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Department of Physiology, University of Michigan, Ann Arbor, Michigan 48109-0622
The Fischer 344 x Brown Norway (F344xBN) rat
has been demonstrated to have a lower incidence of age-related
pathology than other rat strains. Therefore, 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 
-myosin heavy
chain with advanced age and a significant rightward shift in the
tension-pCa curve 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 from 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 in either the
relengthening parameters or the Ca2+ transient, indicating
that relaxation is not directly altered by aging. This latter finding
is at variance with previous studies in rat strains with higher rates
of pathology. We conclude, therefore, that the primary effect of aging
in isolated cardiac 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 compensatory mechanisms induced by pathological conditions.
calcium transient; muscle mechanics
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