Abstract
In an era of molecular biology, “gene therapy,” and increasingly sophisticated technological approaches to treat cardiovascular disease, it is easy to overlook the physical forces generated by and acting on the human cardiovascular system. In this issue of Circulation , Tanaka and colleagues1 report that aerobic exercise training can blunt the age-associated stiffening of large blood vessels in humans. In this context, why is this important, what are some of Tanaka and colleagues’ key observations, and what mechanisms might explain them? It is well known that arterial compliance declines with age even in healthy individuals with no overt cardiovascular disease.2 3 4 This means that the large conducting vessels (ie, the aorta and its major branches) all lose their ability to distend in response to an increase in pressure. As a consequence of this stiffening, when blood is ejected from the heart during systole, there is a smaller change in arterial diameter with aging, and this reduction in arterial compliance appears to be an independent risk factor for the development of cardiovascular disease.5 6 This reduction in compliance also contributes to isolated systolic hypertension in the elderly. Additionally, as the vessels stiffen, the physical forces that oppose aortic valve opening increase and can contribute to ventricular hypertrophy, aortic root dilation, valvular dysfunction, and heart failure.2 3 4 5 To evaluate the impact of physical activity on …
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