Resistance training maintains physical function but does not prevent changes in body composition and biochemical markers after detraining in aging adults.

OBJECTIVE: The objective of the present study was to analyze the effects of 10 weeks of resistance training (RT) and subsequent 4 weeks of detraining on physical function, body composition, and biochemical markers in aging adults. METHODS: The study sample was selected by convenience and consisted of 12 women with a mean age of 58 ± 7 years. Physical function [Latin-American Group of Development for Maturity (GDLAM) general index], body composition, total and fractional cholesterol, triglycerides, and glycemia were assessed before and after RT (10 weeks) and detraining (4 weeks). RESULTS: After 10 weeks of RT, there were improvements in fat-free mass (39.1 ± 4.2 vs. 39.9 ± 4.4 kg; p < 0.05 and d = 0.2), fat mass (39.9 ± 6.3% vs. 38.7 ± 6.4%; p < 0.05 and d = -0.2), conicity index (1.47 ± 0.07 vs. 1.43 ± 0.06; p = 0.001 and d = -0.6), and physical function (GDLAM index [27.2 ± 5.5 vs. 25.0 ± 4.7; p = 0.001 and d = -0.4]). Significant improvements were also found in total cholesterol (271.8 ± 75.7 vs. 217.2 ± 52.2 mg/dL; p < 0.01 and d = -0.8), LDL-cholesterol (196.5 ± 61.6 vs. 159.3 ± 38.5 mg/dL; p < 0.01 and d = -0.7), HDL-cholesterol (53.1 ± 7.3 vs. 64.3 ± 23.7 mg/dL; p < 0.05 and d = 0.7), and triglycerides (165.8 ± 32.6 vs. 139.9 ± 46.6 mg/dL; p = 0.001 and d = -0.6). After the detraining period, all benefits in physical function were successfully maintained. CONCLUSION: RT provided benefits in physical function, body composition, and biochemical markers in aging adults. However, 4-week detraining impaired body composition and biochemical markers in the investigated sample.

The Taurine-Conjugated Bile Acid (TUDCA) Normalizes Insulin Secretion in Pancreatic ß-Cells Exposed to Fatty Acids: The Role of Mitochondrial Metabolism.

Bile acid tauroursodeoxycholic (TUDCA), formed from the association of ursodeoxycholic acid (UDCA) with taurine, has already been shown to increase mitochondrial biogenesis and cell survival, in addition to reduce reticulum stress markers in different cell types. However, its mechanism of action upon insulin secretion control in obesity is still unknown. In this sense, we seek to clarify whether taurine, associated with bile acid, could improve the function of the pancreatic ß-cells exposed to fatty acids through the regulation of mitochondrial metabolism. To test this idea, insulin-producing cells (INS1-E) were exposed to a fatty acid mix containing 500 µM of each palmitate and oleate for 48 hours treated or not with 300 µM of TUDCA. After that, glucose-stimulated insulin secretion and markers of mitochondrial metabolism were evaluated. Our results showed that the fatty acid mix was efficient in inducing hyperfunction of INS1-E cells as observed by the increase in insulin secretion, protein expression of citrate synthase, and mitochondrial density, without altering cell viability. The treatment with TUDCA normalized insulin secretion, reducing the protein expression of citrate synthase, mitochondrial mass, and the mitochondrial membrane potential. This effect was associated with a decrease in the generation of mitochondrial superoxide and c-Jun N-terminal kinase (JNK) protein content. The findings are also consistent with the hypothesis that TUDCA normalizes insulin secretion by improving mitochondrial metabolism and redox balance. Thus, it highlights likely mechanisms of the action of this bile acid on the glycemic homeostasis reestablishment in obesity.

Amino acid restriction alters survival mechanisms in pancreatic beta cells: possible role of the PI3K/Akt pathway.

BACKGROUND AND AIMS: Malnutrition in the early stages of life may lead to changes in the glycemic metabolism during adulthood, such as pancreatic beta cells dysfunction and failure. Therefore, this study aimed to evaluate the effects of an in vitro amino acid restriction model on the function and viability of pancreatic beta cells. METHODS: Insulin-producing cells (INS-1E) were maintained in control or amino acid restricted culture medium containing 1 × or 0.25 × of amino acids, respectively, for 48 h. RESULTS: Amino acid restricted group showed lower insulin secretion and insulin gene expression, reduced mitochondrial oxygen consumption rate and reactive oxygen species production. Besides, amino acid restricted group also showed higher levels of endoplasmic reticulum stress and apoptosis markers and enhanced Akt phosphorylation. However, even with higher levels of apoptosis markers, amino acid restricted group did not show higher levels of cell death unless the PI3K/Akt pathway was inhibited. CONCLUSION: Amino acid restricted beta cell viability seems to be dependent on the PI3K/Akt pathway.

Amino acid restriction increases ß-cell death under challenging conditions.

Malnutrition programs metabolism, favor dysfunction of ß cells. We aimed to establish an in vitro protocol of malnutrition, assessing the effect of amino acid restriction upon the ß cells. Insulin-producing cells INS-1E and pancreatic islets were maintained in RPMI 1640 medium containing 1× (Ctl) or 0.25× (AaR) of amino acids. We evaluated several markers of ß-cell function and viability. AaR Insulin secretion was reduced, whereas cell viability was unaltered. Calcium oscillations in response to glucose increased in AaR. AaR showed lower Ins1 RNAm, snap 25, and PKC (protein kinase C) protein content, whereas phospho-eIF2α was increased. AaR cells exposed to nutrient or chemical challenges displayed higher apoptosis rates. We showed that amino acid restriction programmed ß cell and induced functional changes. This model might be useful for the study of molecular mechanisms involved with ß-cell programming helping to establish novel therapeutic targets to prevent harmful outcomes of malnutrition.

Physical exercises decreases thrombus and neointima formation in atherosclerotic mice.

The practice of physical exercise is highly indicated to prevent cardiovascular diseases and is directly related to the improvement of endothelial function and the regulation of arterial blood pressure. The objective of this study was to analyze the effect of physical exercise in vascular remodeling after FeCl3 chemically induced arterial injury on atherosclerotic mice. To analyze the effect of exercises on thrombus formation, LDL receptor-deficient mice were fed for 6 weeks with a high-fat diet and performed or not physical exercises for 2 weeks before the arterial injury. To verify endothelium recovery the animals were exercised or not 2 weeks before the injury, and 3 weeks after it, when the vessels were analyzed. In this work, we observed that physical exercises done only before arterial injury reduced thrombosis time, protected the endothelial layer, promoted the recruitment of CD34 positive progenitor cells, increased the level of eNOS and gelatinases activities and decreased the number of inflammatory cells in the vessel, but do not avoid the growth of neointima. Otherwise exercises done before and continued after injury, increased gelatinase activities, reduced lipid deposition in the aortic arch and prevented neointima formation. Thus, we could conclude that physical exercises are done before and continued after endothelial injury stimulate endothelial recovery by promoting endothelial cell growth, matrix remodeling and decreasing inflammation in the vessel wall.

Protein malnutrition mitigates the effects of a high-fat diet on glucose homeostasis in mice.

Nutrient malnutrition, during the early stages of development, may facilitate the onset of metabolic diseases later in life. However, the consequences of nutritional insults, such as a high-fat diet (HFD) after protein restriction, are still controversial. We assessed overall glucose homeostasis and molecular markers of mitochondrial function in the gastrocnemius muscle of protein-restricted mice fed an HFD until early adulthood. Male C57BL/6 mice were fed a control (14% protein-control diet) or a protein-restricted (6% protein-restricted diet) diet for 6 weeks. Afterward, mice received an HFD or not for 8 weeks (mice fed a control diet and HFD [CH] and mice fed a protein-restricted diet and HFD [RH]). RH mice showed lower weight gain and fat accumulation and did not show an increase in fasting plasma glucose and insulin levels compared with CH mice. RH mice showed higher energy expenditure, increased citrate synthase, peroxisome-proliferator-activated receptor gamma coactivator 1-alpha protein content, and higher levels of malate and α-ketoglutarate compared with CH mice. Moreover, RH mice showed increased AMPc-dependent kinase and acetyl coenzyme-A (CoA) carboxylase phosphorylation, lower intramuscular triacylglycerol content, and similar malonyl-CoA levels. In conclusion, protein undernourishment after weaning does not potentiate fat accumulation and insulin resistance in adult young mice fed an HFD. This outcome seems to be associated with increased skeletal muscle mitochondrial oxidative capacity and reduced lipids accumulation.

Protein malnutrition blunts the increment of taurine transporter expression by a high-fat diet and impairs taurine reestablishment of insulin secretion.

Taurine (Tau) restores ß-cell function in obesity; however, its action is lost in malnourished obese rodents. Here, we investigated the mechanisms involved in the lack of effects of Tau in this model. C57BL/6 mice were fed a control diet (CD) (14% protein) or a protein-restricted diet (RD) (6% protein) for 6 wk. Afterward, mice received a high-fat diet (HFD) for 8 wk [CD + HFD (CH) and RD + HFD (RH)] with or without 5% Tau supplementation after weaning on their drinking water [CH + Tau (CHT) and RH + Tau (RHT)]. The HFD increased insulin secretion through mitochondrial metabolism in CH and RH. Tau prevented all those alterations in CHT only. The expression of the taurine transporter (Tau-T), as well as Tau content in pancreatic islets, was increased in CH but had no effect on RH. Protein malnutrition programs ß cells and impairs Tau-induced restoration of mitochondrial metabolism and biogenesis. This may be associated with modulation of the expression of Tau-T in pancreatic islets, which may be responsible for the absence of effect of Tau in protein-malnourished obese mice.-Branco, R. C. S., Camargo, R. L., Batista, T. M., Vettorazzi, J. F., Borck, P. C., dos Santos-Silva, J. C. R., Boschero, A. C., Zoppi, C. C., Carneiro, E. M. Protein malnutrition blunts the increment of taurine transporter expression by a high-fat diet and impairs taurine reestablishment of insulin secretion.

Protein malnutrition potentiates the amplifying pathway of insulin secretion in adult obese mice.

Pancreatic beta cell (ß) dysfunction is an outcome of malnutrition. We assessed the role of the amplifying pathway (AMP PATH) in ß cells in malnourished obese mice. C57Bl-6 mice were fed a control (C) or a low-protein diet (R). The groups were then fed a high-fat diet (CH and RH). AMP PATH contribution to insulin secretion was assessed upon incubating islets with diazoxide and KCl. CH and RH displayed increased glucose intolerance, insulin resistance and glucose-stimulated insulin secretion. Only RH showed a higher contribution of the AMP PATH. The mitochondrial membrane potential of RH was decreased, and ATP flux was unaltered. In RH islets, glutamate dehydrogenase (GDH) protein content and activity increased, and the AMP PATH contribution was reestablished when GDH was blunted. Thus, protein malnutrition induces mitochondrial dysfunction in ß cells, leading to an increased contribution of the AMP PATH to insulin secretion through the enhancement of GDH content and activity.

Recreational Anabolic-Androgenic Steroid Use Associated With Liver Injuries Among Brazilian Young Men.

BACKGROUND: The recreational use of anabolic-androgenic steroids (AAS) has reached alarming levels among healthy people. However, several complications have been related to consumption of these drugs, including liver disorders. OBJECTIVE: To evaluate the prevalence of liver injuries in young Brazilian recreational AAS users. METHODS: Between February/2007 and May/2012 asymptomatic bodybuilders who were ≥18 years old and reported AAS use for ≥6 months were enrolled. All had clinical evaluations, abdominal ultrasound (AUS), and blood tests. RESULTS: 182 individuals were included in the study. The median age (interquartile range) was 26.0 years (22.0-30.0) and all were male. Elevated liver enzyme levels were observed in 38.5% (n = 70) of AAS users, and creatine phosphokinase was normal in 27.1% (n = 19) of them. Hepatic steatosis was observed by AUS in 12.1% of the sample. One individual had focal nodular hyperplasia and another had hepatocellular adenoma. One case each of hepatitis B and C virus infection was found. A diagnosis of toxic liver injury was suggested in 23 (12.6%) AAS users without a history of alcohol or other medications/drugs consumption, or evidence of other liver diseases. CONCLUSIONS/IMPORTANCE: Young Brazilian recreational AAS users presented a wide spectrum of liver injuries that included hepatotoxicity, fatty liver, and liver neoplasm. They also presented risk factors for liver diseases such as alcohol consumption and hepatitis B and C virus infection. The results suggest that the risk of AAS use for the liver may be greater than the esthetic benefits, and demonstrate the importance of screening AAS users for liver injuries.

The influence of concomitant use of alcohol, tobacco, cocaine, and anabolic steroids on lipid profiles of Brazilian recreational bodybuilders.

Anabolic-androgenic steroids (AAS) are used to enhance physical performance and/or appearance. The aim of this study was to evaluate the influence of the concomitant use of alcohol, tobacco, cocaine, and AAS on blood lipid profiles of 145 asymptomatic male bodybuilders from the Northeast region of Brazil. Interviews, clinical exams, and serological evaluations were performed on all participants between 2007 and 2009. All subjects' self-reported use of testosterone or its derivatives, 118 individuals reported alcohol intake, 27-reported cigarette smoking, and 33 confirmed cocaine use. Four subjects were users of all drugs at the same time. Higher levels of total cholesterol and LDL-cholesterol were observed among concomitant users of alcohol, tobacco, cocaine, and AAS. The study's limitations are noted.

Decreased insulin secretion in islets from protein malnourished rats is associated with impaired glutamate dehydrogenase function: effect of leucine supplementation.

We herein studied the role of glutamate dehydrogenase (GDH), in response to leucine (LEU) supplementation, upon insulin secretion of malnourished rats. Weaned male Wistar rats were fed normal-protein (17%) or low-protein diet (6%, LP) for 8 weeks. Half of the rats of each group were supplemented with LEU (1.5%) in the drinking water for the following 4 weeks. Gene and protein expressions, static insulin secretion, and cytoplasmic Ca(2+) oscillations were measured. Glutamate dehydrogenase messenger RNA was 58% lower in LP islets, and LEU supplementation augmented it in 28%. The LP islets secreted less insulin when exposed to 20 mmol/L LEU, 20 mmol/L LEU + 2 mmol/L glutamine (with or without 5 mmol/L aminooxyacetic acid, a branched chain aminotransferase inhibitor, or 20 µmol/L epigallocatechin gallate, a GDH inhibitor), 20 mmol/L α-ketoisocaproate, glutamine + 20 mmol/L ß-2-aminobicyclo[2.2.1]heptane-2-carboxylic acid (a GDH activator), and 22.2 mmol/L glucose. Leucine supplementation augmented insulin secretion to levels found in normal-protein islets in all the above conditions, an effect that was blunted when islets were incubated with epigallocatechin gallate. The glutamine + ß-2-aminobicyclo[2.2.1]heptane-2-carboxylic acid-induced increased [Ca(2+)](i) and oscillations were higher than those for LP islets. Leucine supplementation normalized these parameters in LP islets. Impaired GDH function was associated with lower insulin release in LP islets, and LEU supplementation normalized insulin secretion via restoration of GDH function. In addition, GDH may contribute to insulin secretion through ameliorations of Ca(2+) handling in LP islets.

Endurance training activates AMP-activated protein kinase, increases expression of uncoupling protein 2 and reduces insulin secretion from rat pancreatic islets.

Endurance exercise is known to enhance peripheral insulin sensitivity and reduce insulin secretion. However, it is unknown whether the latter effect is due to the reduction in plasma substrate availability or alterations in ß-cell secretory machinery. Here, we tested the hypothesis that endurance exercise reduces insulin secretion by altering the intracellular energy-sensitive AMP-activated kinase (AMPK) signaling pathway. Male Wistar rats were submitted to endurance protocol training one, three, or five times per week, over 8 weeks. After that, pancreatic islets were isolated, and glucose-induced insulin secretion (GIIS), glucose transporter 2 (GLUT2) protein content, total and phosphorylated calmodulin kinase kinase (CaMKII), and AMPK levels as well as peroxisome proliferator-activated receptor-γ coactivator-1-α (PGC-1α) and uncoupling protein 2 (UCP2) content were measured. After 8 weeks, chronic endurance exercise reduced GIIS in a dose-response manner proportionally to weekly exercise frequency. Contrariwise, increases in GLUT2 protein content, CaMKII and AMPK phosphorylation levels were observed. These alterations were accompanied by an increase in UCP2 content, probably mediated by an enhancement in PGC-1α protein expression. In conclusion, chronic endurance exercise induces adaptations in ß-cells leading to a reduction in GIIS, probably by activating the AMPK signaling pathway.

Preliminary report: leucine supplementation enhances glutamate dehydrogenase expression and restores glucose-induced insulin secretion in protein-malnourished rats.

Low-protein diet impairs insulin secretion in response to nutrients and may induce several metabolic disorders including diabetes, obesity, and cardiovascular disease. In the present study, the influence of leucine supplementation on glutamate dehydrogenase (GDH) expression and glucose-induced insulin secretion (GIIS) was investigated in malnourished rats. Four groups were fed with different diets for 12 weeks: a normal-protein diet (17%) without or with leucine supplementation or a low (6%)-protein diet without (LP) or with leucine supplementation (LPL). Leucine (1.5%) was supplied in the drinking water. Western blotting analysis revealed reduced GDH expression in LP, whereas LPL displayed improved GDH expression, similar to control. The GIIS and leucine-induced insulin release were also enhanced in LPL compared with LP and similar to those observed in rats fed a normal-protein diet without leucine supplementation. In addition, GDH allosteric activators produced an increased insulin secretion in LPL. These findings indicate that leucine supplementation was able to increase GDH expression leading to GIIS restoration, probably by improved leucine metabolic pathways.

Effects of aerobic and anaerobic exercise on cardiac risk variables in overweight adults.

BACKGROUND: Aerobic exercise is an important ally in the fight against cardiovascular risk factors. However, the effects of high-intensity exercise on these factors are still poorly known. OBJECTIVE: To compare the effects of aerobic and anaerobic exercise protocols on cardiac risk factors. METHODS: 22 individuals with mean age of 40+/-8 years were distributed into the following groups: control (CO), endurance training (ET) and interval training (IT). The protocols lasted 12 weeks, three times a week, with intensities of 10% below and 20% above the anaerobic threshold (AnT). The following measurements were taken: total body mass (TBM), body mass index (BMI), waist circumference (WC), hip circumference (HC), and body composition, in addition to plasma concentrations of glucose (GLU), total cholesterol (CHO), and triglycerides (TG). Waist-hip ratio (WHR) and conicity index (C index) were also calculated. RESULTS: The TBM, BMI, WC, GLU, and body composition variables showed significant changes in the ET and IT groups. CHO and HC values were significantly reduced in the ET group, whereas WHR showed a significant reduction in the IT group. AnT and C index in the IT group were significantly different in relation to ET. CONCLUSION: In view of the differences found in the results of the variables studied in relation to the training performed, we conclude that an exercise program that includes both high and low-intensity activities is more efficient to ensure the reduction of a greater number of cardiac risk variables.

Efeitos do exercício aeróbico e anaeróbico em variáveis de risco cardíaco em adultos com sobrepeso / Effects of aerobic and anaerobic exercise on cardiac risk variables in overweight adults

FUNDAMENTO: O exercício físico aeróbico é importante aliado no combate aos fatores de risco cardiovascular. No entanto, os efeitos de exercícios de alta intensidade sobre tais fatores ainda são pouco conhecidos. OBJETIVO: Comparar os efeitos de protocolos de exercícios aeróbico e anaeróbico sobre fatores associados ao risco cardíaco. MÉTODOS: Vinte e dois indivíduos com idade média de 40±8 anos foram alocados nos grupos: controle (CO), treinamento de endurance (ET) e treinamento intermitente (IT). Os protocolos tiveram duração de 12 semanas, três vezes por semana; e intensidades de 10 por cento abaixo e 20 por cento acima do limiar anaeróbico (LAn). Foram medidas: massa corporal total (MCT), índice de massa corporal (IMC), circunferências de cintura (CINT) e quadril (QUA) e a composição corporal, além das concentrações plasmáticas de glicose (GLI), colesterol total (CHO) e triglicérides (TG); ainda foram calculados a razão cintura-quadril (PCCQ) e o índice de conicidade (Índice C). RESULTADOS: As variáveis de MCT, IMC, CINT, GLI e a composição corporal apresentaram alterações significativas nos grupos ET e IT. Os valores de CHO e QUA foram significativamente reduzidos no grupo ET, enquanto a PCCQ mostrou redução significativa no grupo IT. O LAn e o índice C, no grupo IT foram significativamente diferentes em relação a ET. CONCLUSÃO: Tendo em vista as diferenças encontradas nas respostas das variáveis estudadas, em razão do treinamento empregado, concluímos que um programa de exercício que contemple atividades de alta e baixa intensidades seja mais completo para garantir a redução de maior número de variáveis de risco cardíaco.

BACKGROUND: Aerobic exercise is an important ally in the fight against cardiovascular risk factors. However, the effects of high-intensity exercise on these factors are still poorly known. OBJECTIVE: To compare the effects of aerobic and anaerobic exercise protocols on cardiac risk factors. METHODS: 22 individuals with mean age of 40±8 years were distributed into the following groups: control (CO), endurance training (ET) and interval training (IT). The protocols lasted 12 weeks, three times a week, with intensities of 10 percent below and 20 percent above the anaerobic threshold (AnT). The following measurements were taken: total body mass (TBM), body mass index (BMI), waist circumference (WC), hip circumference (HC), and body composition, in addition to plasma concentrations of glucose (GLU), total cholesterol (CHO), and triglycerides (TG). Waist-hip ratio (WHR) and conicity index (C index) were also calculated. RESULTS: The TBM, BMI, WC, GLU, and body composition variables showed significant changes in the ET and IT groups. CHO and HC values were significantly reduced in the ET group, whereas WHR showed a significant reduction in the IT group. AnT and C index in the IT group were significantly different in relation to ET. CONCLUSION: In view of the differences found in the results of the variables studied in relation to the training performed, we conclude that an exercise program that includes both high and low-intensity activities is more efficient to ensure the reduction of a greater number of cardiac risk variables.

Anthropometric and physical characteristics of motor disabilited paralympic rowers.

The purpose of this study was to characterize aerobic, anaerobic, handgrip strength, and body fat content (BF) characteristics in paralympic rowers (ROW) in order to determine motor disabled rowers' fitness level and if specific motor disabilities could impair performance in this specific population. Upper body anaerobic threshold (LacT), peak (PK-AnP), mean (M-AnP), and lower (L-AnP) anaerobic power, peak anaerobic power to weight ratio (RelPk-AnP) and fatigue index (FI) were measured by the Wingate test (WinT). Handgrip strength was also measured and skinfold sum was used to estimate BF and were compared with a reference group of recreational disabled athletes (CON). LacT was significantly higher (p < 0.01) in ROW compared with CON. RelPk-AnP and BF were significantly different (p < 0.05) in ROW compared with CON as well. All other measured parameters did not significantly differ between ROW and CON. In most of cases, rowers have shown a relative low performance level, induced probably by specific disabilities.

Determination of the anaerobic threshold and maximal lactate steady state speed in equines using the lactate minimum speed protocol.

Maximal blood lactate steady state concentration (MLSS) and anaerobic threshold (AT) have been shown to accurately predict long distance events performance and training loads, as well, in human athletes. Horse endurance races can take up to 160 km and, in practice, coaches use the 4 mM blood lactate concentration, a human based fixed concentration to establish AT, to predict training loads to horse athletes, what can lead to misleading training loads. The lactate minimum speed (LMS) protocol that consists in an initial elevation in blood lactate level by a high intensity bout of exercise and then establishes an individual equilibrium between lactate production and catabolism during progressive submaximal efforts, has been proposed as a nonfixed lactate concentration, to measure individual AT and at the same time predicts MLSS for human long distance runners and basketball players as well. The purpose of this study was to determine the reliability of the LMS protocol in endurance horse athletes. Five male horses that were engaged on endurance training, for at least 1 year of regular training and competition, were used in this study. Animals were submitted to a 500 m full gallop to determine each blood lactate time to peak (LP) after these determinations, animals were submitted to a progressive 1000 m exercise, starting at 15 km h(-1) to determine LMS, and after LMS determination animals were also submitted to two 10,000 m running, first at LMS and then 10% above LMS to test MLSS accuracy. Mean LP was 8.2+/-0.7 mM at approximately 5.8+/-6.09 min, mean LMS was 20.75+/-2.06 km h(-1) and mean heart rate at LMS was 124.8+/-4.7 BPM. Blood lactate remained at rest baseline levels during 10,000 m trial at LMS, but reached a six fold significantly raise during 10% above LMS trial after 4000 and 6000 m (p<0.05) and (p<0.01) after 8000 and 10,000 m. In conclusion, our adapted LMS protocol for horse athletes proposed here seems to be a reliable method to state endurance horse athletes LT and MLSS.

Alterações em biomarcadores de estresse oxidativo, defesa antioxidante e lesão muscular em jogadores de futebol durante uma temporada competitiva / Blood oxidative stress, antioxidant enzymes and muscle damage biomarkers changes

O exercício físico induz aumento no consumo de oxigênio bem como na demanda energética. O aumento no consumo de O2 induz aumento na produção de espécies reativas de oxigênio (EROs). Dependendo da sua concentração, as EROs reagem com estruturas celulares, oxidando-as. Altos níveis de oxidação alteram sua função e prejudicam a homeostase intracelular. Jogadores de futebol aumentaram odesempenho de forma significativa nas últimas décadas, pela intensificação do processo de treinamento e melhoria das capacidades físicas envolvidas na modalidade. Tal fato sugere um aumento na possibilidade destes atletas estarem mais susceptíveis ao ataque oxidativo de EROs, com conseqüente aumento nos níveis de estresse oxidativo. Por outro lado, o treinamento também age na modulação dos sistemas antioxidantes intracelulares, aumentando sua capacidade de remover EROs. O objetivo deste estudo foi analisar o comportamento de marcadores sangüíneos do sistema de defesa antioxidante, de ataque oxidativo, bem como dos níveis de alteração muscular ao longo de cinco meses e campeonato paulista de um time de futebol,categoria sub-20. Nossos resultados mostram que as enzimas antioxidantes glutationa redutase e catalaseatingiram picos de atividade em momentos distintos da temporada, sugerindo uma ação complementar entre elas. Os marcadores de estresse oxidativo e lesão muscular analisados não mostraram alterações significativas ao longo do estudo. Esses dados sugerem que a capacidade de defesa antioxidante foi eficiente em tamponar o possível aumento na produção de EROs induzido pelos treinamentos e jogos da competição, impedindo a ocorrência de lesões musculares de origem oxidativa ao longo do campeonato.