Soares J M, Duarte J A, Carvalho J, Appell H J
Department of Sport Biology, Faculty of Sport Sciences, University of Porto, Portugal.
Int J Sports Med. 1993 Nov;14(8):437-9. doi: 10.1055/s-2007-1021206.
Little is known about the cellular mechanisms which induce the development of skeletal muscle immobilization atrophy. Initial disturbances in cellular homeostasis seem to occur very early during immobilization. The aim of the study was to investigate whether loss of calcium homeostasis might be of etiological importance for atrophy. Therefore a calcium channel blocker (nifedipine) was administered to mice immobilized for four days, and their soleus muscle was investigated comparatively to immobilized animals without nifedipine. The immobilized muscles showed an atrophy of about 15% which was not the case in nifedipine-treated immobilized muscles. Ultrastructural alterations (lysosomes, mitochondrial damage) were found predominantly in the immobilized muscles, but rarely with nifedipine. It was concluded that nifedipine protected the muscle fibers probably against calcium overload, thereby avoiding an autophagic response and an impairment of mitochondrial respiratory function.
关于诱导骨骼肌固定性萎缩发展的细胞机制，人们了解甚少。细胞内稳态的初始紊乱似乎在固定过程的早期就会出现。本研究的目的是调查钙稳态丧失是否在病因上对萎缩具有重要意义。因此，给固定四天的小鼠施用钙通道阻滞剂（硝苯地平），并将其比目鱼肌与未使用硝苯地平的固定动物进行比较研究。固定的肌肉出现了约15%的萎缩，而在使用硝苯地平治疗的固定肌肉中则未出现这种情况。超微结构改变（溶酶体、线粒体损伤）主要在固定的肌肉中发现，但使用硝苯地平时很少出现。研究得出结论，硝苯地平可能通过保护肌纤维免受钙超载，从而避免自噬反应和线粒体呼吸功能受损。
