The principal features of the cardiovascular responses to endurance training in nonnal subjects were well documented by the late 1960s (2, 23, 35, 84, 88) and are illustrated in Table 1. They include an increase in maximal oxygen uptake, stroke volume, and cardiac output with no change or a small decrease in maximal heart rate. Systemic vascular conductance increases and there is also an increase in the maximal systemic arteriovenous oxygen difference. Cardiac output at submaximal levels of work does not change significantly but the increase in stroke volume is associated with a relative bradycardia at rest and at any given submaximal level of oxygen uptake. These cardiovascular changes are produced by a complex set of central and peripheral mechanisms operating at multiple levels--eg structural, meta bolic, and regulatory (13, 14, 97). Our understanding of how these adapta tions combine to extend aerobic capacity is still incomplete. The classical concept that maximal oxygen uptake is limited by the oxygen transport capacity of the cardiovascular system (37) was challenged during the early 1970s (46) and the oxidative capacity of skeletal muscle was then by some considered to be the primary limiting mechanism. More recent work has reinforced the conclusion that functional capacity of the cardiovascular system is the principal limiting factor. Here we review the interaction between training-induced adaptations affecting the heart, the