Onset of exercise leads to a sudden increase in [K+] in venous plasma from the exercising muscles. Delayed by about 10 s. the arterial [K+] rises nearly at the same rate as the venous concentration. At exercise intensities below 100% of Vo2max, both venous and arterial [K+] stabilize at a steady-state value. At higher intensities, venous and arterial plasma [K+] continue to rise until exhaustion. During the first 5 min of exercise the contracting muscles always lose K+, with a peak in loss rate after 1-2 min. During steady state, the loss rate is minimized or may even be reduced to zero. The loss is caused by an exercise-induced afflux of K+ from the contracting cells which exceeds the exercise-induced influx mediated by the Na, K pump. The Na, K pump is stimulated by catecholamines in vitro and in resting tissue in vivo. However, the loss rate of K+ from steady-state exercising muscles does not show any increase during beta -adrenergic blockade or decrease during beta-adrenergic stimulation. This is probably due to a compensatory change in intracellular [Na+]. During low exercise intensity, arterial [K+] does not increase after 1-2 min. while the exercising muscles lose K+, showing that the extracellular pool of K+ is redistributed. During beta-adrenergic blockade this redistribution is impaired so that the rise in plasma [K+] is accentuated. Conversely alpha-adrenergic blockade reduces the exercise-induced hyperkalaemia. Hence, the adrenergic system plays an important role in regulation of whole-body K+ balance during exercise but its significance in exercising muscles is not clear.