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AIM To identify anthropometric indicators that could predict pelvic floor muscle distress (PFMD) in young women. METHOD A cross-sectional study was conducted, whose sample consisted of 54 women aged between 18 and 35 years. The Pelvic Floor Distress Inventory was used to assess the PFMD. The anthropometric indicators evaluated were body mass index (BMI) being measured the weight and height, body fat percentage (skinfolds), waist circumference (WC), waist-to-hip ratio (WHR), and relative fat mass (RFM), which is calculated from height and WC. Descriptive and inferential statistics (Spearman correlation, simple linear regression, and receiver operating characteristic curve) were used, with a significance level of 5%. RESULTS The PFMD and the anthropometric indicators BMI (r = .43), body fat percentage (r = .42), WC (r = .46), WHR (r = .49), and RFM (r = .48) showed a positive and moderate correlation (P

Major depressive disorder (MDD) is one of the most prevalent forms of mental illness also affecting older adults. Recent evidence suggests a relationship between MDD and neurodegenerative diseases, including Parkinson's disease (PD). Individuals with PD have a predisposition to developing MDD, and both neurobiological conditions are associated with oxidative stress. Thus, we conducted this study to investigate depressive-like behavior and oxidative stress parameters using both animal models of PD and stress. Adult Wistar rats were subjected to chronic mild stress (CMS) protocol by 40 days and then it was used 6-hydroxydopamine (6−OHDA) as a model of PD, into the striatum. The experimental groups were: Control + Sham, Stress + Sham, Control+6−OHDA, and Stress+6−OHDA. Depressive like-behavior was evaluated by the forced swimming test (FST) and spontaneous locomotor activity by open-field test. Oxidative stress parameters were measured in the striatum, hippocampus, and prefrontal cortex (PFC). The results showed effects to increase immobility and decrease climbing times in the FST in Stress + Sham, Control+6−OHDA, and Stress+6−OHDA groups. The number of crossings and rearings were decreased in the Stress+6−OHDA group. The lipid peroxidation was increased in the PFC of Stress + Sham, and the hippocampus and striatum of Stress + Sham and Control+6−OHDA groups. Carbonyl protein levels increased in the PFC of Stress + Sham and striatum in Control+6−OHDA. Nitrite/Nitrate concentration was elevated in the PFC of Stress + Sham, in the hippocampus of Control+6−OHDA, the striatum of Stress + Sham, and Control+6−OHDA groups. Myeloperoxidase (MPO) activity was increased in the PFC and hippocampus of Stress + Sham and Control+6−OHDA groups. The activity of catalase decreased in the PFC of the Stress + Sham group. The activity of the superoxide dismutase (SOD) was decreased in the PFC of the Stress + Sham group, in the hippocampus of Stress + Sham and Control+6−OHDA groups, and the striatum of Control+6−OHDA group. These findings suggest that both stress and 6−OHDA induce depressive-like behavior and oxidative stress in the brain. The joining models have little evidence of the effects. Thus these findings suggest that other pathways are involved in the common point of the pathophysiology of PD and MDD.

OBJECTIVE Test the association between the practice of physical activity (PA) according to the gestational trimesters and the occurrence of cesarean delivery, prematurity, and low birth weight in puerperal women assisted in the Unified Health System of Santa Catarina, Brazil. METHODS A cross-sectional study was conducted with a probabilistic sample of puerperal women who gave birth in public maternity hospitals in Santa Catarina from January to August 2019. The cesarean delivery outcome was self-reported, and information on premature birth (< 37 gestational weeks) and low birth weight (< 2,500 grams) were obtained from medical records. The practice of PA during pregnancy and according to each trimester was self-reported. Multivariate Logistic Regression analyses and interviews with 3,580 puerperal women were carried out. RESULTS PA practice during any period of pregnancy was reported by 20.6% of the sample, with a gradual reduction in prevalence according to the gestational trimester (16.2%, 15.4%, and 12.8%). The highest prevalences of outcomes concerning the total sample were observed in puerperal women who did not practice PA in the third trimester, with 43.9% for cesarean delivery, 7.7% for low birth weight, and 5.5% for premature birth. The odds of cesarean delivery (OR = 1.40; 95%CI 1.10–1.76) and low birth weight (OR = 1.99; 95%CI 1.04–3.79) were, respectively, 40% and 99% higher among puerperal women who did not practice PA in the third trimester of pregnancy when compared to those who practiced PA. There was no association between PA practice and prematurity. CONCLUSION Puerperal women who did not practice PA in the third trimester of pregnancy were more likely to have cesarean delivery and low birth weight newborns.

Blood brain barrier (BBB) permeability and oxidative stress have been reported to be important mechanisms for brain damage following ischemic stroke and stanniocalcin-1 (STC-1), a neuroprotective protein, has anti-inflammatory and anti-oxidative stress properties. Herein, we report the effect of STC-1 on BBB permeability and brain oxidative stress after stroke in an animal model. Male Wistar received an intracerebroventricularly injection of human recombinant STC-1 (100 ng/kg) or saline and were subjected to sham procedure or global cerebral ischemia/reperfusion (I/R) model. Six and 24 h after I/R, neurological evaluation was performed; at 24 h brain water content was evaluated in the total brain, and BBB permeability, nitrite/nitrate (N/N) concentration, lipid peroxidation, protein carbonyls formation, superoxide dismutase (SOD) and catalase (CAT) activity were determined in the hippocampus, cortex, prefrontal cortex, striatum and cerebellum. Rats exhibited neurological deficit at 6 and 24 h after I/R and STC-1 reduction at 24 h. After I/R there were an increase of brain water content, BBB permeability in the hippocampus, cortex and pre-frontal cortex and N/N in the hippocampus, and STC-1 decreased this level only in the hippocampus. STC-1 decreased lipid peroxidation in the hippocampus, cortex and prefrontal cortex and protein oxidative damage in the hippocampus and cortex. SOD activity decreased in the hippocampus, cortex and prefrontal cortex after I/R and STC-1 reestablished these levels in the hippocampus and cortex. CAT activity decreased only in the hippocampus and cortex and STC-1 increased the CAT activity in the hippocampus. Our data provide the first experimental demonstration that STC-1 reduced brain dysfunction associated with cerebral I/R in rats, by decreasing BBB permeability and oxidative stress parameters.

The aim of the study described here was to investigate the effects of pulsed ultrasound and gold nanoparticles (AuNPs) on behavioral, inflammatory and oxidative stress parameters in an experimental model of overuse. Wistar rats performed 21 d of exercise on a treadmill at different intensities and were exposed to ultrasound in the presence or absence of AuNPs. The overuse model promoted behavioral changes and increased creatine kinase, superoxide dismutase and glutathione peroxidase activity, as well as the levels of superoxide, nitrotyrosine, nitric oxide, thiobarbituric acid reactive substance, carbonyl, tumor necrosis factor α and interleukin-6. These values were significantly decreased by AuNPs and by AuNPs plus ultrasound. Catalase activity remained unchanged and the glutathione level increased significantly after exposure to AuNPs plus ultrasound. These results suggest a susceptibility to anxiety as well as elevated levels of oxidative stress. However, therapeutic interventions with AuNPs plus ultrasound reduced the production of oxidants and oxidative damage and improved the anti-oxidant defense system.

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.

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.

The objective of the present study was to investigate the effects of exercise training on behavior and neurochemical parameters in mice exposed to cigarette smoke. To this aim, mice (C57 BL6) male (30-35 g) were exposed to cigarette smoke 60 consecutive days three times a day and they were subjected to treadmill training 8 weeks for 5 days/week. For behavior assessment, mice were tested in the open-field and forced to a swim test. The superoxide anion, thiobarbituric acid reactive substances and protein carbonyl formation were measured as markers of oxidative stress in hippocampus of mice. In addition, the brain-derived neurotrophic factor (BDNF) levels were measured in the hippocampus samples. Cigarette smoke group and cigarette smoke plus exercise group, increased immobility time in forced swimming test in rats compared to the control group, without affecting spontaneous locomotor activity. There was an increase in the levels of superoxide, TBARS and of protein carbonyl and a decreased in BDNF levels in the hippocampus of rats exposed to cigarette smoke and cigarette smoke plus exercise. Exercise alone did not change any of the parameters evaluated in this study. In conclusion, we observed that physical training improves the oxidative stress parameters, but does not alter depressive-like behavior neither prevent the decreases in BDNF levels in hippocampus induced by cigarette smoke.

INTRODUÇÃO: O uso terapêutico do laser de baixa potência na fisioterapia tem aumentado significativamente. OBJETIVO: Avaliar os efeitos da laserterapia de baixa potência nos parâmetros oxidativos na cicatrização de feridas em ratos. MÉTODOS: Dezoito ratos Wistar foram divididos randomicamente em 3 grupos (controle 5 dias, n=6; 5 dias/2 J/cm², n=6; 5 dias/4 J/cm², n=6). Uma única ferida circular medindo 8 X 8 mm foi cirurgicamente realizada no dorso do rato. Trinta minutos após a última irradiação, os ratos foram submetidos à eutanásia, e o tecido irradiado foi removido cirurgicamente e armazenado a -70ºC. Foi determinada a atividade das enzimas da cadeia respiratória: DCIP oxirredutase (complexo II) e succinato desidrogenase solúvel (SDH), atividade do citocromo c oxidase (complexo IV), produção de ânion superóxido, atividade da superóxido dismutase (SOD) e catalase (CAT). A lipoperoxidação foi avaliada pela técnica de TBARS. RESULTADOS: Os resultados mostram uma diminuição na atividade do complexo II nos grupos irradiados por 5 dias com 2 e 4 J/cm², enquanto a produção de ânion superóxido mostrou uma diminuição significativa no grupo irradiado por 5 dias com 4 J/cm² em relação ao grupo controle. Além disso, um aumento significativo na atividade da catalase foi observado no grupo irradiado por 5 dias com 2 J/cm², como também uma diminuição da peroxidação lipídica nos dois grupos irradiados. CONCLUSÕES: Os resultados do presente estudo indicam que o laser estimula a atividade antioxidante e protege a célula contra danos oxidativos durante o processo de cicatrização de feridas cutâneas em ratos. BACKGROUND: Therapeutic use of low-level laser in physical therapy has increased significantly. OBJECTIVE: To assess the effects of low-level laser therapy on the oxidative parameters of wound healing in rats. METHODS: Eighteen Wistar rats were randomly divided into three groups (control, 5 days, n=6; 2 J/cm², 5 days, n=6; 4 J/cm², 5 days, n=6). A single circular wound measuring 8 x 8 mm was surgically created on the rats' backs. Thirty minutes after the last irradiation, the rats were euthanized and the irradiated tissue was surgically removed and stored at -70°C. We determined the activity of the respiratory chain enzymes DCIP oxidoreductase (complex II) and soluble succinate dehydrogenase (SDH); the activity of cytochrome c oxidase (complex IV); the production of superoxide anion; and the activity of superoxide dismutase (SOD) and catalase (CAT). Lipid peroxidation was assessed by means of the TBARS assay. RESULTS: There was a decrease in the complex II activity in the groups irradiated for 5 days with 2 and 4 J/cm², while superoxide anion production decreased significantly in the group irradiated for 5 days with 4 J/cm² when compared with the control group. There was also a significant increase in CAT activity in the group irradiated for 5 days with 2 J/cm² as well as a decrease in lipid peroxidation activity in the two irradiated groups. CONCLUSIONS: The results of the present study indicate that laser stimulates antioxidant activity and protects cells against oxidative damage during the wound healing process in rats.

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-cc(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-EEincreased 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.

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

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 × 15 min/day) and continuous treadmill exercise (45 min/day). Training significantly (P

This study aimed to evaluate the effects of two different protocols for physical exercise (strength and aerobic training) on mitochondrial and inflammatory parameters in the 6-OHDA experimental model of Parkinson’s disease. Six experimental groups were used (n=12per group): untrained + vehicle (Sham), strength training + vehicle (STR), treadmill training + vehicle (TTR), untrained + 6-OHDA (U + 6-OHDA), strength training + 6-OHDA (STR + 6-OHDA), and treadmill training + 6-OHDA (TTR + 6-OHDA). The mice were subjected to strength or treadmill training for 8 weeks. PD was inducedviastriatal injection of 6-OHDA 24 h after the last exercise session. Mice were euthanized by cervical dislocation and the striatum and hippocampus were homogenized to determine levels of tyrosine hydroxylase (TH), nuclear factor kappa B (NF-κB) p65, and sirtuin 1 (Sirt1) by western blot; tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), IL-17, interferon-γ(IFN-γ), and transforming growth factorβ1 (TGF-β1) levels by ELISA; NO content; and complex I (CI) activity. STR + 6-OHDA mice had higher TH levels and CI activity and lower NF-κB p65 and IFN-γlevels in the striatum compared to U + 6-OHDA mice, while TTR + 6-OHDA mice had higher Sirt1 levels and CI activity in both the striatum and the hippocampus, compared to U + 6-OHDA mice. Strength training increased CI activity and TH and Sirt1 levels and reduced NO, NF-κB p65, TNF-α, IFN-γ, IL-1β, and TGF-β1 levels in 6-OHDA mice, while treadmill exercise increased CI activity and NO, TH, and Sirt1 levels and reduced NF-κB p65, TNF-α, IFN-γ, and IL-1βlevels. Our results demonstrated that both treadmill training and strength training promote neuroprotection, possibly by stimulating Sirt1 activity, which may in turn regulate both mitochondrial function and neuroinflammationviadeacetylation of NF-κB p65. Changes in nitric oxide levels may also be a mechanism by which 6-OHDA-induced inflammation is controlled.

Depression is a neuropsychiatric disorder that is commonly found in patients with Parkinson's disease (PD). Many studies have suggested that physical exercise can have an antidepressant effect by increasing the levels of brain-derived neurotrophic factor (BDNF), and may also prevent neurodegenerative disease. However, different forms of training may promote different changes in the brain. The aim of this study was to investigate the effects of two types of physical training on depressive-like behavior, and on the levels of proBDNF, BDNF, and its receptor, TrkB, in a mouse model of PD. C57BL/6 mice were subjected to 60 days of exercise: either running on a treadmill or performing a strength exercise. PD was induced by striatal administration of 6-OHDA 24 h after the last physical exercise session. Seven days after 6-OHDA injection, depressive-like behavior and apomorphine-induced rotational behavior were evaluated. The levels of proBDNF, BDNF, and TRKB were measured in the striatum and the hippocampus of mice by immunoblotting assay. The 6-OHDA-treated animals showed a significant increase in immobility time and rotational behavior compared with the control group. In addition, significant decreases in the levels of proBDNF, BDNF, and its receptor, TrkB were observed in the 6-OHDA group. Both types of physical exercise prevented depressive-like behavior and restored the levels of proBDNF, BDNF, and TrkB in the striatum and hippocampus of mice administered 6-OHDA. Our results demonstrate that exercise training was effective for neuroprotection in the striatum and the hippocampus in an experimental model of PD.

The effect of physical training on the neurochemical and oxidative stress markers were evaluated in the striatum of rats with Parkinson's disease (PD). Untrained+sham-operated (USO), untrained+PD (UPD), trained+sham-operated (TSO), and trained+PD (TPD) were submitted to training on the treadmill. The PD was induced and 7 days after the lesion, the animals underwent a rotational test and euthanasia by decapitation. The striatum was homogenized for Western Blot with anti-tyrosine hydroxylase (TH), anti-brain-derived neurotrophic factor (BDNF), anti-α-synuclein, anti-sarcoplasmic reticulum Ca(2+)-ATPase (SERCA II), anti-superoxide dismutase (SOD), anti-catalase (CAT), anti-glutathione peroxidase (GPX), and specific buffer for oxidative damage (TBARS and carbonyl content). The UPD and TPD groups showed a clear rotational asymmetry, apart from a significant reduction in the level of TH, BDNF, α-synuclein, SOD, CAT, and GPX as well as an increase in the TBARS and carbonyl content, as observed in the UPD group. The TH level was not significantly altered but the TPD group increased the levels of BNDF, SERCA II, SOD, and CAT and decreased the oxidative damage in lipids and protein. The effects of exercise on PD indicate the possibility that exercise, to a certain extent, modulates neurochemical status in the striatum of rats, possibly by improving the oxidative stress parameters.

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.

Considerable evidence has indicated a pro-oxidant status in the brain of people with Down's syndrome (DS), which may contribute to motor and cognitive impairments verified in this condition. On the other hand, previous studies addressing the role of physical exercise on oxidative stress and antioxidant status in DS have indicated conflicting results. Here, we investigated the effects of a supervised judo training of controlled intensity and monitored on the basis of lactate threshold on the blood oxidative stress status and motor coordination in 21 young adults with DS. The training extended over a period of 16 weeks and consisted of three sessions per week. The exercise improved the motor function and significantly decreased lactate production in the DS subjects. However, blood markers of oxidative damage to lipids (TBARS and lipid peroxides) and proteins (carbonyls) were increased by the judo training. Moreover, superoxide dismutase and catalase activity also increased, while glutathione peroxidase activity remained unaltered after exercise. These results reinforce the notion that physical exercise can improve motor disabilities in people with DS. More importantly, our findings demonstrate that the beneficial effects are accompanied by some degree of oxidative stress, suggesting that young adults with DS may be more susceptible to physical training-induced oxidative stress than adolescents with DS, which should be taken into account in physical training programs for this population.