Intense exercise induces pronounced hyperkalemia, where arterial plasma potassium concentration ([K+]a) may reach as high as 7-8 mM, then followed by a rapid decline in recovery from exercise, inducing a transient hypokalemia, with [K+]a less than 3.5 mM. These substantial changes occur over a time-course of minutes. As [K+]a is a modulator of cardiac repolarization during exercise and recovery, we investigated whether the post-exercise decline in [K+]a and hypokalemia affected cardiac repolarization, via QT hysteresis and/or T-wave dispersion. Eleven healthy, normokalemic adults performed 3 min intense rowing exercise, with [K+]a measured at rest, every 30 s during exercise and for 60 min recovery. The QT interval, QT hysteresis, Tpe and Tpe/QT ratio were calculated from ECG (n=8). The Tpeak-Tend interval (Tpe) is thought to reflect dispersion in ventricular repolarization, and abnormalities in Tpe have been associated with increased risk of arrhythmia. [K+]a increased above baseline during exercise (rest, 3.91 ±0.21 vs end-exercise, 7.21 ±0.57 mM, P<0.001, mean±SD) and decreased rapidly during early recovery to below baseline to nadir at 5 min (3.26 ±0.25 mM, P<0.05); restoration was incomplete at 60 min post-exercise (3.70 ±0.32 mM, P<0.05). The post-exercise decline in [K+]a was correlated with QT hysteresis (r=0.326, P<0.05). The decrease in [K+]a from end-exercise by ~4 mM was associated with reduced QT hysteresis by ~75 ms. The recovery-induced hypokalemia was also associated with a prolongation of Tpe compared to pre-exercise baseline (112 ±10 ms vs. 87 ±5 ms, p < 0.05) and an increase in Tpe/QT ratio (0.29 ±0.02 vs. 0.23 ±0.009, p < 0.01). Analyses of serial data revealed [K+]a as a predictor of Tpe (after logarithmic transformation) in these healthy subjects (β = -0.37 ±0.1, p < 0.001) after adjusting for heart rate and recovery state. The [K+]a was also a predictor of Tpe/QT ratio in these healthy participants. Thus post-exercise hypokalemia impaired cardiac repolarization and predicted both Tpe and the Tpe/QT ratio, which could unmask electrophysiological vulnerabilities to arrhythmias, thereby potentially causing sudden cardiac death in susceptible individuals with pre-existing hypokalemia and/or heart disease.