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LETTER TO THE EDITOR
TO THE EDITOR: Perhaps the most important point put forward by Green et al. (3) regards the overall vascular tree effects promoted by exercise. It bears consideration that skeletal muscles and their vasculature remain "plastic" throughout most of the lifetime of humans, being able to remodel in positive, beneficial ways, in response to exercise (1). However, this ability to remodel also can progress in a negative direction, with a lack of exercise and weight-bearing activities associated with aging (5) and as a result of some disease processes (2). As such, the assertion by the authors that exercise training should be the cornerstone of prevention efforts (3) should likely be extended toward consideration of exercise as a lifetime therapeutic regimen, as well as after surgery, and in combination with other treatments. This approach is typically initiated with rehabilitation programs after coronary bypass surgery (1). However, the regimen is usually of a relatively brief time period, originally 1–2 mo, now as much as 3–6 mo, but typically dictated by insurance coverage and other nonmedical considerations. Thus the unmotivated postbypass patient can lapse backward toward a lifestyle that may have contributed to their original need for surgery, forcing "reductive muscle and vascular remodeling" (5), which can be detrimental and increase risk for a subsequent event. Furthermore, the statistical modeling suggesting that nearly half of risk reduction associated with exercise cannot be explained by established risk factors (4), would support the idea put forth by Green et al. (3), that refocus of investigation toward impact of exercise on vascular remodeling and function is warranted, particularly in conjunction with other therapeutic approaches.
REFERENCES
TO THE EDITOR: The article "Exercise and cardiovascular risk reduction: Time to update the rationale for exercise?" by Green et al. (3) addresses the role of exercise in the risk management of cardiovascular disease. The paper emphasizes the importance of the role of shear stress on the vasculature and the concomitant production of nitric oxide (NO), which is a recognized vasodilator. It should also be recognized the role of other local agents that cause exercise hyperemia, e.g., adenosine, potassium, prostaglandins, and ATP. The number of paracrine messengers that contribute to exercise hyperemia suggests a redundancy in the regulation of blood flow during exercise (1). They all contribute to the increase in blood flow to match the metabolic requirements of exercising muscle. Additionally, sympathetic venoconstriction increases venous return and cardiac output.
The nature of an exercise training program is an important independent variable in determining the effect of NO on endothelial function. Aerobic and resistance exercise training programs have been shown to increase the endothelial-dependent vasodilation. Those changes have been noted in young and older men and women (2, 4, 5).
In conclusion, research on the effects of a combined aerobic and resistance training programs on endothelial function is needed. Additionally, it is also important to note that there are gender differences in exercise hyperemia. Young women showed a greater increase in exercise hyperemia than young men (6). The extent to which NO-mediated vasodilation contributes to the gender difference in exercise hyperemia is a subject for future investigations.
REFERENCES
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