MRS OF PATS W/ AIDS DEMENTIA COMPLEX: MULTICENTER ACTG 301 DRUG EVAL PROGRAM

因固定、卧床休息而不活动或停用， 不负重或失神经会导致许多适应性变化 骨骼肌的最终结果是肌肉功能障碍。损失 肌肉肿块或肌肉萎缩是最常见的 不使用的后果。不运动也被证明是导致 骨骼肌的代谢变化，最重要的是 基础无机磷(PI)升高。我们已经追踪了10名受试者 通过8周的小腿石膏固定 随后进行了10周的康复治疗。用于比较变化 在康复过程中，我们对7名患者进行了类似的测试 在十周的时间内控制受试者。 10名受试者的固定导致了骨骼肌的形成 萎缩，基础无机磷增加，力量下降 制作。31P核磁共振仪显示基础值增加了43%。 萎缩组与对照组的无机磷比较 人口。小腿三头肌最大横截面积为 看起来也在减少。 部队损失的程度大于 肌肉横截面积，意味着萎缩、废弃的肌肉 与控制组相比，在生产力量方面变得不那么有效 有相似肌肉CSA的受试者。两者的回归分析 MaxCSA随力验证的萎缩及控制措施 统计学上有意义的是萎缩组产生的 在相似的最大CSA处的作用力(R2=0.55，萎缩组为0.70 控件)。在整个恢复过程中，肌肉的效率 萎缩组增加接近对照组在 戒毒期结束了。这是通过增加 力量，最大CSA，和基础无机磷的减少。这个 制动后肌肉效率的变化，其中 力量丧失的程度和肌肉功能超过了 肌肉的大小表明还有其他重要的因素导致 通过制动导致肌肉效率的全面丧失 除了肌肉萎缩。我们认为升高的无机磷， 伴随着肌肉大小的减少，成为一个重要的贡献 导致制动后肌肉功能下降。

Inactivity or disuse as a result of immobilization, bed rest, non-weight bearing, or denervation causes many adaptive changes in skeletal muscle with muscular dysfunction as a final outcome. Loss of muscle mass or muscular atrophy is one of the most recognized consequences of disuse. Inactivity has also been shown to cause metabolic alterations in skeletal muscle, the most important being elevated basal inorganic phosphate (Pi). We have tracked 10 subjects through an 8 week period of cast immobilization of the lower leg followed by ten weeks of rehabilitation. For comparison of changes seen during rehabilitation, we have performed similar testing on 7 control subjects over a ten week period. Immobilization of the ten subjects resulted in skeletal muscle atrophy, an increase in basal inorganic phosphate and decreased force production. 31P NMR was used to show a 43% increase in basal inorganic phosphate in the atrophy group as compared with the control population. The maximum cross-sectional area of the triceps surae was seen to decrease as well. The extent of force loss was greater than the decrease in muscle cross-sectional area, meaning that the atrophic, disused muscle had become less efficient at producing force as compared to control subjects with similar muscle CSAs. Regression analysis of both atrophy and control measurements of MaxCSA versus Force proved statistically significant with the atrophy group generating lower forces at similar MaxCSAs (R2=0.55 in the atrophy group, and 0.70 in the control). Throughout recovery the muscular efficiency in the atrophy group was seen to increase approaching control values at the end of the rehab period. This was accomplished by an increase in Force, maximum CSA, and a decrease in basal inorganic phosphate. The change in muscular efficiency as a result of immobilization, where the extent of force loss and muscle function exceeded the decrease in muscle size suggests that there are other significant factors caused by immobilization that lead to an overall loss in muscul ar efficiency besides muscle atrophy. We believe elevated inorganic phosphate, along with a decrease in muscle size, to be an important contributor to decreased muscle function following immobilization.