The increase in ventilation caused by exercise is controlled by a combination of neural and chemical events, although the precise contribution and relative importance of these signals is still debated. It is generally agreed that the genesis of exercise hyperpnoea lies within the central nervous system and that peripheral reflexes, both chemical and neural, modulate central drive. Recently, attention has once again focused on the idea that circulating factors, in particular potassium, may play an important role in this modulation by stimulating known areas of peripheral chemoreception. Arterial chemoreceptors, muscle chemoreflex and slowly adapting pulmonary stretch receptors are all excited by hyperkalaemia. When potassium is raised to mimic exercise concentrations it increases ventilation in anaesthetised animals. This response is abolished by surgical denervation of the arterial chemoreceptors and is markedly reduced by chemical denervation with hyperoxia. Hypoxia enhances the ventilatory response to hyperkalaemia, and the stimulatory effects of potassium are further increased when combined with lactic acid or raised concentrations of noradrenaline. Hyperkalaemia can also increase the hypoxic sensitivity of the arterial chemoreflex in exercise. There is a close temporal relationship between potassium and ventilation during exercise, but changes in potassium are not proportionally related to changes in ventilation. When all data are taken together, there is good evidence that potassium has a supporting role in the control of exercise hyperpnoea, predominantly through modulation of the arterial chemoreflex.