Chronic exercise enhances endothelium-mediated dilation of epicardial coronary artery in conscious dogs.

Abstract

Whether endothelium-derived relaxing factor (EDRF)/nitric oxide (NO) plays a role in the dilation of the left circumflex coronary artery during acute exercise and whether endothelium-mediated dilation of this artery is altered after chronic exercise training have not been determined previously. Nine dogs were chronically instrumented for measurements of systemic hemodynamics, left circumflex coronary artery diameter, and blood flow. Acute treadmill exercise (10.9 km/h) caused dilation of the circumflex coronary artery by 4.33 +/- 0.84% and an increase in coronary blood flow by 32 +/- 5.2 mL/min. After the administration of intravenous nitro-L-arginine, the dilation of the circumflex coronary artery was converted to vasoconstriction (-4.13 +/- 1.58%), whereas the increase in coronary blood flow was not altered (24 +/- 3.6 mL/min). Chronic exercise training (2 hours each day at a speed of 10.9 km/h for 7 days) enhanced acetylcholine-induced dilation and reactive dilation (following release of a brief coronary artery occlusion) of the large coronary artery (P < .05), whereas the coronary blood flow responses were not changed. These enhanced acetylcholine-induced and reactive dilations of the circumflex coronary artery were due to a greater release of EDRF/NO since they were eliminated by nitro-L-arginine. Thus, in the circumflex coronary artery, EDRF/NO-dependent dilation was enhanced after 7 days of exercise training. This may represent the mechanism responsible for the perception that chronic exercise induces cardiovascular "well being."

Endothelial Flow-Mediated Dilatation and Exercise Capacity in Highly Trained Endurance Athletes

“…Furthermore, Kingwell et al (1996) demonstrated that enhanced vascular reactivity to acetylcholine in young endurance-trained athletes compared with age-matched sedentary control subjects. Animal experiments have also shown the effects of exercise training on endotheliumdependent responses, both in the resistance and conduit vessels of the coronary and peripheral circulation (Wang et al 1993;Muller et al 1994;Oltman et al 1995). FMD, has consistently been improved by exercise training in a variety of models (Koller et al 1995).…”

Exercise Training Improves Vascular Endothelial Function in Patients with Type 1 Diabetes

“…Endothelial L-arginine uptake, the substrate of NO production, is increased (23); further, NO synthase gene expression in endothelial cells is augmented (24) and NO release of endothelial cells is increased (25). In animals, enhanced NO synthase gene expression, higher NO production, and increased endothelium-dependent dilation of coronary arteries were associated with training (26). Inactivation of NO by oxygenderived free radicals is an important mechanism of endothelial dysfunction in diabetes (27).…”

Modulation of blood flow and tissue perfusion by endothelium‐derived relaxing factor

“…Expression of eNOS is enhanced by exposure of endothelial cells to fluid shear stress over periods of hours, thus explaining up-regulation of the EDRF response to both flow and agonists by relatively short term (-1 week) chronic exercise training in dogs and the increased flow associated with arteriovenous fistulae (Miller & Vanhoutte 1988;Miller & Burnett, 1992;Nishida et al 1992;Wang, Wolin & Hintze, 1993). The response to exercise training may extend throughout the vascular tree, as a 3-fold increase in eNOS is found not only in epicardial conduit arteries but also coronary microvessels (Sessa, Pritchard, Sayedi, Wang & Hintze, 1994).…”