Mij
Senior Member (Voting Rights)
KEY POINTS
Eccentric contractions (ECC) induce excessive intracellular calcium ion (Ca2+) accumulation and muscle structural damage in localized regions of the muscle fibers. In this investigation, we present the novel hypothesis that the ryanodine receptor (RyR) plays a central role in evoking a Ca2+ dynamics profile that is markedly distinguishable from other muscle adaptive responses.
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- Eccentric contractions (ECC) induce muscle damage that persists for several days or weeks and resembles a pathophysiological condition.
- The morphological changes in ECC-induced muscle damage are highly selective and localized within the muscle fibers, suggesting the existence of a mechanism that determines whether a specific region can control its intracellular Ca2+ concentration ([Ca2+]i) and thus is subject to damage or not.
- [Ca2+]i displays both spatial and temporal dynamics to achieve high versatility in regulating various cellular functions. Ryanodine receptors (RyR) and their interactions with mitochondria likely drive the distinctive Ca2+ dynamics that result in the selective and persistent muscle damage that follows ECC.
Eccentric contractions (ECC) induce excessive intracellular calcium ion (Ca2+) accumulation and muscle structural damage in localized regions of the muscle fibers. In this investigation, we present the novel hypothesis that the ryanodine receptor (RyR) plays a central role in evoking a Ca2+ dynamics profile that is markedly distinguishable from other muscle adaptive responses.
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