Effects of different physical training protocols on ventricular oxidative stress parameters in infarction-induced rats.

AIM: Physical exercise is important in the prevention and treatment of cardiovascular diseases. Nevertheless, controversy remains around type and intensity of effort required for significant biochemical protective changes. This study investigates two exercise protocols on ventricular oxidative parameters in rats post-infarction. MAIN METHODS: Thirty-six 2-month-old male Wistar rats were divided in two groups (n=18): Sham and acute myocardial infarction (AMI) conducted by blocking the coronary artery. Thirty days after AMI, animals were divided in 6 subgroups (n=6): sham, sham+continuous training (60 min), sham+interval training, AMI, AMI+continuous training, and AMI+interval training. Training was conducted in water (30-32°C) 5 times a week for 6 weeks. Animals were sacrificed 48 h after the last exercise routine. Left ventricles were used for oxidative stress analyses (antioxidant enzyme activity and level, oxidative damage) and HIF1α and cit c oxidase expression. KEY FINDINGS: After AMI, both exercise models decreased superoxide levels significantly. Training routines did not alter SOD expression and activity, though CAT expression increased with continuous training and GPX level diminished in both training groups, which coincided with the increase in GPX activity. Lipid damage decreased only in the continuous training group, while protein damage decreased only in the interval training group. Cytochrome C increased in both groups, while HIF-1 α dropped significantly after both exercise protocols. SIGNIFICANCE: Significant improvement occurred in myocardium redox status in rats challenged with AMI after different training routines. However, continuous training seems to be more efficient in improving the parameters analyzed.

Alterations in muscular oxidative metabolism parameters in incremental treadmill exercise test in untrained rats.

The present study investigates the effects of incremental exercise test on muscular oxidative metabolism. Thirty-six 2-month-old male Wistar rats were distributed in seven groups that performed exercise at different levels: first level (control), second level (0.6 km/h), third level (0.6 and 0.8 km/h), fourth level (0.6, 0.8 and 1.0 km/h), fifth level (0.6, 0.8, 1.0 and 1.2 km/h), sixth level (0.6, 0.8, 1.0, 1.2 and 1.4 km/h), and seventh level (0.6, 0.8, 1.0, 1.2, 1.4 and 1.6 km/h). At the end of the exercise challenge, level of blood lactate (BL), glycogen content (MG), creatine kinase (CK), complexes (CI, CII, CIII, CIV), oxidative damage, succinate dehydrogenase (SDH), cytochrome c oxidase as well as antioxidant enzymes (SOD and CAT) expression were measured. The speed of 1.0 km/h increased BL level, while 1.2 km/h decreased MG and increased serum CK. Increased SDH expression was observed after intensity levels 6 and 7, and cytochrome c oxidase expression increased after levels 5, 6 and 7, in comparison with lower intensity levels, ETC enzyme activities increased when exercise was applied at intensities of 0.8 km/h (CI), 1.0 km/h (CII and CIII), and 1.2 km/h (CIV). The increase in SOD expression did not occur as observed for superoxide production, except for rats that underwent exercise at level 7, but CAT expression increased significantly in all levels, starting from level 3. Our results show interesting alterations in the muscular metabolism parameters, and suggest a differential response of muscle oxidative metabolism when intense exercise is applied at different speeds.

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.

Vitamin E supplementation decreases muscular and oxidative damage but not inflammatory response induced by eccentric contraction.

The purpose of this study was to investigate the effects of vitamin E supplementation on muscular and oxidative damage, as well as the inflammatory response induced by eccentric exercise (EE) in humans. Twenty-one participants with a mean age of 22.5 +/- 4 years, weight of 68.2 +/- 4.9 kg, and height of 173 +/- 4.3 cm were selected and divided randomly into two groups: supplemented (S) (n = 11) and placebo (P) (n = 10). Fourteen days after starting supplementation, subjects performed EE (three sets until exhaustion with elbow flexion and extension on the Scott bench, 80% 1 RM). Blood samples were collected on days 0, 2, 4, and 7 after EE. Muscle soreness (MS), lactate dehydrogenase (LDH) activity, lipid peroxidation, protein carbonylation, tumor necrosis factor-alpha (TNF-alpha), and interleukin 10 (IL-10) levels were determined. We measured a significant increase in MS, LDH, lipid peroxidation, and carbonylation in both groups on days 2, 4, and 7 after eccentric contractions (EC). Values of the supplement group were lower than those of the placebo group at 4 and 7 days after EC in all parameters. Both groups showed significantly increased TNF-alpha on the second day and IL-10 concentration on the fourth and seventh days after EE. The results suggest that vitamin E supplementation represents an important factor in the defense against oxidative stress and muscle damage but not against the inflammatory response in humans.

Effect of different models of physical exercise on oxidative stress markers in mouse liver.

The aim of this study was to investigate the effect of different protocols of physical exercise on oxidative stress markers in mouse liver. Twenty-eight male CF1 mice (30-35 g) were distributed into 4 groups (n = 7) - untrained (UT), continuous running (CR), downhill running (D-HR), and intermittent running (IR) - and underwent an 8-week training program. Forty-eight hours after the last training session, the animals were killed, and their livers were removed. Blood lactate, creatine kinase, citrate synthase, thiobarbituric acid reactive species, carbonyl, superoxide dismutase (SOD), and catalase (CAT) activities were assayed. Results show a decrease in the level of lipoperoxidation and protein carbonylation in the CR and D-HR groups. SOD activity was significantly increased and CAT activity was reduced in the CR and D-HR groups. Our findings indicate that CR and D-HR may be important for decreasing oxidative damage and in the regulation of antioxidant enzymes (SOD and CAT) in the livers of trained mice.

Physical exercise increases mitochondrial function and reduces oxidative damage in skeletal muscle.

The present study investigated mitochondrial adaptations and oxidative damage after 4 and 8 weeks of running training in skeletal muscle of mice. Twenty-one male mice (CF1, 30-35 g) were distributed into the following groups (n = 7): untrained (UT); trained-4 weeks (T4); trained-8 weeks (T8). Forty-eight hours after the last training session the animals were killed by decapitation and quadriceps (red portion) were removed and stored at -70 degrees C. Succinate dehydrogenase (SDH), complexes I, II, II-III and IV, lipoperoxidation (TBARS), protein carbonyls (PC) and total thiol content were measured. Results show that endurance training (8-wk) increases the SDH activity and complexes (I, II, III, IV), decreases oxidative damage (TBARS, CP) and increases total thiol content in skeletal muscle when compared to untrained animals. In conclusion, eight weeks of running training are necessary for increases in mitochondrial respiratory chain enzyme activities to occur, in association with decreased oxidative damage.

N-acetylcysteine supplementation and oxidative damage and inflammatory response after eccentric exercise.

The objective of the study was to verify the effect of N-acetylcysteine (NAC) supplementation on parameters of oxidative damage and inflammatory response after high-intensity eccentric exercise (EE). 29 participants with a mean age of 21.3+/-4 yr, weight of 74.5+/-7.7 kg, and height of 177.2+/-6.9 cm were selected and divided randomly into 3 groups: placebo (21 days; n=8), NAC (21 days; n=9), and NAC plus placebo (14 days; n=8). Four participants withdrew from the study for personal reasons. 14 days after starting supplementation, the participants performed EE: 3 sets until exhaustion (elbow flexion and extension on the Scott bench, 80% 1RM). Blood samples were collected before and on the 2nd, 4th, and 7th day after EE. Muscle soreness (MS), lipoperoxidation, protein carbonylation, tumor-necrosis factor- (TNF-), and interleukin 10 (IL-10) were determined. Results showed a significant increase in MS in all the groups on the 2nd day after EE and a decrease in the following days. A significant increase was observed in malondialdehyde and carbonyl levels on the 4th and 7th days after EE in all groups. TNF- increased significantly on the 2nd day after eccentric exercise and decreased in the following days irrespective of NAC supplementation; concentration of IL-10 increased significantly on the 4th day in all groups. Only the supplemented groups maintained high levels of IL-10 on the 7th day after EE. The results suggest that treatment with NAC represents an important factor in the defense against muscle soreness and has different effects on oxidative damage and pro- and anti-inflammatory cytokines.

Intense exercise induces mitochondrial dysfunction in mice brain.

There are conflicts between the effects of free radical over-production induced by exercise on neurotrophins and brain oxidative metabolism. The objective of this study was to investigate the effects of intense physical training on brain-derived neurotrophic factor (BDNF) levels, COX activity, and lipoperoxidation levels in mice brain cortex. Twenty-seven adult male CF1 mice were assigned to three groups: control untrained, intermittent treadmill exercise (3 x 15 min/day) and continuous treadmill exercise (45 min/day). Training significantly (P < 0.05) increased citrate synthase activity when compared to untrained control. Blood lactate levels classified the exercise as high intensity. The intermittent training significantly (P < 0.05) reduced in 6.5% the brain cortex COX activity when compared to the control group. BDNF levels significantly (P < 0.05) decreased in both exercise groups. Besides, continuous and intermittent exercise groups significantly (P < 0.05) increased thiobarbituric acid reactive species levels in the brain cortex. In summary, intense exercise promoted brain mitochondrial dysfunction due to decreased BDNF levels in the frontal cortex of mice.

Mitochondrial IV complex and brain neurothrophic derived factor responses of mice brain cortex after downhill training.

Twenty-four adult male CF1 mice were assigned to three groups: non-runners control, level running exercise (0 degrees incline) and downhill running exercise (16 degrees decline). Exercise groups were given running treadmill training for 5 days/week over 8 weeks. Blood lactate analysis was performed in the first and last exercise session. Mice were sacrificed 48 h after the last exercise session and their solei (citrate synthase activity) and brain cortices (BDNF levels and cytochrome c oxidase activity) were surgically removed and immediately stored at -80 degrees C for later analyses. Training significantly increased (P<0.05) citrate synthase activity when compared to untrained control. Blood lactate levels classified the exercise intensity as moderate to high. The downhill exercise training significantly reduced (P<0.05) brain cortex cytochrome c oxidase activity when compared to untrained control and level running exercise groups. BDNF levels significantly decreased (P<0.05) in both exercise groups.