Effect of Vitamin E on the Exhaustive Exercise-Induced Damage in the Skeletal Muscle of Adult Male Albino Rat: A Functional, Histological and Ultrastructural Study

Background: Swimming is a minor traumatic exercise for animals and has been commonly used to elucidate the physiologic and molecular responses of the muscle to exercise stress. Short term exhausting exercise increases the formation of harmful reactive oxygen species (ROS). Vitamin E (α-tocopherol) is a fat soluble vitamin that can inhibit the generation of ROS in the body as it acts as an antioxidant. Aim of the Study: The present study was designed to investigate the possible protective effect of vitamin E against the untrained exhaustive exercise-induced damage in the skeletal muscle, and on the plasma levels of proinflammatory cytokines in adult male albino rat. Material and Methods: 24 adult male albino rats, age 3 months and about 90-120g body weight were purchased from Animal House, Faculty of Medicine, Assiut University. All animals were kept in stainless-steel cages at room temperature at a natural photoperiod with free access to standard rat chow and tap water. Animals were randomly divided into 3 groups (8 rats each): Group C (control group), Group S (submitted to exhaustive swimming stress group), and Group SE (submitted to exhaustive swimming stress plus vitamin E-received group). The animals from groups S and SE were submitted to bouts of swimming stress for 1 hour daily for a week. The rats from SE group received oral gavage administration of vitamin E (100mg/kg/day) before swimming stress. Results: Exhaustive swimming stress in group S significantly elevated plasma tumor necrosis factor-alpha (TNF-α), interferon gamma (INF-γ) and C reactive protein (CRP). Light microscopy of gastrocnemius muscle specimens showed in group S hypervascularity, apparent increase in the number of interstitial nuclei, splitting of muscle fibers, and central location of nuclei compared to C group. Transmission electron microscopy revealed marked skeletal muscle cell damage with destructed myofibrils and loss of some myofilaments, and areas of degeneration and vacuolation, with irregularity of the Z lines, and apparent irregular shape and small size of mitochondria were present in group S compared to group C. Administration of vitamin E before exposure to exercise in group SE significantly decreased TNF-α and INF-γ, but didn t change CRP level. Vitamin E supplementation also increased animal total body weight, and increased endothelial nitric oxide synthase (eNOS) expression as detected by immunohistochemistry, and ameliorated the structural changes in the gastrocnemius muscle as shown both by light and transmission electron microscopy in group SE compared to groups C and S. Conclusion: Vitamin E supplementation has promising protective role against exercise-induced elevation of cytokines and muscular damage.