Cardiovascular sensitivity to epinephrine in the trained and untrained states.
Heart rate (HR), blood pressure (BP) and inotropic responses to acute exercise are partially mediated by sympathetic stimulation. Physical conditioning reduces exercise HR and improves maximal stroke volume and cardiac output. Uncertainty exists regarding the role of altered catecholamine sensitivity in producing these changes in man. In 6 highly trained men, noninvasive methods were used to serially assess the effect of cessation of training on the resting HR, BP and left ventricular contractile function in response to constant epinephrine infusion. Plasma epinephrine concentration during infusion did not vary with inactivity and was similar to that attained with strenuous exercise. Two subjects showed an increase in chronotropic sensitivity to epinephrine and 4 showed no consistent change. Despite a significant decline in exercise capacity and no apparent change in cardiac loading conditions, there was no persistent effect of inactivity on BP or left ventricular function as assessed by echocardiography and systolic time intervals. Therefore, an alteration in sensitivity to epinephrine is unlikely to account for the hemodynamic adaptations to endurance exercise training in healthy men.
D000222:Adaptation, Physiological; D000328:Adult; D001794:Blood Pressure; D002320:Cardiovascular Physiological Phenomena; D002319:Cardiovascular System / Q000187:drug effects*; D004452:Echocardiography; D004837:Epinephrine / Q000097:blood / Q000494:pharmacology*; D006339:Heart Rate; D006801:Humans; D008297:Male; D009200:Myocardial Contraction; D010101:Oxygen Consumption; D010806:Physical Education and Training; D005082:Physical Exertion; D013318:Stroke Volume
D004837:Epinephrine