Protection against severe hypokalemia but impaired cardiac repolarization after intense rowing exercise in healthy humans receiving salbutamol

Author:

Atanasovska Tania1,Smith Robert12,Graff Claus3,Tran Cao T.4,Melgaard Jacob3,Kanters Jørgen K.5,Petersen Aaron C.1,Tobin Antony6,Kjeldsen Keld P.378,McKenna Michael J.1ORCID

Affiliation:

1. Institute for Health and Sport, Victoria University, Melbourne, Victoria, Australia

2. Department of Anaesthesia, Western Hospital, Melbourne, Victoria, Australia

3. Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Aalborg, Denmark

4. Division of Cardiology, John Hopkins University School of Medicine, Baltimore, Maryland

5. Laboratory of Experimental Cardiology, Department of Biomedical Sciences, Copenhagen University, Copenhagen, Denmark

6. Intensive Care Unit, St. Vincent Hospital, Melbourne, Victoria, Australia

7. Medical Department, Copenhagen University Hospital (Holbæk Hospital), Holbæk, Denmark

8. Institute of Clinical Medicine, Faculty of Medicine, Copenhagen University, Copenhagen, Denmark

Abstract

Intense exercise induces pronounced hyperkalemia, followed by transient hypokalemia in recovery. We investigated whether the β2 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+]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. NEW & NOTEWORTHY Intense rowing exercise induced a marked increase in arterial potassium, followed by a pronounced decline to hypokalemic levels. The β2 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.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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