Examining the effects of exercise on vascular function in obstructive sleep apnea

摘要： 阻塞性睡眠呼吸暂停(OSA)是一种严重的疾病，估计有1500万美国成年人受到影响 以反复发作上呼吸道阻塞、反复觉醒和发作为特征 睡眠时氧合血红蛋白降低饱和度。这些异常导致血管的亚临床改变。 增加心血管疾病发病率和死亡率的功能。相比之下，锻炼 减少心血管事件的风险，促进体力活动继续位居榜首 我们的国家公共卫生议程，从1996年美国卫生局局长关于 体力活动和健康。虽然这种保护性利益的确切机制还不完全清楚，但有 是运动通过直接影响血管内皮细胞而提供心脏保护的有力证据 功能。美国睡眠医学院建议将锻炼作为一种行为治疗选择 奥萨。然而，这一建议所基于的大多数临床试验都集中在建立 改变生活方式的有效性(例如，饮食诱导的减肥和更多的体力活动参与) 用于改善肥胖个体的OSA严重程度，而OSA是否会受到较少关注 缓和运动对心血管疾病底物的影响。我们最重要的假设是 OSA减弱运动对肥胖者血管功能的有益影响 患有未经治疗的阻塞性睡眠呼吸暂停综合症。本研究的目的是：1)检测患者的血管功能参数 有无阻塞性睡眠呼吸暂停的肥胖者，2)评估一次急性运动对臂动脉的影响 有无阻塞性睡眠呼吸暂停的肥胖者的血流介导的扩张，以及3)检查6周的 运动训练对阻塞性睡眠呼吸暂停患者和非阻塞性睡眠呼吸暂停患者血管功能的影响。我们的数据将立即有用 在临床实践中，并告知我们如何处方锻炼和实施生活方式的改变，以减少 阻塞性睡眠呼吸暂停综合征患者的心血管疾病风险。

Abstract: Obstructive sleep apnea (OSA) is a serious medical condition that affects an estimated 15 million US adults and is characterized by repeated episodes of upper airway obstruction, recurrent arousals and episodic oxyhemoglobin desaturations during sleep. These abnormalities contribute to subclinical alterations in vascular function that increase the risk of cardiovascular disease morbidity and mortality. In contrast, exercise decreases the risk of cardiovascular events and the promotion of physical activity continues to be at the top of our national public health agenda, as seen in the publication of the 1996 report of the US Surgeon General on physical activity and health. While the exact mechanisms for this protective benefit are not entirely clear, there is good evidence that exercise confers cardioprotection through its direct impact on vascular endothelial function. The American College of Sleep Medicine recommends exercise as a behavioral treatment option for OSA. Yet, most clinical trials upon which this recommendation is based have focused on establishing the effectiveness of lifestyle change (e.g., dietary induced weight loss and increased physical activity participation) for improving OSA severity in obese individuals, whereas less attention has been given to whether OSA moderates the effects of exercise on the cardiovascular disease substrate. Our overarching hypothesis is that OSA attenuates the beneficial effect of exercise on vascular function in obese individuals suffering from untreated OSA. The aims of the study are to 1) examine parameters of vascular function in obese persons with and without OSA, 2) evaluate the effects of an acute bout of exercise on brachial artery flow mediated dilation in obese persons with and without OSA, and 3) examine the effects of 6 weeks of exercise training on vascular function among those with and without OSA. Our data will be immediately useful in clinical practice and inform how we prescribe exercise and implement lifestyle changes to reduce cardiovascular disease risk in OSA patients.