IS MUSCLE METABOLISM AFFECTED BY CHANGES IN BODY WEIGHT?

在美国，大约34%的成年人是 超重 一些研究人员推测， 保持体重减轻与骨骼肌的变化有关 代谢和体重波动。 我们正在调查此事 假设通过测量基础磷酸盐含量和体内 根据PCr再合成率（kPCr）的氧化能力， 肥胖和非肥胖者的体重变化更大。 初始 对MRS测量结果的分析表明， 与Pi含量的增加有关。 在肥胖和 非肥胖者体重下降10%， 基础磷含量分别提高12%。 相反，10% 非肥胖者体重增加导致体重下降6%， Pi含量。 对照组kPcr（s-1）升高 有重量。 对照组的骨骼肌变得更多 在增加重量时效率高，而在较低重量时效率低。 肥胖组在骨骼肌容量方面表现出不同的变化 因为体重减轻。 -20%时的k Pcr为2.45，而-20%时为1.99。 基线。 -10%时的值与基线相比保持不变，为1.95。 这表明，在肥胖人群中， 伴随着骨骼肌氧化能力的增加。 肥胖组kPCr和基础Pi含量的变化 一组支持体重波动影响骨骼的假设， 肌肉代谢，随着氧化能力的增加， 体重减轻和氧化能力随体重增加而降低。 对照组的基础Pi分析显示出与对照组相同的趋势。 肥胖组与对照组比较，差异有统计学意义（P < 0. 05）。 验证性 使用肌肉活组织检查的体外生物化学测量的研究， 低强度运动时全身耗氧量的测定 目前正在执行。 这些数据证明， 代谢改变可能导致体重的高复发率 体重减轻后增加。 未来的研究将集中在使用光谱定位 技术，更具体地看内侧腓肠肌在 体重减轻和增加的不同阶段。 局部基线 迄今为止，已经对一个对象进行了测量。

Approximately 34% of the adult population in the United States is overweight. Several investigators have postulated that the difficulty to maintain weight loss is linked to changes in skeletal muscle metabolism with weight perturbations. We are investigating this hypothesis by measuring the basal phosphate content and the in vivo oxidative capacity based on the PCr resynthesis rate (kPCr) after larger weight alterations in both obese and non-obese. Initial analysis of MRS measurements shows that a reduction in body weight is associated with an increase in the Pi content. In both the obese and non-obese a 10% decrease in body weight was associated with a 16% and 12% increase in basal Pi content respectively. Conversely, a 10% increase in body weight in the non-obese resulted in a 6% decrease in Pi content. The k Pcr(s-1) in the control group was shown to increase with weight. The skeletal muscle of the control group becomes more efficient at increased weight, and less efficient at lower weights. The obese group showed different changes in skeletal muscle capacity due to weight loss. The k Pcr at -20% was 2.45 as compared to 1.99 at baseline. The value at -10% was unchanged from baseline at 1.95. This suggests that in the obese population a decrease in weight was accompanied by an increase in the skeletal muscle oxidative capacity. Both the changes in kPCr and basal Pi content in the obese group support the hypothesis that weight perturbations affect skeletal muscle metabolism, with an increase in the oxidative capacity with weight loss and a decrease in oxidative capacity with weight gain. Analysis of basal Pi in the control group showed the same trend as the obese group, but k PCr measurements did not agree. Confirmative studies using in vitro biochemical measures of muscle biopsies and whole body oxygen consumption measurements during low level exercise are currently being performed. These data provide evidence that metabolic alterations may contribute to the high recidivism of weight increase after weight loss. Future studies will focus on using a spectra localization technique to look more specifically at the medial gastrocnemius at the different stages of weight loss and gain. Localized baseline measurements have been performed on one subject to date.