Obesity is associated with an elevated risk of pathological cardiac hypertrophy, whereas exercise confers cardioprotective effects; however, the cellular mechanisms underlying these opposing influences remain incompletely defined, particularly in females. We investigated how obesity and exercise affect cardiomyocyte ultrastructure, Ca2+ release, and contractility in female Zucker Diabetic Fatty rats and their lean littermates. Animals were assigned at 12 weeks to sedentary or aerobic exercise-trained groups and maintained on a standard diet. By 18 weeks, obese rats exhibited increased body mass and myocardial hypertrophy in the absence of diabetes. Sedentary obese animals showed a reduced fraction of compact dyads and diminished stimulated and caffeine induced Ca2+ release, while contractility remained preserved. In lean rats, exercise increased dyad density but reduced Ca2+ release, whereas in obese rats, exercise enhanced both dyad compactness and Ca2+ release. Across all groups, global cardiomyocyte ultrastructure and contractile function were similar. Type III ANOVA revealed a significant obesity x exercise interaction for dyadic structure and Ca2+ release. These findings demonstrate that obesity itself, independent of diabetes, triggers early dyadic remodeling and altered Ca2+ handling in female myocardium before detectable impairment of global cardiomyocyte structure or contractile function. Furthermore, exercise exerts beneficial effects on dyadic ultrastructure and Ca2+ signaling in obese animals.
Novak, A., Baglaeva, I., Nejati Bervanlou, R., Iaparov, B., Zahradnikova, A., Cagalinec, M., Novotova, M., Zahradnikova, A.
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