Weiss Edward P, Racette Susan B, Villareal Dennis T, Fontana Luigi, Steger-May Karen, Schechtman Kenneth B, Klein Samuel, Holloszy John O
Division of Geriatrics and Nutritional Sciences, Department of Internal Medicine, Washington University School of Medicine, St Louis, MO, USA.
Am J Clin Nutr. 2006 Nov;84(5):1033-42. doi: 10.1093/ajcn/84.5.1033.
Weight loss, through calorie restriction or increases in energy expenditure via exercise, improves glucose tolerance and insulin action. However, exercise-induced energy expenditure may further improve glucoregulation through mechanisms independent of weight loss.
The objective was to assess the hypothesis that weight loss through exercise-induced energy expenditure improves glucoregulation and circulating factors involved in insulin action to a greater extent than does similar weight loss through calorie restriction.
Sedentary men and women aged 50-60 y with a body mass index (kg/m(2)) of 23.5-29.9 were randomly assigned to 1 of 2 weight-loss interventions [12 mo of exercise training (EX group; n = 18) or calorie restriction (CR group; n = 18)] or to a healthy lifestyle (HL) control group (n = 10). The insulin sensitivity index and areas under the curve for glucose and insulin were assessed with an oral-glucose-tolerance test. Adiponectin and tumor necrosis factor alpha concentrations were measured in fasting serum. Fat mass was measured by dual-energy X-ray absorptiometry.
Yearlong energy deficits were not significantly different between the EX and CR groups, as evidenced by body weight and fat mass changes. The insulin sensitivity index increased and the glucose and insulin areas under the curve decreased in the EX and CR groups, remained unchanged in the HL group, and did not differ significantly between the EX and CR groups. Marginally significant increases in adiponectin and decreases in the ratio of tumor necrosis factor alpha to adiponectin occurred in the EX and CR groups but not in the HL group.
Weight loss induced by exercise training or calorie restriction improves glucose tolerance and insulin action in nonobese, healthy, middle-aged men and women. However, it does not appear that exercise training-induced weight loss results in greater improvements than those that result from calorie restriction alone.
通过热量限制或运动增加能量消耗来减轻体重,可改善葡萄糖耐量和胰岛素作用。然而,运动诱导的能量消耗可能通过独立于体重减轻的机制进一步改善血糖调节。
评估以下假设:与通过热量限制实现的类似体重减轻相比,通过运动诱导的能量消耗实现的体重减轻在更大程度上改善血糖调节和参与胰岛素作用的循环因子。
将年龄在50 - 60岁、体重指数(kg/m²)为23.5 - 29.9的久坐不动的男性和女性随机分配至两种减肥干预措施之一[12个月的运动训练(EX组;n = 18)或热量限制(CR组;n = 18)]或健康生活方式(HL)对照组(n = 10)。通过口服葡萄糖耐量试验评估胰岛素敏感性指数以及葡萄糖和胰岛素的曲线下面积。测量空腹血清中的脂联素和肿瘤坏死因子α浓度。通过双能X线吸收法测量脂肪量。
体重和脂肪量变化表明,EX组和CR组全年的能量亏空没有显著差异。EX组和CR组的胰岛素敏感性指数升高,葡萄糖和胰岛素曲线下面积降低,HL组保持不变,EX组和CR组之间无显著差异。EX组和CR组脂联素略有显著升高,肿瘤坏死因子α与脂联素的比值降低,而HL组未出现此情况。
运动训练或热量限制引起的体重减轻可改善非肥胖、健康的中年男性和女性的葡萄糖耐量和胰岛素作用。然而,运动训练引起的体重减轻似乎并不比单纯热量限制带来的改善更大。