[Aging of heart function in man].

In normal subjects at rest neither heart rate nor ejection volume are influenced by age. The loss of elasticity of the great arteries, and in particular the aorta which becomes tortuous and wider, results in an increase of impedance at ejection. At systole time pressure rises in the whole cardiovascular system, so that the left ventricle is subjected to an increase of parietal tension to which it adapts itself by hypertrophy which normalizes this tension. Ejection fraction and end-systolic volume are thus preserved, and the systolic function at rest globally remains unmodified by age. The delay and slowing down of relaxation due to hypertrophy of the left ventricle, to the reflection waves and to other changes in cardiac muscle physical properties during senescence reduce the importance of the initial phase of left ventricular filling. This major modification of diastolic dynamics at rest is compensated, at the end of diastole, by a more vigorous contraction of the left atrium, which increases its contribution to left ventricular filling. The global filling volume is thus preserved and the end-diastolic volume remains appropriate, these two conditions being necessary to start off a normal ejection. In normal subjects at exercise the cardiac function is also modified by age. Maximum heart rate is reduced in the elderly, whereas the ejection volume increases more than in younger subjects, which maintains the appropriate cardiac output. This adaptation takes place owing to an increase of cardiac volume and through Starling's mechanism which ensures a greater ejection volume. Only the maximum exercise level (VO2 max) decreases with age, mainly because of the decrease of skeletal muscle mass. Filling of the left ventricle seems to continue to rely, at rest as at exercise, on atrial compensation. Cardiac output therefore is globally maintained with age during a dynamic effort. During isometric exercise, which in the elderly results in a higher rise in blood pressure, the ejection fraction decreases, the end-systolic volume increases and the initial filling decreases but is compensated by a greater contribution of the atrium. Thus, cardiac work at rest and during exercise is well preserved in the ageing man, due to secondary homeostatic adaptations which counterbalance the primary age-related changes. The principal primary changes are loss of elasticity of the great vessels and reduction of efficacy in response to adrenergic stimulation. The principal secondary adaptations are left ventricular hypertrophy, increased atrial contribution and, during exercise, intervention of Starling's mechanism.