Adrenergic modulation of potassium metabolism during exercise in normal and diabetic humans.

The effect of acute and chronic beta- and alpha-adrenergic blockade on potassium homeostasis during moderate intensity exercise (40% VO2max) was investigated in control and insulin-dependent diabetic subjects. In protocol I, subjects were studied during exercise alone, exercise plus intravenous propranolol, and exercise plus intravenous phentolamine. In both the control and diabetic groups, exercise alone produced a modest increase in the plasma potassium concentration (0.31 +/- 0.06 meq/l), while propranolol exacerbated this hyperkalemic response. In contrast, the increment in plasma potassium during phentolamine was similar to exercise alone in normals but was 26% (P less than 0.05) lower in the diabetic group. In protocol II, the effect of chronic (5 days) beta-adrenergic blockade on potassium homeostasis was examined. Subjects participated in three studies: exercise alone, exercise plus propranolol (beta 1/beta 2-antagonist), and exercise plus metoprolol (beta 1 antagonist). In the nondiabetic group, both propranolol and metoprolol were associated with a 40% greater increase in potassium compared with exercise alone. In the diabetic group, propranolol, but not metoprolol, was associated with a deterioration in potassium tolerance. In no study could the alterations in potassium homeostasis be explained by a change in urinary potassium excretion. In summary, alpha-adrenergic blockade ameliorates exercise-induced hyperkalemia in diabetic but not in control subjects, nonspecific beta-adrenergic blockade causes a greater increment in potassium when compared with exercise alone, and specific beta 1-adrenergic blockade exacerbates exercise-induced hyperkalemia in control, but not in diabetic subjects. These results indicate that both alpha- and beta-adrenergic regulation of extrarenal potassium metabolism is altered in insulin-dependent diabetes mellitus.