Chronic Exercise Increases Antioxidant Activity and Decreases Lipid Peroxidation in the Skeletal Muscle of Rats

Abstract

No relationships reported) PURPOSE:The goal of the present study was to analyze the activity of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase as well as a lipid peroxidation biomarker (thiobarbituric acid reactant substances; TBARs) in the skeletal muscle of rats subjected to aerobic swimming exercise. METHODS:Eighteen male Wistar rats (60 days of age at the beginning of the experiment) were used. With 90 days of age, the animals were divided into two groups: Control Group (C; n=10): rats maintained as sedentary controls; Trained Group (T: n=8): rats subjected to aerobic swimming exercise. The exercise protocol consisted of 1h/day of continuous swimming exercise, 5x/week, during 8 weeks. The animals carried out overload equivalent to 5% of body weight. At the end of the experiment, the rats were killed by CO2 inhalation and cervical dislocation; samples of gastrocnemius muscles (200mg) of all rats were collected for antioxidant enzymes activities (Cayman Chemical, Michigan, USA) and lipid peroxidation biomarker (Cayman Chemical, Michigan, USA) determinations. The data were analyzed using "t" Student test (p value of ≤ 0.05) to verify the difference between means. RESULTS:The antioxidant enzymes activities levels were significantly higher in the skeletal muscle of T group [CAT (µmol/min.mg protein): 0.87 ± 0.04; SOD (U/ml): 6.49 ± 0.04; GPx (nmol/min.protein): 6.57 ± 0.52] if compared to C group (CAT: 0.51 ± 0.03; SOD: 4.01 ± 0.37; GPx: 2.94 ± 0.56). On the other hand, the TBARs levels (nmol/mg.protein) were significantly lower in the skeletal muscle of T group (2.34 ± 0.41) when compared to C group (8.94 ± 0.56). CONCLUSION:Our data suggest that the antioxidant mechanisms were improved in the skeletal muscle of rats subjected to chronic aerobic swimming exercise. Such results indicated that regular physical exercise may protect the organism against the oxidative stress caused by the sedentarism condition.Financial Support: Fundação de Amparo à Pesquisa do Estado de Mato Grosso (Brazilian Foundation; Process number: 450794/2009). (No relationships reported)Doxorubicin is an effective antitumor agent used in cancer treatment. However, doxorubicin can also cause muscle toxicity and can result in significant reduction in skeletal muscle mass and function. The mechanism(s) by which doxorubicin induces toxicity in skeletal muscle is unclear. However, doxorubicininduced toxicity is associated with increased generation of reactive oxygen species and oxidative damage within muscle fibers. In this regard, autophagy can be induced by oxidative stress and it is also a constitutively active catabolic process that degrades oxidized proteins. PURPOSE:We hypothesized that systemic doxorubicin administration in rats would promote increased autophagy in skeletal muscle as evidenced by increased components of the autophagy system. METHODS:To test this postulate, adult, male Sprague-Dawley rats were randomly assigned to placebo or doxorubicin groups. The doxorubicin animals received do...