The extent of physical activity and the dynamic performance capacity show a
n inverse relationship to cardiovascular mortality, independent of the infl
uence of other risk factors, but the underlying mechanism remains uncertain
. Most concepts assume that the aerobic capacity of the peripheral musculat
ure is increased by training, and thus improved cardiocirculatory regulatio
n and especially a more favorable stress reaction pattern are attained. Thi
s adaptation is essentially an inverse adaptation mechanism as in establish
ed cardiocirculatory insufficiency.
Based on an extended stress concept, it can be seen that training effects,
especially in autonomic circulatory regulation, occur under physiological c
onditions to a lower degree in the renin-angiotensin-aldosterone system and
in inflammatory reaction. The training effects depend on the form of exerc
ise, the baseline condition, the extent of training, and genetic predisposi
tion. It can be particularly demonstrated when the aerobic capacity has bee
n sufficiently enlarged in an adequate proportion of the peripheral muscula
ture. To what extent and under what conditions these training effects can b
e used under the pathophysiological conditions of established cardiocircula
tory insufficiency is presently under investigation.