Physical training increases insulin stimulated glucose uptake in adipocytes and decreases insulin secretion from pancreatic islets. The mechanism behind these adaptations is not known. Because in acute exercise adrenergic activity influences both adipocytes and pancreatic islets, the sympathetic nervous system was examined as the possible mediator. Rats were either adrenodemedullated or sham adrenodemedullated and underwent either unilateral abdominal sympathectomy or were sham sympathectomized. Resting plasma adrenaline concentration in adrenodemedullated rats was 32% of the concentration in sham adrenodemedullated rats (P < 0.0001) and muscle noradrenaline content in sympathectomized leg was 9% of content in sham sympathectomized leg (P < 0.0001). After operations rats were either swim trained for 10 weeks or remained sedentary. Insulin stimulated 3-O-[14C]methylglucose transport was measured in adipocytes from epididymal fat pads, and insulin secretion and glucose metabolism were measured in glucose stimulated pancreatic islets. Training increased insulin stimulated glucose transport in adipocytes (P < 0.0001) and decreased their size (P < 0.0001), but neither adrenodemedullation nor sympathetic denervation affected these parameters significantly. Training decreased insulin secretion (P < 0.01) and increased glucose oxidation (P = 0.02) and utilization (P = 0.08) in pancreatic islets, but none of these parameters was affected significantly by adrenodemedullation. It is concluded that adrenergic activity is not important for the training induced decrease in size and increase in insulin stimulated glucose transport of adipocytes. Neither is an intact adrenal medulla necessary for training-induced adaptations in pancreatic beta cell function. Finally, in response to training, beta cell insulin secretion and glucose metabolism changed in opposite directions.