title: Exercise training in coronary artery disease and coronary vasomotion.
abstract: Exercise training has assumed a major role in cardiac rehabilitation, mostly because of its positive effects on myocardial perfusion in patients with coronary artery disease. The mechanisms involved in mediating this key effect have long been debated: both regression of coronary artery stenosis and improvement of collateralization have been suggested as potential adaptations. However, the comparatively minute changes in luminal diameter and myocardial contrast staining do not fully explain the significant changes in myocardial perfusion. During the last decade, endothelial dysfunction was identified as a trigger of myocardial ischemia. The impaired production of endothelium-derived nitric oxide (NO) in response to acetylcholine and flow leads to paradoxic vasoconstriction and exercise-induced ischemia. Recently, it was confirmed in humans that training attenuates paradoxic vasoconstriction in coronary artery disease and increases coronary blood flow in response to acetylcholine. Data from cell-culture and animal experiments suggest that shear stress acts as a stimulus for the endothelium to increase the transport capacity for L-arginine (the precursor molecule for NO), to enhance NO synthase activity and expression, and to increase the production of extracellular superoxide dismutase, which prevents premature breakdown of NO. Exercise also affects the microcirculation, where it sensitizes resistance arteries for the vasodilatory effects of adenosine. These novel findings provide a pathophysiological framework to explain the improvement of myocardial perfusion in the absence of changes in baseline coronary artery diameter. Because endothelial dysfunction has been identified as a predictor of coronary events, exercise may contribute to the long-term reduction of cardiovascular morbidity and mortality.
authors.affiliation: Universität Leipzig, Herzzentrum GmbH, Klinik für Innere Medizin/Kardiologie, Leipzig, Germany.
authors.forename: S
authors.initials: S
authors.lastname: Gielen
authors.forename: G
authors.initials: G
authors.lastname: Schuler
authors.forename: R
authors.initials: R
authors.lastname: Hambrecht
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity / Q000502:physiology*; D001792:Blood Platelets / Q000166:cytology / Q000378:metabolism; D001809:Blood Viscosity / Q000502:physiology; D003097:Collateral Circulation / Q000502:physiology; D003324:Coronary Artery Disease / Q000473:pathology / Q000534:rehabilitation; D003326:Coronary Circulation / Q000502:physiology; D003327:Coronary Disease / Q000473:pathology / Q000503:physiopathology / Q000534:rehabilitation*; D003331:Coronary Vessels / Q000201:enzymology / Q000502:physiology* / Q000503:physiopathology; D004285:Dogs; D004730:Endothelium, Vascular / Q000166:cytology / Q000201:enzymology / Q000503:physiopathology; D005081:Exercise Therapy; D006801:Humans; D008833:Microcirculation / Q000502:physiology / Q000503:physiopathology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III; D012074:Remission Induction; D013314:Stress, Mechanical; D013482:Superoxide Dismutase / Q000145:classification / Q000378:metabolism; D014655:Vascular Resistance / Q000502:physiology
chemical_list: C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D013482:Superoxide Dismutase