Jaspers S R, Tischler M E
Muscle Nerve. 1986 Jul-Aug;9(6):554-61. doi: 10.1002/mus.880090613.
Adrenalectomy did not prevent atrophy of rat soleus muscle during 6 days of tail cast suspension. Cortisol treatment enhanced this atrophy and caused atrophy of the weight-bearing soleus and both extensor digitorum longus (EDL) muscles. Unloading led to increased sarcoplasmic protein concentration in the soleus, but cortisol administration increased the myofibrillar (+stromal) protein concentration in both muscles. Suspension of hindlimbs of adrenalectomized animals led to faster protein degradation, slower sarcoplasmic protein synthesis, and faster myofibrillar protein synthesis in the isolated soleus, whereas with cortisol-treated animals, the difference in synthesis of myofibrillar proteins was enhanced and that of sarcoplasmic proteins was abolished. Both soleus and EDL of suspended, cortisol-treated animals showed faster protein degradation. It is unlikely that any elevation in circulating glucocorticoids was solely responsible for atrophy of the soleus in this model, but catabolic amounts of glucocorticoids could alter the response of muscle to unloading.
在尾部悬吊6天期间，肾上腺切除术并不能防止大鼠比目鱼肌萎缩。皮质醇治疗加剧了这种萎缩，并导致负重比目鱼肌和两块趾长伸肌（EDL）萎缩。卸载导致比目鱼肌肌浆蛋白浓度增加，但给予皮质醇会增加两块肌肉的肌原纤维（+基质）蛋白浓度。切除肾上腺动物的后肢悬吊导致分离的比目鱼肌中蛋白质降解加快、肌浆蛋白合成减慢、肌原纤维蛋白合成加快，而对于接受皮质醇治疗的动物，肌原纤维蛋白合成的差异增强，肌浆蛋白合成的差异消失。悬吊并接受皮质醇治疗的动物的比目鱼肌和EDL均显示蛋白质降解加快。在该模型中，循环糖皮质激素的任何升高不太可能是比目鱼肌萎缩的唯一原因，但分解代谢量的糖皮质激素可能会改变肌肉对卸载的反应。
