Exercise-induced lipolysis and hormones possibly involved in the regulation of lipid metabolism in association with exercise (plasma catecholamines, ACTH, HGH, TSH, insulin) were studied in 11 WHO stage 1 to 2 hypertensive men (mean age 37 years) during a 30-min steady-state submaximal (65% of VO2 max) and near-maximal exercise seated on a bicycle ergometer. To assess the contribution of the sympathetic system to the regulation of lipolysis and to define the type of beta-receptors mediating the catecholamine effects on lipolysis, all patients were again studied under identical conditions after a 4-week treatment with the beta-1-beta-2-receptor antagonist pindolol (15 mg daily) and with the beta-1-receptor blocker acebutolol (500 mg daily). Eight patients were even restudied after a 16-month treatment with acebutolol. Plasma glycerol levels increased progressively (P less than 0.001) during exercise reflecting increased exercise-induced lipolysis. The concomitant significant rise of noradrenaline, adrenaline, ACTH, and HGH and the parallel fall in plasma insulin suggest that all these hormones are involved in the adjustment of exercise-induced lipolysis. However, the impaired catecholamine-induced lipolysis under beta-receptor blockade was not accompanied by significant compensatory increases of ACTH, HGH, or TSH or a fall in insulin during exercise. Both beta-receptor antagonists resulted in a similar 27% inhibition of lipolysis confirming that the catecholamine-induced increase of lipolysis is mainly mediated via beta-1-adrenoceptors. After 16 months of treatment with acebutolol, the degree of inhibition of the exercise-induced lipolysis was unchanged. However, FFA were significantly reduced (28%, P less than 0.05) and HGH significantly (100%, P less than 0.05) increased.