The Fischer 344 x Brown Norway (F344xBN) rat has been demonstrated to have
a lower incidence of age-related pathology than other rat strains. Therefor
e, to elucidate the effects of aging on cardiac function, uncomplicated by
compensatory effects caused by age-related pathology, cardiac myocytes were
isolated from female F344xBN rats at 6 (young) and 32-33 (old) mo of age.
Myocytes showed an increase in the relative amount of beta-myosin heavy cha
in with advanced age and a significant rightward shift in the tension-pCa c
urve from 5.78 +/- 0.02 pCa units in young adult myocytes to 5.66 +/- 0.03
pCa units. Consistent with a shift to a slower myosin isoform, the time fro
m stimulation to peak sarcomere shortening increased with age from 50.5 +/-
1.3 to 58.9 +/- 1.0 ms. In contrast, no age-related difference was found i
n either the relengthening parameters or the Ca2+ transient, indicating tha
t relaxation is not directly altered by aging. This latter finding is at va
riance with previous studies in rat strains with higher rates of pathology.
We conclude, therefore, that the primary effect of aging in isolated cardi
ac myocytes from the F344xBN rat model is a shift in the myosin heavy chain
isoform. Changes in relaxation seen in other rat strains may result from c
ompensatory mechanisms induced by pathological conditions.