Abstract
Excessive long-term accumulation of calcium ions in the myoplasm of skeletal muscles can negatively affect mitochondria and lead to muscle dysfunction. The aim of our study was to identify the role of L-type calcium channels in the development of increased fatigue rat soleus muscle under functional unloading. Young male Wistar rats were divided into three groups of 8 animals each: the vivarium control group (C), the group subjected to hind limb unloading for 7 days (7HS) and the group with 7 days of hindlimb unloading with daily intraperitoneal injections of nifedipine (7 mg/kg body weight). The administration of nifidipine during hindlimb unloading prevented the upregulation of calcium-dependent phosphorylation of calcium-calmodulin kinase II (CaMK II), prevented the increase in fatigue and contributed to the preservation of mitochondrial proteins, DNA and mRNA expression of a number of genes that regulate mitochondrial biogenesis.
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