LAUSR

Numerous scientific findings have concluded that individuals who are active tend to develop less cardiovascular disease than those who enjoy more sedentary lifestyles. Animal models have further demonstrated that the beneficial effects of training on the heart effects of training are related to the signaling pathways of myocardial hypertrophy and fibrosis. As such, fibroblasts represent a very important population of cells within the myocardium as they play a crucial role in both cardiac development and response to injury. Fibroblasts establish and maintain the biochemical, electrical and mechanical environment of the heart through their complex interactions with cardiomyocytes. Cardiac injury disrupts the balance between fibroblasts and cardiomyocytes and creates a state favouring inflammation and fibrosis. Although this adaptive response initially serves to increase wound healing, it may eventually lead to increased cardiac damage and cardiac failure if homeostasis is not restored. Myofibroblasts are mediators of both the adaptive and maladaptive components of this reaction. This review focuses on the beneficial effects of exercise in cardiac fibrosis as demonstrated in basic research studies. Attention will be given to the characterisation of the relationship between exercise and cardiac remodelling, including the cellular and molecular adaptations of the heart in response to exercise as well as benefits of exercise in preventing or reversing the pathological remodelling of the fibrotic heart. By furthering our understanding of the beneficial and deleterious roles of cardiac fibroblasts and myofibroblasts and how these roles are related to each other in cardiac development and in heart disease, we may be able to design interventions to prevent the progression of cardiac fibrosis.