ABSTRACT
Habitual endurance exercise promotes improved heart function in both young and old populations, while chronic inactivity impairs cardiac function and elevates the risk of heart disease. As we grow older contractile function of the heart and work capacity are reduced as a function of impaired Ca2+ homeostasis and mechanical remodeling. Mechanical remodeling in the heart that occurs with advancing age includes (a) loss of cardiac myocytes, (b) hypertrophy and weakness of the remaining cardiac myocytes, and (c) increased connective tissue and altered geometry. Mounting evidence indicates that oxidative stress, mitochondrial dysfunction, and impaired stress response contribute to the etiology of age-induced mechanical remodeling. Our laboratory has collected novel data which demonstrate that exercise training ameliorates apoptosis, linked to the mitochondrial Bcl-2 pathway, as well as accumulation of connective tissue in the aging rat heart. Recent interest has also focused on fi brosis, which limits
early diastolic fi lling in the heart. However, there is a paucity of studies seeking to elucidate the upstream mechanisms by which exercise training mitigates ageinduced remodeling, including cardiomyocyte apoptosis and fi brosis, in the heart. Th e lack of such knowledge impedes progress in elucidating the mechanisms by which exercise protects against impaired cardiac function in aging populations.
