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

由于固定、卧床休息， 非负重或去神经支配引起许多适应性变化， 骨骼肌与肌肉功能障碍作为最终结果。 损失 肌肉质量或肌肉萎缩是最公认的 废弃的后果。 不活动也会导致 骨骼肌的代谢改变，最重要的是 基础无机磷（Pi）升高。 我们追踪了10个实验对象 经过8周的小腿石膏固定 然后进行十周的康复治疗 用于比较变化 在康复期间，我们对7名患者进行了类似的测试， 对照组在10周内。 十名受试者的固定导致骨骼肌 萎缩，基础无机磷酸盐增加和力量下降 生产 使用31P NMR显示基础浓度增加了43%。 萎缩组与对照组相比， 人口 小腿三头肌的最大横截面积为 也看到了下降。 力损失的程度大于 肌肉横截面积，这意味着萎缩，废用肌肉 与对照组相比， 肌肉CSA相似的受试者。 两者的回归分析 MaxCSA与力的萎缩和对照测量证明 统计学显著性，萎缩组产生的 在相似MaxCSA下的力（萎缩组R2=0.55， 控制）。 在整个恢复过程中， 萎缩组的增加接近对照值， 康复期结束。 这是通过增加 用力，最大CSA，基础无机磷酸盐减少。 的 由于固定，肌肉效率发生变化， 力量损失和肌肉功能的程度超过了 肌肉大小表明，还有其他重要因素导致 通过固定导致肌肉效率的整体损失 除了肌肉萎缩 我们认为无机磷酸盐含量过高， 沿着肌肉尺寸的减少， 导致肌肉功能下降

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.