Role of exercise-induced potassium fluxes underlying muscle fatigue: a brief review

Abstract

The site of exercise-induced muscle fatigue is suggested to be the muscle membrane, which includes the sarcolemma and T-tubule membrane; the excitability of the membrane is dependent on the membrane potential. Significant potassium flux from the intracellular space of contracting muscle may decrease the membrane potential to half its resting value. This is true for isolated muscle preparations as well as for the whole body exercise in humans. Specific K+ channels have been identified, that may account for the intracellular K+ loss. Calcium-sensitive K+ channels open when intracellular Ca2+ concentrations increase, as during excitation. ATP-sensitive K+ channels may be involved but may open only at ATP concentrations well below those attained at exhaustion. However, ATP may be compartmentalized and only the membrane-bound ATP concentration may be of significance. Ca2+ accumulation and ATP depletion cause cell destruction; these changes induce an increased K+ conductance, which may inactivate the membrane and consequently prevent tension development. It is hypothesized that such a safety mechanism is identical to the fatigue mechanism.