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Hypobaric hypoxia, a condition of low oxygen availability at high altitude, has a great impact on health via producing oxidative stress which could lead to protein modifications and skeletal muscle damage. Enhanced calpain activity has a major role in hypobaric hypoxia induced protein modifications and protein degradation in the skeletal muscle. The pilot study was designed to investigate the role of a calpain inhibitor, calpeptin in amelioration of hypoxia induced skeletal muscle damage. Male Sprague Dawley rats were exposed to hypobaric hypoxia (HH) with and without calpeptin (50 µg/kg, ip) treatment. HH exposure was given for 6 h at 25,000 ft. Following exposure, the animals were sacrificed and hind limb skeletal muscle was excised for analysis. Calpeptin administration inhibited protein oxidation (decrease protein carbonyl and AOPP content). Decrease in oxidized tryptophan and bityrosine content was also observed in calpeptin pre-treated group in comparison to HH exposed group. Beside this, HH induced reactive oxygen species (ROS) was also ameliorated via calpeptin treatment. Conclusively, calpeptin administration better maintained the oxidative homeostasis in skeletal muscle under hypobaric hypoxia and significantly protected against the protein damage and degradation. However, the exact mechanism is still unknown. Therefore, further research needs to be done to unravel the underlying mechanism.

Role of Calpeptin in Amelioration of Hypobaric Hypoxia Induced Skeletal Muscle Damage in Rats: A Pilot Study