We investigated whether potassium (K(+)) disturbances during and following intense exercise may be pronounced when utilizing a large contracting muscle mass, examining maximal 2,000-m rowing exercise effects on radial arterial plasma K(+) concentration ([K(+)]a) in 11 healthy adults. Blood was sampled at baseline, preexercise, each 30 s during rowing, and for 30 min postexercise. Time to complete 2,000 m was 7.26 ± 0.59 min; power output at 30 s was 326 ± 81 W (mean ± SD). With exercise time expressed in deciles, power output fell 16.5% from the first to fourth decile (P < 0.05) and 19.9% at the ninth decile (P < 0.05); EMG median frequency declined 4.6% by the third decile and 5.5% by the eighth decile (P < 0.05). Plasma [K(+)]a increased from 3.89 ± 0.13 mM at rest to 6.13 ± 0.46 mM by 90 s rowing (P < 0.001) and was then sustained until end exercise (P < 0.001). In recovery, [K(+)]a decreased abruptly, reaching 3.33 ± 0.22 mM at 5 min postexercise (P < 0.001) and remaining below preexercise after 30 min (P < 0.005). At end exercise, blood [lactate]a (preexercise 0.64 ± 0.18 mM) reached 10.87 ± 1.33 mM, plasma volume decreased 9.7 ± 2.3% from preexercise, and pHa decreased to 7.10 ± 0.07 units (P < 0.001). In conclusion, arterial hyperkalemia was sustained during exhaustive rowing reflecting a balance between K(+) release and reuptake in contracting muscles and K(+) uptake by inactive muscles. While high, the [K(+)]a was lower than anticipated compared with maximal cycling or sprinting, possibly reflecting greater adrenergic response and Na(+),K(+)-ATPase activity in contracting muscles; fatigue was evidenced by reduced power output and EMG median frequency. A prolonged hypokalemia after rowing likely reflected continuing muscular Na(+),K(+)-ATPase activity.

Intense exercise induces pronounced hyperkalemia, followed by transient hypokalemia in recovery. We investigated whether the β 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 µg salbutamol (SAL) or placebo (PLAC) by inhalation. Arterial plasma potassium concentration ([K]) 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] 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] 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] 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] was correlated with QT hysteresis ( r = 0.343, n = 112, pooled data, P = 0.001). Therefore, the decrease in [K] from end-exercise by ~4 mM was associated with reduced QT hysteresis by ~75 ms. Although salbutamol lowered [K] 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. NEW & NOTEWORTHY Intense rowing exercise induced a marked increase in arterial potassium, followed by a pronounced decline to hypokalemic levels. The β agonist salbutamol lowered potassium during exercise and late recovery but not during early postexercise, suggesting a protective effect against severe hypokalemia. The decreased potassium in recovery was associated with impaired cardiac QT hysteresis, suggesting a link between postexercise potassium and the heart, with implications for increased risk of cardiac arrhythmias and, potentially, sudden cardiac death.

The cardiac T-wave peak-to-end interval (Tpe) is thought to reflect dispersion in ventricular repolarisation, with abnormalities in Tpe associated with increased risk of arrhythmia. Extracellular K + modulates cardiac repolarisation and since arterial plasma K + concentration ([K + ]) rapidly increases during and declines following exercise, we investigated the relationship between [K + ] and Tpe with exercise. MethodsSerial ECGs (Tpe, Tpe/QT ratio) and [K + ] were obtained from 8 healthy, normokalaemic volunteers and 22 patients with end-stage renal disease (ESRD), at rest, during and after exhaustive exercise. ResultsPost-exercise [K + ] nadir was 3.1 ±0.1, 5.0 ±0.2 and 4.0 ±0.1 mmol.L -1 (mean ± SEM) for healthy participants and ESRD patients before and after HD, respectively. In healthy participants, compared to pre-exercise, recovery-induced low [K + ] was associated with a prolongation of Tpe (110 ±8 vs. 87 ±5 ms, respectively, p=0.03) and an increase in Tpe/QT ratio (0.28 ±0.01 vs. 0.23 ±0.01, respectively, p=0.01). Analyses of serial data revealed [K + ] as a predictor of Tpe in healthy participants (β = -0.54 ±0.11, p=0.0007), in ESRD patients (β = -0.72 ±0.1, p < 0.0001) and for all data pooled (β = -0.64 ±0.52, p = 0.0007). The [K + ] was also a predictor of Tpe/QT ratio in healthy participants and ESRD patients. ConclusionsTpe and Tpe/QT ratio are predicted by [K + ] during exercise. Low [K + ] during recovery from exercise was associated with increased Tpe and Tpe/QT, indicating accentuated dispersion of ventricular repolarisation. The findings suggest that variations in [K + ] with physical exertion may unmask electrophysiological vulnerabilities to arrhythmia.