Role of intracellular calcium and metabolites in low-frequency fatigue of mouse skeletal muscle.
We have examined the extent to which prolonged reductions in low-frequency force (i.e., low-frequency fatigue) result from increases in intracellular free Ca2+ concentration ([Ca2+]i) and alterations in muscle metabolites. Force and [Ca2+]i were measured in mammalian single muscle fibers in response to short, intermediate, and long series of tetani that elevated the [Ca2+]i-time integral to 5, 17, and 29 microM x s, respectively. Only the intermediate and long series resulted in prolonged (>60 x min) reductions in Ca2+ release and low-frequency fatigue. When fibers recovered from the long series of tetani without glucose, Ca2+ release was reduced to a greater extent and force was reduced at high and low frequencies. These findings indicate that the decrease in sarcoplasmic reticulum Ca2+ release associated with fatigue has at least two components: 1) a metabolic component, which, in the presence of glucose, recovers within 1 h, and 2) a component dependent on the elevation of the [Ca2+]i-time integral, which recovers more slowly. It is this Ca2+-dependent component that is primarily responsible for low-frequency fatigue.
Chin
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ER
Institute for Biomedical Research and Department of Physiology, University of Sydney, New South Wales, Australia.
Balnave
C D
CD
Allen
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DG
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004558:Electric Stimulation / Q000379:methods; D007425:Intracellular Membranes / Q000378:metabolism*; D051379:Mice; D009119:Muscle Contraction; D018763:Muscle Fatigue / Q000502:physiology*; D018482:Muscle, Skeletal / Q000502:physiology*; D013997:Time Factors
D002118:Calcium