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目的 观察有氧运动对慢性睡眠剥夺（CSD）引发胰岛素抵抗(IR)的影响，并明确其可能机制。方法 采用改良多平台水环境睡眠剥夺法(MMPM)对大鼠进行为期8周的睡眠剥夺建立CSD模型。雄性Sprague-Dawley大鼠30只，随机分为5组：对照组、睡眠剥夺组、睡眠剥夺+低强度运动组、睡眠剥夺+中强度运动组、睡眠剥夺+高强度运动组。通过测定空腹血清胰岛素、空腹血糖、胰岛素抵抗指数(homeostasis model assessment for insulin resistance,HOMA-IR)、心肌葡萄糖摄取、腹腔糖耐量和空腹胰岛素敏感性等手段观察有氧运动对CSD引发大鼠IR的影响；采用彩色多普勒超声诊断仪检测短轴缩短率(Fractional Shortening,FS)及左心室射血分数(Left Ventricular Ejection Fraction, LVEF)；采用放射免疫法测量血清中肿瘤坏死因子-α（tumor necrosis factor-α，TNF-α）、白介素-1β(interleukin-1β，IL-1β)、白介素-6（interleukin -6，IL-6）水平；通过Western blot法检测外周血单核细胞核因子（NF-kappa B，NF-κB）以及抑制蛋白（I-kappa B，I-κB），观察有氧运动对慢性睡眠剥大鼠体内炎症因子水平及心功能的影响。结果 CSD可引起大鼠HOMA-IR、腹腔糖耐量和胰岛素敏感性的明显异常，降低心肌葡萄糖摄取和心脏功能，同时可降低抑炎因子I-κB水平，增加促炎因子NF-κB和血浆炎症因子水平（P<0.05）。低强度运动干预对上述各指标无明显影响；而中强度运动干预则可明显改善大鼠机体IR、心肌IR及心脏射血功能，增加抑炎因子I-κB，降低机体促炎因子NF-κB以及外周各炎症因子的水平（P<0.05）；但高强度运动干预则可引起机体IR加重、心肌葡萄糖摄取能力下降及心脏射血分数下降，体内促炎因子NF-κB以及外周各炎症因子水平升高，而抑炎因子IκB表达水平下降（P<0.05）。结论 适量有氧运动可以通过降低体内炎症反应改善大鼠睡眠剥夺引发的IR及心功能下降。
Objective To observe the effect of aerobic exercise on insulin resistance (IR) induced by chronic sleep deprivation (CSD) and to clarify its possible mechanism. Methods CSD model was established by sleep deprivation with modified multi-platform water environment sleep deprivation (MMPM) for 8 weeks in rats. Thirty male Sprague-Dawley rats were randomly divided into five groups: control group, sleep deprivation group, sleep deprivation + low intensity exercise group, sleep deprivation + moderate intensity exercise group, sleep deprivation + high intensity exercise group. The effects of aerobic exercise on the IR of CSD-induced rats were observed by measuring fasting serum insulin, fasting blood glucose, homeostasis model assessment for insulin resistance (HOMA-IR), myocardial glucose uptake, peritoneal glucose tolerance and fasting insulin sensitivity (Fractional Shortening, Left Ventricular Ejection Fraction, Left Ventricular Ejection Fraction, LVEF) were detected by color Doppler sonography. Serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in peripheral blood mononuclear cells were detected by Western blot. κB) and I-kappa B (I-κB) in rats with chronic sleep deprivation, and to observe the effect of aerobic exercise on the levels of inflammatory cytokines and cardiac function in rats with chronic sleep deprivation. Results CSD induced obvious abnormalities of HOMA-IR, peritoneal glucose tolerance and insulin sensitivity, decreased myocardial glucose uptake and cardiac function, decreased the level of I-κB and increased the expression of proinflammatory cytokines NF-κB and plasma inflammation Factor levels (P & lt; 0.05). Low-intensity exercise intervention had no significant effect on the above indexes; while moderate-intensity exercise intervention could significantly improve IR, myocardial IR and cardiac ejection function, increase I-κB and decrease proinflammatory cytokine NF-κB (P <0.05). However, high-intensity exercise intervention could cause the increase of IR, decrease of myocardial glucose uptake, decrease of cardiac ejection fraction, in vivo proinflammatory cytokine NF-κB and peripheral inflammatory cytokines Increased, while the expression of anti-inflammatory factor IκB decreased (P <0.05). Conclusions Moderate aerobic exercise can improve sleep deprivation-induced IR and cardiac dysfunction in rats by reducing inflammation in vivo.