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1 Human Movement, Recreation and Performance; Centre for Ageing, Rehabilitation, Exercise and Sport, Victoria University, Melbourne, Victoria, Australia
2 Copenhagen Muscle Research Centre, Institute of Sport and Exercise Sciences, University of Copenhagen, Copenhagen, Denmark
3 Cellular and Molecular Medicine, University of Ottawa, Ottawa, Canada
* To whom correspondence should be addressed. E-mail: michael.mckenna{at}vu.edu.au.
Membrane excitability is a critical regulatory step in skeletal muscle contraction and is modulated by local ionic concentrations, conductances, ion transporter activities, temperature and humoral factors. Intense fatiguing contractions induce cellular K+ efflux, Na+ and Cl- influx, causing pronounced perturbations in extracellular (interstitial) and intracellular K+ and Na+ concentrations. Muscle interstitial K+ concentration may increase 1 to 2-fold to 11-13 mM and intracellular K+ concentration fall by 1.3 to 1.7-fold; interstitial Na+ concentration may decline by 10 mM and intracellular Na+ concentration rise by 1.5 to 2.0-fold. Muscle Cl- concentration changes reported with muscle contractions are less consistent, with reports of both unchanged and increased intracellular Cl- concentrations, depending upon contraction type and the muscles studied. When considered together, these ionic changes depolarize sarcolemmal and t-tubular membranes to depress tetanic force and are thus likely to contribute to fatigue. Interestingly, less severe local ionic changes can also augment sub-tetanic force, suggesting they may potentiate muscle contractility early in exercise. Increased Na+ ,K+ -ATPase activity during exercise stabilize Na+ and K+ concentration gradients and membrane excitability and thus protects against fatigue. However, during intense contraction some Na+ ,K+ -pumps are inactivated and together with further ionic disturbances, likely precipitate muscle fatigue.
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