Sarcoplasmic reticulum Ca(2+) release and 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.
Favero
T G
TG
Department of Biology, University of Portland, Portland, Oregon 97203, USA.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D009119:Muscle Contraction / Q000502:physiology; D018763:Muscle Fatigue / Q000502:physiology*; D009124:Muscle Proteins / Q000378:metabolism; D018482:Muscle, Skeletal / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*
D015220:Calcium Channels; D009124:Muscle Proteins; D017382:Reactive Oxygen Species; D002118:Calcium