It has been reported that catecholamine release is associated with stressful events and that adrenaline administration induces hyperfibrinolysis. To examine the possible involvement of the adrenoreceptor mechanism in the regulation of fibrinolytic activity at rest and to maximum exercise, 12 healthy volunteers (six males and six females, age range 19–21 yr) were orally medicated with two formulations of a beta blocker. The drug treatments consisted of 1) a single dose of OM756 alpha 10 mg propranolol “Inderal” tablet, 2) a single dose of a generic 10 mg propranolol tablet, and 3) a single dose of generic placebo. The drug administrations were assigned to the subjects using a complete Latin square design and double-blind procedure and were separated by 7 d. Two hours after the administration of the respective drug treatment, subjects exercised to maximal capacity using a graded exercise protocol on a bicycle ergometer. Prior to and 2 h after the drug administration and immediately after maximum exercise, heart rate, blood pressure, and oxygen consumption were measured and venous blood was removed and analyzed for fibrinolytic activity using a standard fibrin plate method. ANOVA showed that the resting and maximum heart rates were significantly reduced (P< 0.05) following oral premedication with either of the two formulations of beta blocker, while blood pressure and oxygen consumption were unaffected. ANOVA also showed no difference in the resting fibrinolytic activity 2 h post-administration of the drug treatments but a significant decrease (P< 0.05) in the normal fibrinolytic response to maximum exercise. It was concluded, therefore, that the resting level of fibrinolytic activity is not mediated via an adrenergic pathway but that the enhanced fibrinolytic activity to maximum exercise is partially regulated via an adrenoreceptor mechanism.