Physical performance and serum potassium under chronic beta-blockade

Summary

Various publications have described a beta₂-receptor regulated potassium transport system in the cellular membrane of human skeletal muscle. To examine the suggestion that serum potassium alterations are among the causes of premature muscular fatigue during physical exercise under pharmacological blockade of Β-receptors, we have compared the influence of sustained blockade with a beta₁-selective blocker and a non-selective beta-blocker on the levels of serum potassium before, during and after a physical exercise test.

63 healthy physical education students received in random order and under double blind conditions either 100 mg Metoprolol (Β₁-selective) or 80 mg Propranolol (non-selective), or placebo daily for 3 months. Serum potassium was measured before, during (at 150 Watt and at the end of exercise) and after a bicycle exercise with a stepwise increase in work loads. After three months of beta-blocker treatment serum potassium levels during exercise were significantly higher than in control subjects receiving the placebo, and it took longer for the serum potassium levels to return to the resting level in the beta-blocker treated subjects. At rest, however, the levels were not found to be statistically different. In the subjects receiving Propranolol the post-exercise serum potassium levels were higher than in the subjects receiving Metoprolol. Three days after cessation of the medication these differences were no longer perceptible.

Our findings confirm the existence of a beta-receptor regulated potassium transport system in human skeletal muscle and indicate that the transmembranous potassium transport in human skeletal muscle is predominantly regulated via beta₂-receptors, although beta₁-receptors seem also to be involved. The registered differences in serum potassium levels possibly contribute to the unequal impairment of physical performance capacity under beta₁- as opposed to non-selective beta-blockade.