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Resumo Este estudo teve por objetivo comparar os efeitos do exercício agudo com carga de trabalho relativa em gastrocnêmio de ratos Wistar com três e 18 meses. Os animais foram divididos em quatro grupos (n = 6): controle de três e 18 meses; exercício de três e 18 meses. Os grupos exercitados foram submetidos a uma única sessão de corrida na esteira com 60 minutos em velocidade de 0,8 km/h e 1,2 km/h. Foram analisados parâmetros do metabolismo (níveis de lactato, conteúdo de glicogênio, níveis de succinato desidrogenase, citocromo c oxidase e de estresse oxidativo (SOD, CAT e GPX). Os resultados mostraram um aumento nos marcadores metabólicos após o exercício agudo independentemente da idade dos animais e similaridade nos danos oxidativos apesar de as enzimas antioxidantes apresentarem modulação diferenciada nos animais mais velhos em comparação com animais jovens. Abstract The effects of exercise on the generation of reactive oxygen species and the response to muscle oxidative stress determines longevity. This study compares the effects of acute exercise with similar relative workload in rats with 3 and 18 months. The animals were divided into four groups (n = 6): control 3-months; exercise 3-months; control 18-months and exercise 18-months. Exercised groups underwent to a single bout of running with 60 minutes in the speed 0.8 km/h (18 months) and 1.2 km/h (3 months). Metabolic parameters (lactate levels, glycogen content, succinate dehydrogenase levels, cytochrome c oxidase) and oxidative stress (activity of superoxide dismutase, catalase and glutathione peroxidase). The results showed an increase in metabolic markers after acute exercise regardless of the age and similarity in oxidative damage even if the antioxidant enzymes are age-dependent. These results suggest that the effects of acute exercise at moderate intensity, affects the metabolism independent of age, and, that the differential response in enzymatic antioxidant system between groups do not promote protection against oxidative damage. Este estudio ha tenido como objetivo comparar los efectos del ejercicio agudo con carga de trabajo relativamente similar en el gastrocnemio de ratas Wistar con 3 y 8 meses. Se separó a los animales en cuatro grupos (n = 6): control de 3 y 18 meses, y ejercicio de 3 y 18 meses. Se sometió a los grupos de ejercicio a una sola sesión de carrera en la cinta durante 60 minutos con una velocidad de 0,8 km/h y 1,2 km/h. Se analizaron algunos parámetros del metabolismo (niveles de lactato, contenido de glucógeno, niveles de succionato-deshidrogenasa, citocromo c-oxidasa e de estrés oxidativo [superóxido-dismutasa, catalasa y glutatión-peroxidasa]). Los resultados mostraron un aumento de los marcadores metabólicos después del ejercicio agudo independientemente de la edad de los animales y la similitud de los daños oxidativos aunque las enzimas antioxidantes presentan modulación diferenciada en animales viejos en comparación con animales jóvenes.

Aims: The present study investigated the effect of different frequencies (three and five times a week) on electron transport chain and oxidative stress after 8 weeks of run training. Methods: Eighteen male mice (CF1, 30-35g) were distributed into the following groups (n=6): untrained (UT); trained three-time per week (T3) and trained five- time per week (T5). All training sessions were at the same intensity and duration (45min/day) in a treadmill for small animals. Forty-eight hours after the last training session, the animals were killed by decapitation and quadriceps (red portion) was removed and stored at -70ºC. Succinate dehydrogenase (SDH), complexes I, II, II-III, IV and hydroperoxides were measured. Results: Training sessions for five times per week were more effective in increasing the mitochondrial respiratory chain enzyme activities (SDH, complexes I, II, II-III, IV) as well as in decreasing the formation hydroperoxides than sessions performed for three times training per week (p

Age-associated decline in skeletal muscle mass and strength is associated with oxidative stress and Ca(2+) homeostasis disturbance. Exercise should be considered a viable modality to combat aging of skeletal muscle. This study aimed to investigate whether continuous and fractionated training could be useful tools to attenuate oxidative damage and retain calcium-handling proteins. We conducted the study using 24-month-old male Wistar rats, divided into control, continuous, and fractionated groups. Animals ran at 13 m min(-1) for five consecutive days (except weekends) for 6 weeks, for a total period of 42 days. Each session comprised 45 min of exercise, either continuous or divided into three daily sessions of 15 min each. Metabolic and oxidative stress markers, protein levels of mitochondrial transcription factors, and calcium-handling proteins were analyzed. Continuous exercise resulted in reduced ROS production as well as showed a decrease in TBARS levels and carbonyl content. On the other hand, fractionated training increased the antioxidant enzyme activities. The ryanodine receptor and phospholamban protein were regulated by continuous training while sodium calcium exchange protein was increased by the fractionated training. These data suggest that intracellular Ca(2+) can be modulated by various training stimuli. In addition, the modulation of oxidative stress by continuous and fractionated training may play an important regulatory role in the muscular contraction mechanism of aged rats, due to changes in calcium metabolism.

Exercise increases both the consumption of oxygen and the production of reactive species in biological tissues, and this is counterbalanced by antioxidant adaptations to regular physical training. When the intensity of exercise fluctuates between mild and moderate, it improves the status of reduction-oxidation balance in the brain and induces neuroplasticity. However, intense exercise can oxidize the brain and impair neurological function. The effect of the frequency of exercise, which is an important factor in physical training, is still unknown. The effect of periodic exercise on biomarkers of oxidative stress in the hippocampus of mice was evaluated in this study. Mice were made to run on a treadmill for 8 weeks, two, three, or five times per week, and their hippocampi and quadriceps femoris muscles were then dissected. Biomarkers of oxidative damage were negatively correlated with the frequency of exercise and mitochondrial muscular activity, while the sulfhydryl contents were positively correlated with exercise frequency. A logistic analysis revealed a dose-dependent effect of exercise on these biomarkers. In summary, these results suggested that manipulating the frequency of physical exercise could induce antioxidant-related adaptations in the hippocampi of adult mice.

The purpose of the present study was to investigate the effects of taurine supplementation on muscle performance, oxidative stress, and inflammation response after eccentric exercise (EE) in males. Twenty-one participants (mean age, 21 ± 6 years; weight, 78.2 ± 5 kg; height, 176 ± 7 cm) were selected and randomly divided into two groups: placebo (n = 10) and taurine (n = 11). Fourteen days after starting supplementation, subjects performed EE (3 sets until exhaustion, with EE of the elbow flexors on the Scott bench, 80% 1 repetition maximum (RM)). Blood samples were collected and muscle performance was measured on days 1, 14, 16, 18, and 21 after starting the supplements. Then, performance, muscle damage, oxidative stress, and inflammatory markers were analyzed. The taurine supplementation resulted in increased strength levels and thiol total content and decreased muscle soreness, lactate dehydrogenase level, creatine kinase activity, and oxidative damage (xylenol and protein carbonyl). Antioxidant enzymes (superoxide dismutase, catalase, and gluthatione peroxidase) and inflammatory markers (tumor necrosis factor, interleukin-1β (IL-1β), and interleukin-10 (IL-10)) were not altered during the recovery period compared with the placebo group. The results suggest that taurine supplementation represents an important factor in improving performance and decreasing muscle damage and oxidative stress but does not decrease the inflammatory response after EE.

The objective of the present study was to investigate the effects of eccentric training on the activity of mitochondrial respiratory chain enzymes, oxidative stress, muscle damage, and inflammation of skeletal muscle. Eighteen male mice (CF1) weighing 30-35 g were randomly divided into 3 groups (N = 6): untrained, trained eccentric running (16°; TER), and trained running (0°) (TR), and were submitted to an 8-week training program. TER increased muscle oxidative capacity (succinate dehydrogenase and complexes I and II) in a manner similar to TR, and TER did not decrease oxidative damage (xylenol and creatine phosphate) but increased antioxidant enzyme activity (superoxide dismutase and catalase) similar to TR. Muscle damage (creatine kinase) and inflammation (myeloperoxidase) were not reduced by TER. In conclusion, we suggest that TER improves mitochondrial function but does not reduce oxidative stress, muscle damage, or inflammation induced by eccentric contractions.

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.

It is well known that high-fat diets (HFDs) induce obesity and result in an increase in oxidative stress in adipose tissue, which leads to an impairment of fat mobilization by a downregulation of the lipases, such as hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL). On the other hand, exercise training leads to a reduction in adipose tissue and an improvement of antioxidant status and the lipolytic pathway. Our aim was to examine the influence of exercise and moderate intensity training on oxidative stress parameters and the relationship between the proteins involved in the lipolysis of animals subjected to a high-fat fed diet. Twenty-four mice were used and divided into 4 groups (n=6): standard diet (SD); standard diet plus exercise (SD+Ex); high-fat diet (HFD); and high-fat diet plus exercise (HFD+Ex). The animals received HFD for 90 days and submitted to a daily training protocol in swinging. The animals were euthanized 48 h after the last session of exercise. White adipose tissue epididymal fat was excised for the measurement of oxidative stress parameters and protein levels of lipolytic enzymes by Western blotting. The results show an increase in body weight after 90 days of HFD, and exercise training prevented great gain. In adipose tissue, lipid peroxidation and protein carbonylation increased after HFD and decreased significantly after exercise training. The protein level of CGI-58 was reduced, and FAS was increased in the HFD than in SD, whereas ATGL exhibited an increase (p0.05) in HFD than in SD. The exercise plays a significant role in reducing oxidative damage, along with the regulation of proteins that are involved in the lipolysis of animals exposed to HFD.

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.

To investigate the effects physical training exerts on markers of oxidative stress in rats with chronic kidney disease (CKD).Twenty-four male Wistar rats were divided into four groups (n=6): sham, CKD, exercise-sham and exercise-CKD. Surgical reduction of the renal mass was performed (5/6 nephrectomized) and exercise was conducted on a treadmill (50 min/day up to 1 km/h for, 5 days/week for eight weeks). Forty-eight hours after the last exercise session, blood (1 mL) was collected from the abdominal aorta and animals were decapitated. The left kidney was surgically removed and stored at -70 °C for subsequent analysis.An increase was observed in creatinine and urea levels, superoxide production, antioxidant enzymes, and oxidative damage in the CKD group, as compared to sham animals (p0.05). Physical training made superoxide production and oxidative damage decrease in the CKD group (p0.05), increasing SOD and GPX activity, though it did not increase the antioxidant effects of CAT, and renal parameters.Even without altering renal function in animals induced to CKD model, the results show that physical training is an important component in the treatment of CKD, because it exerted a positive influence on oxidative stress parameters, especially on the reduction in superoxide production and oxidative damage, as well as an improvement in the antioxidant defense system, like SOD and GPX.

Background The aim of the present study was to evaluate the protective effect of concurrent exercise in the degree of the insulin resistance in mice fed with a high-fat diet, and assess adiponectin receptors (ADIPOR1 and ADIPOR2) and endosomal adaptor protein APPL1 in different tissues. Methods Twenty-four mice were randomized into four groups (n = 6): chow standard diet and sedentary (C); chow standard diet and simultaneous exercise training (C-T); fed on a high-fat diet and sedentary (DIO); and fed on a high-fat diet and simultaneous exercise training (DIO-T). Simultaneously to starting high-fat diet feeding, the mice were submitted to a swimming exercise training protocol (2 x 30 minutes, with 5 minutes of interval/day), five days per week, for twelve weeks (90 days). Animals were then euthanized 48 hours after the last exercise training session, and adipose, liver, and skeletal muscle tissue were extracted for an immunoblotting analysis. Results IR, IRs, and Akt phosphorylation decreased in the DIO group in the three analyzed tissues. In addition, the DIO group exhibited ADIPOR1 (skeletal muscle and adipose tissue), ADIPOR2 (liver), and APPL1 reduced when compared with the C group. However, it was reverted when exercise training was simultaneously performed. In parallel, ADIPOR1 and 2 and APPL1 protein levels significantly increase in exercised mice. Conclusions Our findings demonstrate that exercise training performed concomitantly to a high-fat diet reduces the degree of insulin resistance and improves adipoR1-2/APPL1 protein levels in the hepatic, adipose, and skeletal muscle tissue.