THE POSSIBLE ROLE OF INTRACELLULAR CA2+ ACCUMULATION FOR THE DEVELOPMENT OF IMMOBILIZATION ATROPHY

Little is known about the cellular mechanisms which induce the develop ment of skeletal muscle immobilization atrophy. Initial disturbances i n cellular homeostasis seem to occur very early during immobilization. The aim of the study was to investigate whether loss of calcium homeo stasis might be of etiological importance for atrophy. Therefore a cal cium 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 sh owed an atrophy of about 15% which was not the case in nifedipine-trea ted immobilized muscles. Ultrastructural alterations (lysosomes, mitoc hondrial 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.