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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1239.)
© 2002 American Heart Association, Inc.

Letters to the Editor

Exercise-Induced Suppression of Postprandial Lipemia: A Possible Mechanism of Endothelial Protection?

Pornpat Chandrruangphen; Peter Collins

Department of Cardiac Medicine, National Heart and Lung Institute, Imperial College School of Medicine, London, United Kingdom

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We wish to propose a novel hypothesis of how exercise may beneficially modulate endothelial function. The benefit of exercise in the prevention of cardiovascular disease is undisputed, but the underlying mechanisms responsible for this beneficial effect, which are independent of traditional cardiovascular risk factors, remain poorly understood. Recently, attention has been focused on the influence of exercise on the endothelium, its functions, and its interactions with blood components.^1,2 Exercise training enhances NO and suppresses endothelin-1 production by the endothelium,³ thus potentially shifting the balance toward vasodilation and anti-atherosclerosis. Improved endothelium-dependent vasodilation (EDV) in both the coronary and peripheral vessels following exercise training has been demonstrated by a number of studies in human subjects of different age and risk groups.^4,5 In hypercholesterolemic patients, this improvement is independent of fasting lipid profile modification.⁶

In cell culture experiments, shear stress induces an upregulation of endothelial NO synthase with resultant increase in NO production and release. With exercise training of small muscle groups, such as a handgrip exercise, the local increase in blood flow directly enhances EDV through shear stress mechanisms.⁷ However, dynamic exercises that use larger muscle groups, such as bicycle ergometer training, produce a systemic enhancement of EDV.^4,8 In this setting, the systemic increase in shear stress is small, and it has been suggested that the systemic enhancement of EDV may be the result of metabolic or neurohormonal factors, which are modified by exercise.⁹ However, to date no likely candidates have been identified.

It has long been known that exercise training lowers . . . [Full Text of this Article]