Skeletal Muscle Contraction - pediagenosis
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Thursday, September 6, 2018

Skeletal Muscle Contraction

Skeletal Muscle Contraction
Summary of sequence of events in the contraction of muscle
   The arrival of the action potential at the neuromuscular junction (NMJ) leads to an influx of Ca2+ and the release of vesicles containing acetylcholine (ACh).
   ACh then binds to the nicotinic ACh receptor (AChR) on the muscle fibre leading to its depolarization.
   Ca2+ is then released from the sarcoplasmic reticulum (SR) of the muscle.
 Ca2+ release leads to the removal of the blocking calcium-binding protein complex of tropomyosin and troponin from actin, the main component of the thin filament.
   Removal of this stearic block allows myosin, the major component of the thick filaments, to bind to actin via a cross-bridge.
   The fibres are then pulled past each other; the cross-bridge between the two fibres is broken at the end of this power stroke by the hydrolysis of adenosine triphosphate (ATP).
The cycle of cross-bridge formation and breakage can then be repeated and the muscle contracts in a ratchet-like fashion.

Sequence of events in the contraction of muscle
   Stage 1
In the resting state the troponin complex holds the tropomyosin in such a position that it blocks myosin from binding to actin (stearic block).
   Stage 2
The arrival of an action potential at the NMJ causes a postsynaptic action potential to be initiated, which is propagated down the specialized invagination of the muscle membrane known as the transverse tubule (T-tubule). This T-tubule conducts the action potential down into the muscle, so that all the muscle fibres can be activated. It lies adjacent to the terminal cisternae of the SR in a structure known as a triad, i.e. a T-tubule lies between two terminal cisternae of the SR (muscle equivalent of smooth endoplasmic reticulum) which contain high concentrations of Ca2+.
The T-tubules are linked to the SR by foot processes, which are part of a calcium ion channel. The arrival of the action potential at the triad leads to the release of Ca2+ from the terminal cisternae, by a process of mechanical coupling. The action potential opens a common Ca2+ ion channel between the T-tubule and SR, which then allows Ca2+ to influx down its electrochemical gradient towards the myofibrils. The Ca2+ then binds to the troponin complex and this leads to a rearrangement of the tropomyosin so that the myosin head can now bind to the actin, forming a cross- link or cross-bridge.
   Stage 3
Once the myosin has bound to the actin there is a delay before tension develops in the cross-bridge. The tension pulls and rotates the actin past the myosin and this causes the muscle to contract. The cross-bridge at the end of this power stroke detaches the myosin from actin with hydrolysis of ATP, a process that is also calcium dependent.
The whole cycle can then be repeated. The process of cross- bridge formation with filament movement is called the sliding filament hypothesis of muscle contraction, as the two filaments slide past each other in a ratchet-like fashion as the cycle repeats. The Ca2+ released by the terminal cisternae of the SR, allowing the process of cross-bridge formation and breakage, is actively taken back up into this structure by a specific Ca2+ pump.

Skeletal Muscle Contraction

Disorders of muscle contraction
Diseases of the muscles, which disrupt their anatomy, will lead to weakness as a consequence of a disorganization of contractile proteins. However, there are some disorders in which there is a disruption of the contractile process itself and examples of this are the rare periodic paralyses and malignant hyperthermia/ hyperpyrexia. In this latter condition there is an abnormality in the ryanodine receptor which is part of the protein complex linking the T-tubule to the SR. This leads, under certain circumstances such as general anaesthesia, to sustained depolarization, contraction and necrosis of muscles resulting in an increase in body temperature and multiorgan dysfunction. In contrast, the periodic paralyses involve abnormalities in the ion channels that can lead to prolonged inexcitability of muscles, which thus become weak and paralysed. These are rare disorders and respiratory muscles are not involved; the paralysis can be provoked by a number of insults such as exercise or high carbohydrate meals.
It is also important to remember that disorders of muscle con- traction occur as a consequence of abnormalities at the NMJ (see Chapter 16), as well as with some inborn errors of metabolism. These latter metabolic myopathies involve inherited defects in either carbohydrate or lipid metabolism, which lead to either episodic exercise-induced symptoms or chronic progressive weakness.

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