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1 Division of Sport and Recreation, Auckland University of Technology, Auckland, Auckland, New Zealand; Department of Physiology, University of Auckland, Auckland, Auckland, New Zealand
2 Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada
* To whom correspondence should be addressed. E-mail: simeon.cairns{at}aut.ac.nz.
A possible role of extracellular Cl- concentration ([Cl-]o) in fatigue was investigated in isolated skeletal muscles of the mouse. When [Cl-]o was lowered from 128 to 10 mM, the peak tetanic force was unchanged, fade was exacerbated (wire electrodes), and a hump appeared during relaxation of the tetanus, in both non-fatigued slow-twitch soleus and fast-twitch extensor digitorum longus (EDL) muscles. Low [Cl-]o increased the rate of fatigue: 1) with prolonged continuous tetanic stimulation in soleus, 2) with repeated intermittent tetanic stimulation in soleus or EDL, and 3) to a greater extent with repeated tetani when using wire than plate stimulation electrodes in soleus. In non-fatigued soleus muscles, application of 9 mM K+ with low [Cl-]o caused a more rapid and greater tetanus depression, along with greater depolarization, than at normal [Cl-]o. These effects of raised [K+]o and low [Cl-]o were synergistic. From these data we suggest that normal [Cl-]o provides protection against fatigue involving high-intensity contractions in both fast- and slow-twitch mammalian muscle. This possibly involves attenuation of the depolarization caused by a stimulation or exercise-induced run-down of the trans-sarcolemmal K+ gradient.
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