Mechanisms of Exercise-Induced Cardiac Remodeling Differ Between Young and Aged Hearts

Emily E. Schmitt; Benjamin D. McNair; Sydney M. Polson; Ross F. Cook; Danielle R. Bruns


Exerc Sport Sci Rev. 2022;50(3):137-144. 

In This Article

Abstract and Introduction


Aging induces physiological and molecular changes in the heart that increase the risk for heart disease. Several of these changes are targetable by exercise. We hypothesize that the mechanisms by which exercise improves cardiac function in the aged heart differ from those in the young exercised heart.


Regular exercise is widely recognized to induce beneficial cardiac adaptations and is among the most cardioprotective interventions identified to date. Cross-sectional studies in humans strongly support the notion that lifelong physical activity is associated with fewer or delayed age-related changes in the heart in both males and females.[1,2] In addition, exercise protects against cardiovascular disease and is a significant component of cardiac rehabilitation. This well-established protection by exercise occurs through modification of risk factors, activation of biochemical mechanisms to protect the heart against stress, and exercise-induced cardiac remodeling. Exercise-induced cardiac remodeling is defined as structural and functional changes to the heart due to changes in cardiac size, mass, geometry, and function.[3] Although exercise-induced cardiac remodeling has been well described in the young heart, the mechanisms by which the aged heart undergoes these structural and functional changes are less clear and are likely distinct from those in the young. To date, few investigations have directly compared exercise-induced cardiac remodeling in the young and aged hearts, and much of what is known about exercise-mediated cardioprotection has been extrapolated from findings reported uniquely in young or aged animals, rather than a rigorous comparison of the two age groups under the same study design. The purpose of this brief review is to identify several mechanisms by which exercise protects the heart and to discuss how these adaptations differ in young and aged hearts. We hypothesize that exercise-induced cardiac remodeling is age specific, resulting in distinct molecular and physiological mechanisms in the aged heart compared with the young. We discuss exercise-induced cardiac remodeling in the setting of chronic adaptations to exercise training, although acute increases in cardiac work also likely differ between young and aged models. Furthermore, although our focus is on cardiac remodeling, we suspect that changes in cardiovascular disease risk factors and activation of cardioprotective pathways also vary in young and aged organisms in response to chronic exercise.