Acceleration Stress and Effects of Propranolol on Cardiovascular Responses

Heart rate, arterial pressure and cardiac output were recorded in six physically well‐trained, young male volunteers in the sitting position at normal gravity and at 3 G acting in the head‐seat direction, before and after beta‐adrenergic blockade by propranolol. Studies were performed both at rest and during leg exercise at a load corresponding to 50 % of the maximal oxygen uptake. After propranolol, the heart rate response to increased G at rest averaged 38 % of that observed without blockade, indicating that G‐induced cardioaccelera‐tion is predominantly due to sympathetic stimulation. G‐induced decline of cardiac output was more marked after propranolol, this effect being entirely due to the reduced response of the heart rate. In spite of the cardioinhibitory effects of propranolol, subjective G tolerance was well preserved; the response of the arterial mean pressure to increased G was unaffected due to a 65 % rise in systemic vascular resistance as against 43 % before propranolol. Hence, sympathetic chronotropic stimulation of the heart is not essential for the circulatory defense against increased gravitational stress. Transition from rest to exercise at 3 G produced a larger increase in stroke volume than in heart rate; after beta‐adrenergic blockade the dominance of the stroke xolume increase was exaggerated.