Physical exercise in rats provokes an increase in plasma glucagon and free fatty acid concentrations. The persistence of exercise-induced glucagon stimulation in adrenodemedullated animals and conversely, its inhibition by immunosympathectomy, (-)-ropranolol, and pindolol substantiate the conclusion that stimulation of the alpha2 cells in exercise involves sympathetic stimulation of the beta-adrenergic receptors. The reduction of free fatty acid mobilization by immunosympathectomy and (-)-propranolol and its persistence after adrenodemedullation suggest that it is similarly mediated, at least in part, by adipose cell beta-sympathetic receptors.