Role of L-Type Calcium Channels in Increased Fatigue of the Rat Soleus Muscle under Functional Unloading

Excessive long-term accumulation of calcium ions in the myoplasmof skeletal muscles can negatively affect mitochondria and leadto muscle dysfunction. The aim of our study was to identify therole of L-type calcium channels in the development of increasedfatigue of the rat soleus muscle under functional unloading. Youngmale Wistar rats were divided into three groups of 8 animals each:vivarium control group (C), group exposed to 7-day hindlimb unloading(7HS), and group exposed to 7-day hindlimb unloading with dailyintraperitoneal injections of nifedipine (7 mg/kg body weight) (7HS+N).Nifedipine administration during hindlimb unloading prevented the upregulationof calcium-dependent phosphorylation of calcium-calmodulin kinaseII (CaMKII) and an increase in fatigue, as well as promoted thepreservation of mitochondrial proteins, mtDNA, and mRNA expressionof a number of regulatory genes of mitochondrial biogenesis in the ratsoleus muscle.