for
attachment, and by reducing the production of antibodies, respectively.

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