Intense exercise induces pronounced hyperkalemia, followed by transient hypokalemia in recovery. We investigated whether the 2 agonist salbutamol attenuated the exercise hyperkalemia and exacerbated the postexercise hypokalemia, and whether hypokalemia was associated with impaired cardiac repolarization (QT hysteresis). Eleven healthy adults participated in a randomized, counterbalanced, double-blind trial receiving either 1,000 g salbutamol (SAL) or placebo (PLAC) by inhalation. Arterial plasma potassium concentration ([K]a) was measured at rest, during 3 min of intense rowing exercise, and during 60 min of recovery. QT hysteresis was calculated from ECG (n 8). [K]a increased above baseline during exercise (rest, 3.72 0.7 vs. end-exercise, 6.81 1.4 mM, P 0.001, mean SD) and decreased rapidly during early recovery to below baseline; restoration was incomplete at 60 min postexercise (P 0.05). [K]a was less during SAL than PLAC (4.39 0.13 vs. 4.73 0.19 mM, pooled across all times, P 0.001, treatment main effect). [K]a was lower after SAL than PLAC, from 2 min preexercise until 2.5 min during exercise, and at 50 and 60 min postexercise (P 0.05). The postexercise decline in [K]a was correlated with QT hysteresis (r 0.343, n 112, pooled data, P 0.001). Therefore, the decrease in [K]a from end-exercise by ~4 mM was associated with reduced QT hysteresis by ~75 ms. Although salbutamol lowered [K]a during exercise, no additive hypokalemic effects occurred in early recovery, suggesting there may be a protective mechanism against severe or prolonged hypokalemia after exercise when treated by salbutamol. This is important because postexercise hypokalemia impaired cardiac repolarization, which could potentially trigger arrhythmias and sudden cardiac death in susceptible individuals with preexisting hypokalemia and/or heart disease.