Key result
Exercise slows cardiac aging and lowers HF risk by improving endothelial function and reducing fibrosis.
Why the study?
Aging causes structural and functional cardiac deterioration that increases heart failure risk, prompting interest in exercise-mediated molecular and cellular adaptations that could serve as therapeutic targets.
Does exercise prevent age-related cardiac deterioration and mitigate the risk of heart failure in aging populations?
Does exercise prevent age-related cardiac deterioration and mitigate the risk of heart failure in aging populations?
Exercise promotes cardiac resilience during aging by mitigating pathological remodeling, restoring endothelial function, and reducing fibrosis, highlighting its value in preventing age-related heart failure.
Hypothesis-generating for exercise in aging; leaves open whether RCTs will confirm benefits before changing practice.
Aging leads to structural and functional deterioration of the heart, reducing its capacity to withstand internal and external stressors and consequently increasing the risk of heart failure. Exercise is a potent modulator of cardiovascular and metabolic health, offering numerous physiological benefits that can persist throughout the aging process. Studies suggest that exercise can decelerate age-related cardiac deterioration and mitigate the risk of heart failure. In this review, we discuss recent advances in our understanding of exercise-mediated molecular and cellular adaptations that could serve as therapeutic targets for age-related cardiac remodeling and functional decline. We also explore how exercise-induced changes may enhance cardiac resilience with age, examine sex differences in cardiac aging and response to exercise, and highlight the value of murine exercise models as research tools for identifying novel therapeutic targets and strategies to combat heart failure.
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Saini et al. (2025) conducted a review in Cardiac aging and heart failure. Exercise vs. Sedentary lifestyle was evaluated. Exercise decelerates age-related cardiac deterioration and mitigates the risk of heart failure by promoting physiological cardiac growth, improving endothelial function, and reducing cardiac fibrosis.
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