Abstract

Current hemodynamic dogma suggests that the increase in central blood pressure during exercise is largely driven by augmentation of pressure from wave reflections. However, this hemodynamic presupposition lacks teleological and physiological support. During dynamic aerobic exercise, there are marked reductions in terminal impedance because of peripheral metabolic vasodilation. Moreover, despite an increase in central artery stiffness and potential muscle pump–mediated pressure counterpulsations during exercise, increases in aortic diameter coupled with peripheral vasodilation and reductions in peripheral artery stiffness result in central-peripheral impedance matching favorably altering pressure wave timing/magnitude. This hemodynamic milieu would foster transmission of minimal wave reflections and thus optimize ventricular–vascular …

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