MISCELLANEOUS TRAINING & DISSEMINATION ACTIVITIES

美国大约34%的成年人口是 超重。一些调查人员推测，这一困难 保持体重减轻与骨骼肌的变化有关 体重紊乱时的新陈代谢。我们正在调查这件事 通过测量基础磷酸盐含量和体内实验提出假说 氧化能力的基础上的聚合酶链式反应再合成率(KPCR)后 肥胖者和非肥胖者的体重变化都更大。首字母 MRS测量的分析表明，体重的减轻是 与PI含量的增加有关。在肥胖者和 非肥胖者体重减轻10%与16%和 基础PI含量分别增加12%。相反，10% 非肥胖者体重增加导致体重减少6% PI内容。对照组K-PCR值(S-1)明显升高 有分量的。对照组的骨骼肌变得更多 在增加重量时效率较高，而在较低重量时效率较低。 肥胖组表现出不同的骨骼肌能力变化 由于体重减轻。在-20%时的kPCr为2.45，而在-20%时为1.99。 基线。-10%的数值与基线1.95持平。 这表明，在肥胖人群中，体重的下降 伴随着骨骼肌氧化能力的增强。 肥胖者KPCR值和基础PI含量的变化 研究小组支持体重波动会影响骨骼的假设 肌肉新陈代谢，随着氧化能力的增加 体重减轻，氧化能力随体重增加而降低。 对照组基础PI分析显示与对照组相同的趋势 肥胖组，但k-PCR测量结果并不一致。确认式 肌肉活组织和肌肉组织体外生化检测方法的研究 低强度运动时全身耗氧量的测定 目前正在进行中。这些数据提供了证据 代谢改变可能导致体重的高复发率 减肥后增加。 未来的研究将集中在使用光谱定位 更具体地观察内侧腓肠肌的技术 体重下降和增加的不同阶段。本地化基线 到目前为止，已经对一个受试者进行了测量。

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.