Hodnett Benjamin L, Hester Robert L
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi 39216-4505, USA.
Microcirculation. 2007 Jun-Jul;14(4-5):273-88. doi: 10.1080/10739680701282143.
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.
肥胖已被证明会损害人体肌肉的血流。由于胰岛素抵抗、高血糖、血脂异常、炎症、氧化应激和内皮功能障碍，肥胖可能会损害代谢控制、肌源性机制、传导性血管舒张和内皮衍生因子释放等血管舒张控制机制。这些血流控制机制的生理重要性主要是在因运动相关代谢增加而发生的血流增加（功能性充血）过程中确定的。本综述探讨了肥胖可能损害功能性充血的机制，并指出了需要进一步研究的领域。肥胖引起的肌肉血流变化研究最广泛的领域是内皮衍生介质在静息血流和运动诱导充血过程中的作用。氧化应激升高会改变内皮衍生因子，导致血管舒张反应受损。肥胖对血流的代谢和传导性血管舒张调节的改变尚未得到广泛研究，这是一个潜在的研究领域。
