Reductions in sarcoplasmic reticulum Ca2+ release during intense muscle contraction compromise tension development via elevated Ca2+, metabolic alterations, and reactive oxygen species.
This review highlights the molecular mechanisms by which intense contractile activity alters sarcoplasmic reticulum Ca2+ handling, leading to skeletal muscle fatigue.
Efforts to examine the relevant mechanisms involved in skeletal muscle fatigue are focusing on Ca(2+) handling within the active muscle cell. It has been demonstrated time and again that reductions in sarcoplasmic reticulum (SR) Ca(2+) release resulting from increased or intense muscle contraction will compromise tension development. This review seeks to accomplish two related goals: 1) to provide an up-to-date molecular understanding of the Ca(2+)-release process, with considerable attention devoted to the SR Ca(2+) channel, including its associated proteins and their regulation by endogenous compounds; and 2) to examine several putative mechanisms by which cellular alterations resulting from intense and/or prolonged contractile activity will modify SR Ca(2+) release. The mechanisms that are likely candidates to explain the reductions in SR Ca(2+) channel function following contractile activity include elevated Ca(2+) concentrations, alterations in metabolic homeostasis within the "microcompartmentalized" triadic space, and modification by reactive oxygen species.
Terence G. Favero (Sun,) conducted a review in Muscle fatigue. Reductions in sarcoplasmic reticulum Ca2+ release during intense muscle contraction compromise tension development via elevated Ca2+, metabolic alterations, and reactive oxygen species.
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