Impact of different resistance training protocols on muscular oxidative stress parameters.

This study analyzes oxidative stress in skeletal muscle using different resisted training protocols. We hypothesize that different types of training produce different specifics. To test our hypothesis, we defined 3 resistance training protocols and investigated the respective biochemical responses in muscle. Twenty-four male Wistar rats were distributed in 4 groups: untrained (UT), muscular resistance training (RT), hypertrophy training (HT), and strength training (ST). After 12 weeks of training on alternate days, the red portion of the brachioradialis was removed and the following parameters were assessed: lactate and glycogen content, superoxide production, antioxidant enzyme content, and activities (superoxide dismutase, SOD; catalase, CAT; GPx, glutathione peroxidase). Thiobarbituric acid-reactive substances (TBARS), carbonyl, and thiol groups were also measured. Results showed increased superoxide production (UT = 5.348 ± 0.889; RT = 5.117 ± 0,651; HT = 8.412 ± 0.431; ST = 6.354 ± 0.552), SOD (UT = 0.078 ± 0.0163; RT = 0.101 ± 0.013; HT = 0.533 ± 0.109; ST = 0.388 ± 0.058), GPx (UT = 0.290 ± 0.023; RT = 0.348 ± 0.014; HT = 0.529 ± 0.049; ST = 0.384 ± 0.038) activities, and content of GPx (HT = 3.8 times; ST = 3.0 times) compared with the UT group. CAT activity was lower (UT = 3.966 ± 0.670; RT = 3.474 ± 0.583; HT = 2.276 ± 0.302; ST = 2.028 ± 0.471) in HT and ST groups. Oxidative damage was observed in the HT group (TBARS = 0.082 ± 0.009; carbonyl = 0.73 ± 0.053; thiol = 12.78 ± 0.917) compared with the UT group. These findings indicate that HT causes an imbalance in oxidative parameters in favor of pro-oxidants, causing oxidative stress in skeletal muscle.

Cigarette smoke inhibits brain mitochondrial adaptations of exercised mice.

Physical exercise and smoking are environmental factors that generally cause opposite health-promoting adaptations. Both physical exercise and smoking converge on mitochondrial adaptations in various tissues, including the pro-oxidant nervous system. Here, we analyzed the impact of cigarette smoking on exercise-induced brain mitochondrial adaptations in the hippocampus and pre-frontal cortex of adult mice. The animals were exposed to chronic cigarette smoke followed by 8 weeks of moderate-intensity physical exercise that increased mitochondrial activity in the hippocampus and pre-frontal cortex in the non-smoker mice. However, mice previously exposed to cigarette smoke did not present these exercise-induced mitochondrial adaptations. Our results suggest that smoking can inhibit some brain health-promoting changes induced by physical exercise.

Oxidative stress and inflammatory parameters after an Ironman race.

OBJECTIVE: The aim of the present study was to investigate oxidative stress markers and inflammatory response in triathletes after an Ironman race (IR). DESIGN: Descriptive research. PARTICIPANTS: Eighteen well-trained male triathletes (mean age, 34.7 +/- 2.15 years; weight, 69.3 +/- 1.9 kg; height, 1.81 +/- 0.58 cm) participated in the study. SETTING: Ironman Triathlon (3.8-km swim, 180-km cycle, 42.2-km run). Mean environmental conditions ranged from 20 to 25 degrees C and from 79% to 85% relative humidity. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Before the race and up to 20 minutes after completing the full race, the weights and heights of volunteers were measured and a 10 mL blood sample was drawn from an antecubital vein. Aliquots of washed/lysed red blood cells and plasma/serum samples were stored at -80 degrees C. Lipid peroxidation, protein carbonylation, superoxide dismutase and catalase activities, and cytokines levels [tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-6, IL-10, and IL-1ra] were determined. RESULTS: After the IR, the results showed a significant increase in TBARS levels (prerace = 1.15 +/- 0.11; postrace = 1.98 +/- 0.27), lipid hydroperoxide content (prerace = 0.75 +/- 0.03; postrace = 1.46 +/- 0.18), protein carbonylation (prerace = 0.67 +/- 0.12; postrace = 2 0.15 +/- 0.60), superoxide dismutase (prerace = 2.67 +/- 0.62; postrace = 3.97 +/- 1.48), and catalase (prerace = 1.48 +/- 0.18; postrace = 2.84 +/- 0.39). TNF-alpha, IL-6, and IL-10 were not detected at basal conditions, but all markers were significantly increased after the IR (TNF-alpha: prerace = ND and postrace = 67.47 +/- 10.34; IL-6: prerace = ND and postrace = 55.41 +/- 3.45; IL-10: prerace = ND and postrace = 122.53 +/- 9.69; IL-1ra: prerace = 127.79 +/- 25.65 and postrace = 259.51 +/- 32.9). CONCLUSIONS: An Ironman race provokes significant alterations in oxidative stress and inflammatory parameters. Thus, more studies with other markers and different designs are needed to elucidate the cellular alterations induced by an IR.

Physical exercise prevents the exacerbation of oxidative stress parameters in chronic kidney disease.

OBJECTIVE: Reactive oxygen species play an important role in the pathogenesis of chronic kidney disease (CKD). Physical exercise was suggested as a useful approach to diminish impaired oxidative defense mechanisms. This study sought to observe the effects of physical training before the induction of renal lesions on oxidative stress parameters in animals induced for CKD. METHODS: Twenty-four male Wistar rats were divided into four groups (n = 6): sham, sham plus exercise, CKD, and CKD plus exercise. Exercise groups performed physical training on a treadmill for 8 weeks (up to 1 km/h for 50 min/day, 5 days/week). Forty-eight hours after the final exercise session, a surgical reduction of renal mass was performed (5/6 nephrectomized). Thirty days later, blood samples were collected to determine serum creatinine and urea concentrations, and the right kidney was surgically removed and stored at -70 degrees C for later analysis of superoxide production, antioxidant enzymes (superoxide dismutase and catalase), and oxidative damage of lipids (thiobarbituric acid reactive susbstances level) and proteins (carbonyl groups and sulfhydryl content). RESULTS: A significant increase occurred in creatinine and urea levels, superoxide production, antioxidant enzymes, and oxidative damage in the CKD group, compared with sham-treated animals (P < .05). Physical training prevented superoxide production, and decreased the oxidative damage in the CKD group (P < .05), but did not increase the effect of antioxidants. CONCLUSION: Physical training before induction of a renal lesion is capable of improving oxidative damage parameters and oxidant production, without altering renal function and the antioxidant defense system.