Previous studies in our laboratory indicate that a marked rise in plasma pancreatic glucagon occurs in rats subjected to non-exhausting exercise (forced swim or FOSWI). Male albino rats fas led overnight Were subjected to FOSWI for thirty to sixty minutes in tepid water. Blood for glucose, free fatty acids, insulin and glucagon determinations was obtained by cardiac puncture immediately after exercise or after a rest period in control animals. The FOSWI-induced rise in plasma glucagon was of pancreatic origin since it was significant with an antiserum highly specific for pancreatic glucagon and an antiserum weakly cross-reacting with gut GLI but absent with a nonspecific antiserum. Theglucagon rise was even more important in hypophysectomized rats. Intraperitoneal glucose injection (0.2 gnu per kilogram) decreased plasma glucagon in resting animals but did not abolish FOSWI-induced glucagon secretion. Adrenalectomy slightly reduced the glucagon response to FOSWI, whereas propranolol pretreatment (5 mg per kilogram intraperitoneally) completely blocked the glucagon rise. Phentolamme (25 mg. per kilogram) increased blood glucose, plasma IRI and glucagon in resting animals. FOSWI did not further increase the already elevated glucagon levels in the phentolamine-treated rats. The exercise-induced glucagon rise persisted in rats pretreated with phentolamine (5 mg. per kilogram) and practolol (12.5 mg. per kilogram). It is concluded that catecholamines and, in particular, sympathetic innervation of the islets play a major role in the exercise-induced glucagon secretion ana tfiat the adrenergic receptors involved are likely of the β2 type.