The extent of physical activity and the dynamic performance capacity show an inverse relationship to cardiovascular mortality, independent of the influence of other risk factors, but the underlying mechanism remains uncertain. Most concepts assume that the aerobic capacity of the peripheral musculature is increased by training, and thus improved cardiocirculatory regulation and especially a more favorable stress reaction pattern are attained. This adaptation is essentially an inverse adaptation mechanism as in established cardiocirculatory insufficiency. Based on an extended stress concept, it can be seen that training effects, especially in autonomic circulatory regulation, occur under physiological conditions to a lower degree in the renin-angiotensin-aldosterone system and in inflammatory reaction. The training effects depend on the form of exercise, the baseline condition, the extent of training, and genetic predisposition. It can be particularly demonstrated when the aerobic capacity has been sufficiently enlarged in an adequate proportion of the peripheral musculature. To what extent and under what conditions these training effects can be used under the pathophysiological conditions of established cardiocirculatory insufficiency is presently under investigation.