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In skeletal muscle, which substance(s) are required for excitation-contraction (EC) coupling and cross-bridge cycling?
Excitation-Contraction Coupling and Cross-Bridge Cycling
The physical contraction of muscles helps us perform our every day activities without a second thought, however there are many molecular steps involved that occur behind the scenes. Two of these steps include excitation-contraction coupling and cross-bridge formation.
First coined by Alexander Sandow in 1952, the term excitation–contraction coupling (ECC) describes
the rapid communication between electrical events occurring in the
plasma membrane of skeletal muscle fibres and Ca2+ release from the SR,
which leads to contraction. The sequence of events in twitch skeletal muscle involves:
initiation and propagation of an action potential along the plasma membrane,
spread of the potential throughout the transverse tubule system (T-tubule system),
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dihydropyridine receptors (DHPR)-mediated detection of changes in membrane potential,
allosteric interaction between DHPR and sarcoplasmic reticulum (SR) ryanodine receptors (RyR),
release of Ca2+ from the SR and transient increase of Ca2+ concentration in the myoplasm,
activation of the myoplasmic Ca2+ buffering system and the contractile apparatus,
followed by Ca2+ disappearance from the myoplasm mediated mainly by its reuptake
by the SR through the SR Ca2+ adenosine triphosphatase (SERCA),
and under several conditions movement to the mitochondria and extrusion by the Na+/Ca2+ exchanger (NCX).
In this text, we review the basics of ECC in skeletal muscle and the techniques used to study it.
Moreover, we highlight some recent advances and point out gaps in knowledge on particular issues
related to ECC such as DHPR-RyR molecular interaction, differences regarding fibre types,
its alteration during muscle fatigue, the role of mitochondria and store-operated Ca2+ entry
in the general ECC sequence, contractile potentiators, and Ca2+ sparks.