Pathologic vasoconstriction of epicardial vessels in response to 7.2 μg of acetylcholine was reduced by 54% after 4 weeks of exercise training. In contrast, the sensitivity of vascular smooth muscle for sensing exogenous NO does not seem to be altered by exercise training, suggesting that the early phase of vascular remodeling does not primarily involve vascular smooth muscle.33 NO also appears to be of minor importance in regard to the vasorelaxation of small arterioles with diameters <100 μm, because these vessels are primarily regulated by myogenic factors.41, 42, Further remodeling in response to long‐term exercise training involves the expression of cytokines and growth factors (eg, vascular endothelial growth factor A, transforming growth factor ß, platelet‐derived growth factor, fibroblast growth factors 1 and 2, and insulin‐like growth factor), which leads to the proliferation and growth of endothelial cells and smooth muscle cells and ultimately drives the arteriolarization of capillaries2, 43, 44, 45, 46 (Figure 2). Lack of exercise also is associated with coronary artery disease and some of its risk factors, as well. In patients with acute coronary syndrome, studies have shown that cardiac catheterization can decrease heart attacks and improve survival. Coronary artery calcification (CAC) is correlated with CHD events. 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