Exercise training-induced coronary vascular adaptation

Abstract

Aerobic exercise training induces an increase in coronary vascular transport capacity. This increased transport capacity is the result of increases in both blood flow capacity and capillary exchange capacity. These functional changes are the result of two major types of adaptive responses, structural vascular adaptation and altered control of vascular resistance. Structural vascular adaptation occurs in response to exercise training in at least two forms, increases in the cross-sectional area of the proximal coronary arteries and angiogenesis. Angiogenesis has been demonstrated in that training causes moderate cardiac hypertrophy while maintaining or increasing capillary density and increasing arteriolar density. Training-induced changes in coronary vascular control have been shown to include altered coronary responses to vasoactive substances, changes in endothelium-mediated vasoregulation, and alterations in the cellular-molecular control of intracellular free Ca2+ in both endothelial and vascular smooth muscle cells isolated from coronary arteries of exercise-trained animals. The signal or signals for these adaptive responses remain unknown. The hypothesis that the adaptive strategy entails maintenance of normal shear stress in coronary arterial vessels is discussed. We propose that as a result of training-induced structural vascular adaptations and alterations in the control of vascular resistance, shear stress throughout the coronary vasculature is returned to the level present in sedentary animals. The signal for adaptation may be peak shear stress during exercise and/or average shear stress over a 24-h period of time.

Time-course of vascular adaptations during 8 weeks of exercise training in subjects with type 2 diabetes and middle-aged controls

“…There are limited animal data on the interaction between arterial function and structure in response to prolonged exercise training, but our findings suggest that adaptations may differ in groups with antecedent endothelial dysfunction. This may be due to differences in the impact of oxidative stress or inflammation, but future studies examining the impact of (short-and long-term) exercise training (in those with endothelial dysfunction) on a molecular level will be required to shed further light on (Laughlin and McAllister 1992;Laughlin et al 1998). Exercise training improves smooth muscle cell sensitivity in animals via the regulation of intracellular Ca 2+ and an enhanced K + channel regulation of tone (Bowles et al 2000).…”

Low-intensity interval exercise training attenuates coronary vascular dysfunction and preserves Ca2+-sensitive K+ current in miniature swine with LV hypertrophy

“…Accumulating evidence regarding the beneficial effects of exercise in stable compensated HF, combined with established exercise-induced alterations to coronary vascular function (6,15,30), illustrate the validity of examining exercise as a treatment for preserving normal coronary vascular function in HF. Although the use of exercise in this context has become largely accepted, a major area of need is the determination of the appropriate intensity, frequency, and duration for optimal health benefits in a clinical setting (11,20,27,38,40) and identification of the mechanisms underlying these responses.…”

“…Recent evidence from our laboratory and others suggests exercise training is an effective treatment in both animal models and human HF, as illustrated by improved survival and delayed onset of decompensated HF, increased peripheral flow-mediated dilation, and improved quality of life (9,17,53). The beneficial effects of exercise on coronary vascular function are well known (6,15,30). Training-induced alterations to the coronary vasculature include both increases in smooth muscle cell K ϩ channel activity (6) and reductions in coronary artery sensitivity to ET-1 mediated, in part, by an increase in smooth muscle cell K ϩ channel activation (23).…”

Von Willebrand Factor And The Right Ventricle: The MESA-Right Ventricle Study

“…16 Alternatively, elevated vWF activity may indicate coronary endothelial dysfunction accompanied by the inability of coronaries to dilate and provide increased blood flow to support cardiac growth. 1,17 Inhibiting angiogenesis and/or coronary dysfunction leads to decreased cardiac mass and volumes in otherwise healthy animal models. 18 If elevated vWF activity does reflect the inability to augment blood flow in active cardiac muscle, this may contribute to the increased mortality we previously described in patients with pulmonary hypertension and elevated vWF activity.…”