Chronic exercise training protects aged cardiac muscle against hypoxia.

Abstract

To test the hypothesis that chronic exercise may improve tolerance to hypoxia in aged hearts, we compared cardiac function of exercised rats to that of their age-matched, nonexercised controls. Right ventricular papillary muscles were removed from young adult (9 mo) and old (24-26 mo) male Fischer 344 rats that were chronically exercised on a rodent treadmill and from their age-matched, nonexercised controls. During isometric contraction, hypoxia depressed contraction and relaxation in all muscles, but to a lesser extent in the exercised groups. A significant exercise effect was observed in the following variables: the maximum developed tension, the maximum rate of tension development, the maximum rate of tension decline, and the time required for the hypoxia to reduce maximum tension by 20%. The maximum rate of tension decline was more sensitive to hypoxia than was the maximum rate of tension development in all groups. Exercise also had an effect on the temperature dependence of cardiac performance during hypoxia. Thus, chronic exercise results in the preservation of both contraction and relaxation during hypoxia for aged as well as young adult hearts.

Left Ventricular Diastolic Filling and Cardiovascular Functional Capacity in Older Men

“…In addition, the absence of a change in HR kinetics during the exercise transient suggests that the cardiovascular improvement of an increased stroke volume consequent to a greater ventricular pre-load was the important change with calcium channel blockade or training. Thus, the improved stroke volume appears to be secondary to an improved LVDF and ultimately a consequence of improved ventricular calcium handling (Wei et al 1989). Functional cardiovascular changes as a consequence of the improvement in stroke volume and LVDF and possible improvements in calcium handling have been previously examined.…”

“…Functional cardiovascular changes as a consequence of the improvement in stroke volume and LVDF and possible improvements in calcium handling have been previously examined. Others (Penpargkul et al 1977;Wei et al 1989) have shown that exercise training in older rats will result in improved calcium re-uptake (an energy-dependent removal of cytosolic calcium and re-uptake by the sarcoplasmic reticulum (Movsesian et al 1985), consequent improved diastolic filling and maximal exercise capacity in the absence of changes in resting systolic indices of left ventricular dysfunction. Also, in an earlier study, we have shown that verapamil ingestion alone improved LVDF and ýOµ,max (Petrella et al 1994).…”

“…A decline in diastolic filling is observed among the elderly with a sedentary life style (Cacciapuoti et al 1992) while middle-aged athletes (Douglas & O'Toole, 1992) have left ventricular diastolic filling parameters similar to the young. Following exercise training in older animals (Wei et al 1989), left ventricular filling was improved resulting in increased maximal exercise indices. In aged humans, ventricular diastolic filling is improved with exercise training and these alterations may be linked to improved maximal exercise performance (Petrella et al 1997).…”

Heart failure and the aging myocardium: Possible role of cardiac mitochondria

“…Further, when animals are chronically exercised, it results in the preservation of both contraction and relaxation during hypoxia for young and senescent hearts [76]. Senescent rats that were endurance trained for 14 months exhibited an enhanced cardiac output, stroke volume, and external work performed [49] compared with sedentary controls.…”

“…While ageassociated morphologic changes (e.g., increased left ventricular mass and interstitial fibrosis) and abnormal calcium handling are likely contributors to congestive heart failure, the importance of energetic factors, especially mitochondrial function, has remained incompletely understood. The significance of cardiac metabolism to heart disease in old age is highlighted by the findings that (1) more patients over 80 years of age have diastolic dysfunction than systolic dysfunction [88], and (2) diastole requires more oxygen and ATP than does systole [89]. While CHF and aging are clearly not identical and CHF does not necessarily result from aging, certain mitochondrial changes associated with CHF may be similar to those observed with old age.…”