Sympathetic and Immune Interactions During Dynamic Exercise Mediation Via a f-Adrenergic-Dependent Mechanism

Background. The relation between the sympathetic nervous system and the immune system has not been fully defined. Recent investigations have suggested an adrenergically driven efflux of specific P2-receptorrich lymphocyte subsets into the circulation with either exercise or infusion of exogenous catecholamines. Methods and Results. To determine whether acute sympathetic stimulation mediates immunoregulatory cell trafflic and function via a A3-receptor mechanism, we exercised 20 healthy volunteers before and after 1 week of treatment with either the nonselective (-antagonist propranolol or the PI-selective antagonist metoprolol. Before treatment, exhaustive exercise according to the Bruce protocol led to a marked lymphocytosis. Tsupporicotoxc (Tj,,) and natural killer cells, subtypes with the largest density of p-receptors, showed the most pronounced increases after exercise, with less impressive elevations in Th,1pe, and B cells. With respect to function, exhaustive exercise led to a decrease in concanavalin A-stimulated IL-2 receptor expression and [3lHlthymidine incorporation while enhancing natural killer cell activity. One week of propranolol therapy blunted the exercise-induced increases in circulating T,S/ and natural killer subpopulations as well as the previously observed alterations in cellular immune function. Treatment with the P,-selective antagonist metoprolol, however, did not impair the influence of exercise on any of the above parameters. Conclusions. Acute sympathetic stimulation by exhaustive exercise leads to selective release of immunoregulatory cells into the circulation with subsequent alterations in cellular immune function, either secondary to subset changes or as a result of direct catecholamine effects on function. These changes are attenuated by propranolol but not metoprolol, suggesting a (32-mediated mechanism. (Circulation 1992;86:203-213)