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Muscle uses Ca2+ as a messenger to control contraction and relies on ATP tomaintain the intracellular Ca2+ homeostasis. Mitochondria are the majorsub-cellular organelle of ATP production. With a negative inner membranepotential, mitochondria take up Ca2+ from their surroundings, a process calledmitochondrial Ca2+ uptake. Under physiological conditions, Ca2+ uptake intomitochondria promotes ATP production. Excessive uptake causes mitochondrialCa2+ overload, which activates downstream adverse responses leading to celldysfunction. Moreover, mitochondrial Ca2+ uptake could shape spatio-temporalpatterns of intracellular Ca2+ signaling. Malfunction of mitochondrial Ca2+uptake is implicated in muscle degeneration. Unlike non-excitable cells,mitochondria in muscle cells experience dramatic changes of intracellular Ca2+levels. Besides the sudden elevation of Ca2+ level induced by actionpotentials, Ca2+ transients in muscle cells can be as short as a fewmilliseconds during a single twitch or as long as minutes during tetaniccontraction, which raises the question whether mitochondrial Ca2+ uptake isfast and big enough to shape intracellular Ca2+ signaling duringexcitation-contraction coupling and creates technical challenges forquantification of the dynamic changes of Ca2+ inside mitochondria. This reviewfocuses on characterization of mitochondrial Ca2+ uptake in skeletal muscle andits role in muscle physiology and diseases.

Mitochondrial Ca2+ uptake in skeletal muscle health and disease