Plasma potassium rises during muscular exercise and falls rapidly when exercise is stopped. Since the sympathoadrenal system is stimulated with exertion and both α- and β-adrenergic agonists affect internal potassium homeostasis, we studied the influence of catecholamines on potassium shifts during and after exercise. Six healthy subjects were given maximal exercise stress tests under three conditions: with no medication (control), during β-blockade with propranolol, and during α-blockade with phentolamine. Compared with a peak rise in plasma potassium of 1.23±0.27 mmol per liter (mean ±S.E.M.) during the control study, propranolol caused a rise of 1.89±0.35 (P<0.01) and a sustained elevation during recovery. Phentolamine diminished the rise of potassium (0.70+0.21 mmol per liter; P<0.01) and lowered the potassium level throughout recovery. These effects of catecholamines were independent of the venous pH, the plasma bicarbonate and serum glucose levels, and urinary potassium excretion, and they did not appear to be due to insulin. High norepinephrine and epinephrine levels confirmed the release of catecholamines capable of stimulating α- and β-receptors. Exercise work did not differ among the groups. β-Adrenergic receptors appear to moderate the acute hyperkalemia of exercise, whereas α-adrenergic receptors act to enhance hyperkalemia and may protect against hypokalemia when exertion ceases. (N Engl J Med 1985; 312:823–7.).
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