Regular exercise training confers beneficial effects to the heart as well as to the entire body. This occurs partly because exercise training improves skeletal muscle work capacity and reduces resistance, thus increasing conductance in the peripheral circulation. More directly, exercise training also alters extrinsic modulation of the heart and improves the intrinsic pump capacity of the heart. Together, these effects allow for improved exercise capacity. Accumulating evidence suggests that the magnitude of these benefits increases proportionally with the intensity of individual exercise training sessions constituting the exercise training program. It has emerged that regular exercise training also confers beneficial effects to patients at risk for, or who have, established heart dysfunction and disease and, moreover, that exercise training may reduce the dysfunction of the heart itself and, at least, partly restore its ability to effectively function as a pump. The most recent studies in patients with established heart disease suggest that a high relative, yet aerobic, intensity of the exercise training improves the intrinsic pump capacity of the myocardium, an effect not previously believed to occur with exercise training. However, more and larger studies are needed to establish the safety and efficacy of such exercise training in patients with heart disease. Here, we consider the nature of the intensity dependence of exercise training and the causes of the improved heart function.
Recent trials suggest that exercise training in the management of heart disease may be more effective if carried out with a high relative aerobic intensity, although safety and efficacy remain unclear. This review discusses these trials, including why high-intensity exercise training may improve the cardiac pump function.
Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow, United Kingdom (Dr Kemi); and Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway (Dr Wisløff).
Corresponding Author: Ole Johan Kemi, PhD, Institute of Biomedical and Life Sciences, University of Glasgow, West Medical Bldg, Glasgow, G12 8QQ, United Kingdom (firstname.lastname@example.org).