In exercise, potassium (K+) is released from contracting muscle predominately through K+ channels associated with the repolarization phase of the action potential. Increases in extracellular K+ are directly related to increases in metabolic rate and may reach concentrations as high as 8-9 mM in the arterial blood during exhaustive work. Exercise-induced hyperkalaemia has been implicated in several physiological processes, in particular skeletal muscle fatigue, hyperaemia, pressor reflex, arterial chemosensitivity and myocardial stability. There is no direct evidence to show that hyperkalaemia causes muscle fatigue, although raised extracellular [K+] may contribute to fatigue during prolonged tetani by depressing the propagation of the action potential down the t-tubule system, thus impairing the release of Ca2+ from the sarcoplasmic reticulum. The vasodilating properties of K+ may transiently contribute to the early phase of exercise hyperaemia and interact synergistically with other vasoactive substances to cause relaxation by hyperpolarizing K+ channels in vascular smooth muscle. Hyperkalaemia has been implicated in the regulation of arterial blood pressure through activation of the muscle afferent reflex where potassium-depolarized C fibres may contribute to a reflex increase in arterial blood pressure. K+ can also increase ventilation and the sensitivity of the ventilatory response to hypoxia through direct excitation of the arterial chemoreceptors. Finally, to maintain myocardial electrical stability in exercise, there is a beneficial interaction between raised K+ and catecholamines on the heart, so that when they combine, each offsets the other's deleterious effects.