One of the likely contributing factors to compensate for slowly developing coronary vascular disease is the enlargement of collateral blood vessels between the left and right coronary arterial systems or among parts of each system. In the healthy heart of a sedentary person, collateral arterial vessels are rare, but arteriolar collaterals (internal diameter, <100 |xm) do occur in small numbers. The expansion of existing collateral vessels and the limited formation of new collaterals provide a partial bypass for blood flow to areas of muscle whose primary supply vessels are impaired. Subendocardial arteriolar collaterals usually enlarge more than epicardial collaterals. In part, the greater collateral enlargement in the endocardium compared to the epicardium may be due to the lower pressure and blood flow in reaching the endocardial vessels.
The exact mechanism responsible for the development of collateral vessels is unknown. However, periods of inadequate blood flow to the heart muscle caused by experimental flow reduction do stimulate collateral enlargement in healthy animals. It is assumed that in humans with coronary vascular disease who develop functional collateral vessels, the mechanism is related to occasional or even sustained periods of inadequate blood flow. Whether or not routine exercise aids in the development of collaterals in healthy humans is debatable; the benefits of exercise may be by other mechanisms, such as enlargement of the primary perfusion vessels and the reduction of atherosclerosis. However, there is no doubt that frequent and relatively intense aerobic exercise is beneficial to cardiac vascular function.
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