Mechanisms for the responses of cardiac muscle to physical activity in old age

The decline of maximal cardiac output (Qmax) is a major factor responsible for the lower maximal oxygen consumption of elderly mammals. The lower Qmax is associated with aging-related decreases in maximal heart rate (HR-max) and maximal stroke volume (SVmax). The mechanism(s) for the slower HRmax, u...

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Bibliographic Details
Published in:Medicine and science in sports and exercise 1994-05, Vol.26 (5), p.561-567
Main Authors: Tate, C A, Hyek, M F, Taffet, G E
Format: Article
Language:English
Subjects:
Aged
Aging - physiology
Calcium-Transporting ATPases - genetics
Calcium-Transporting ATPases - metabolism
Cardiac Output - physiology
Heart - physiology
Heart Rate - physiology
Humans
Motor Activity - physiology
Myocardial Contraction - physiology
Myosins - genetics
Myosins - metabolism
Sarcoplasmic Reticulum - enzymology
Space life sciences
Stroke Volume - physiology
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Summary:The decline of maximal cardiac output (Qmax) is a major factor responsible for the lower maximal oxygen consumption of elderly mammals. The lower Qmax is associated with aging-related decreases in maximal heart rate (HR-max) and maximal stroke volume (SVmax). The mechanism(s) for the slower HRmax, unchanged by exercise training, is unknown. The decrement in SVmax, however, can be improved, as shown by the enhanced systolic and diastolic properties of the elderly heart after exercise training. One major problem is diastolic dysfunction observed in the absence of disease. Diastolic dysfunction (a decrease in peak ventricular filling after systole or a prolonged relaxation of contracted muscle) results from in part a downregulation of the sarcoplasmic reticulum's (SR) calcium ATPase that sequesters cytosolic calcium via the hydrolysis of ATP. Exercise training of sedentary old mammals produces a faster relaxation and an upregulation of the SR calcium ATPase. Yet the characteristic shift of myosin toward the slower isoform is unaltered by exercise training. The molecular signals and mechanisms underlying these aging-related alterations in sedentary and physically active individuals are unknown. An enhancement of cardiac function by exercise training, though, is preserved in advanced age.
ISSN:0195-9131
DOI:10.1249/00005768-199405000-00007