Regular endurance exercise training increases oxygen transport and utilization 15-25 % by causing structural and regulatory adaptations of the cardiovascular system. The primary adaptations include expansion of plasma volume and intrinsic and neurally mediated adjustments in the heart and vasculature. Autonomic neural activity and hormonal and intrinsic cardiac pacemaker activity constitute redundant mechanisms that contribute to the reduction of heart rate at rest and during submaximal exercise. The arterial baroreflex has greater heart rate responses due to increased vagal tone but the sympathetic arm of the baroreflex is inhibited by an increased central blood volume load on the cardiopulmonary baroreceptors resulting in a greater sympathoinhibition. Other hormonal influences increase vagal tone; these include an up-regulation of dopaminergic receptors and a down-regulation of enkephalin receptors in the heart. Aortic rheoreceptor activation by the increased stroke volume and decreased reflex signals from the trained skeletal muscles also reduce sympathetic outflow to the heart and vasculature. The mechanism by which intrinsic heart rate is lowered remains unexplained but appears to involve structural adaptation within the pacemaker cells.