The role of intracellular calcium and metabolites in low frequency
fatigue of mouse skeletal muscle .
Chin, E. R., C. D. Balnave & D. G. Allen.
Institute for Biomedical Research and Department of Physiology F13,
University of Sydney, NSW 2006 Australia
APStracts 3:0293C, 1996.
We have examined the extent to which prolonged reductions of low
frequency force (ie. 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 fibres in response to a short, intermediate and long
series of tetani which elevated the [Ca2+]i -time integral to 5, 17
and 29 [mu]M*s, respectively. Only the intermediate and long series
resulted in prolonged (> 60 min) reductions in Ca2+ release
and low frequency fatigue. When fibres recovered from the long series
of tetani without glucose, Ca2+ release was reduced to a greater
extent and force was reduced at both high and low frequencies. These
findings indicate that the decrease in SR Ca2+ release associated
with fatigue has at least two components - a metabolic component
which, in the presence of glucose, recovers within one hour and a
component dependent on the elevation of the [Ca2+]i -time integral
which recovers more slowly. It is this Ca2+ -dependent component
which is primarily responsible for low frequency fatigue.
Received 29 May 1996; accepted in final form 9 September 1996.
APS Manuscript Number C294-6.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 7 October 1996