Abstract
Obesity has been shown to impair muscle blood flow in humans. Vasodilatory control mechanisms such as metabolic control, myogenic mechanisms, conducted vasodilation, and release of endothelium-derived factors may be impaired in obesity due to insulin resistance, hyperglycemia, dyslipidemia, inflammation, oxidative stress, and endothelial dysfunction. The physiological importance of these blood flow control mechanisms has predominately been determined during the increase in blood flow (functional hyperemia) that occurs in response to the increased metabolism associated with exercise. This review examines the mechanisms by which functional hyperemia may be impaired in obesity and indicates areas where further studies are needed. The most extensively studied area of obesity-induced changes in muscle blood flow has been the role of endothelium-derived mediators during resting blood flow and exercise-induced hyperemia. Elevations in oxidative stress alter endothelium-derived factors, resulting in impaired vasodilatory responses. Alterations in metabolic and conducted vasodilatory regulation of blood flow have not been extensively studied in obesity, providing a potential area of research.
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This work was supported by grants from the National Institutes of Health (HL-51971, HL-63958).