Independent of disease, age-associated changes in cardiovascular function include anatomical, physiological, and haemodynamic alterations that are generally without pathological consequence. Decrements in adrenergic receptor response, arterial distensibility, ventricular compliance, and contractile performance seem to be compensated for by enhanced atrial contribution to ventricular filling, prolongation of systole, and increased reliance on the length-tension relationship of cardiac muscle. Summarily, these compensations constitute increased utilisation of the Frank-Starling mechanism.
Endurance training beneficially alters aging cardiovascular function both at rest and during exercise. An increase in end diastolic volume and ejection fraction demonstrate an enhancement of the length-tension relationship of myocardial tissue in maintaining resting and exercise cardiac outputs. The decline in maximal cardiovascular function is not preventable. It was also concluded that endurance exercise improves clinical and psychosocial factors that enhance the quality of life for elderly individuals.
Future research efforts should attempt to determine if and by what mechanisms endurance training may contribute to the regression of atherosclerotic lesions and the development of collateral vessels in senescent myocardium.