Search

Aline David-Silva,1 João Victor Esteves,1 Mychel Raony PT Morais,2 Helayne Soares Freitas,1 Telma Maria Zorn,2 Maria Lucia Correa-Giannella,3 Ubiratan Fabres Machado1 1Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil; 2Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil; 3Laboratório de Carboidratos e Radioimunoensaio, LIM-18, Hospital das Clinicas HCFMUSP, Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo, BrazilCorrespondence: Ubiratan Fabres MachadoDepartment of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, Av. Prof. Lineu Prestes 1524, São Paulo, SP 05508-900, BrazilTel +55 11 30917494Email ubiratan@icb.usp.brPurpose: NAFLD is a hepatic component of type 2 diabetes mellitus (T2D), in which impaired hepatic glucose production plays an important role. Inhibitors of sodium glucose transporter 2 (SGLT2) reduce glycemia and exert beneficial effects on diabetic complications. Recently, dual SGLT1/2 inhibition has been proposed to be more effective in reducing glycemia. We hypothesized that improving hepatic glucose metabolism induced by SGLT1/2 inhibition could be accompanied by beneficial effects on NAFLD progression.Methods: Glycemic homeostasis, hepatic glucose production and NAFLD features were investigated in obese T2D mice, treated with SGLT1/2 inhibitor phlorizin for 1 week.Results: T2D increased glycemia; insulinemia; hepatic expression of phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphatase (G6Pase) and glucose transporter 2 (Slc2a2 gene); hepatocyte nuclear factors 1A/4A/3B-binding activity in Slc2a2; endogenous glucose production; liver weight, plasma transaminase concentration as well as hepatic inflammation markers, and induced histological signals of non-alcoholic steatohepatitis (NASH, according to NASH-CRN Pathology Committee System). Phlorizin treatment restored all these parameters (mean NASH score reduced from 5.25 to 2.75 P< 0.001); however, plasma transaminase concentration was partially reverted and some hepatic inflammation markers remained unaltered.Conclusion: NAFLD accompanies altered hepatic glucose metabolism in T2D mice and that greatly ameliorated through short-term treatment with the dual SGLT1/2 inhibitor. This suggests that altered hepatic glucose metabolism participates in T2D-related NAFLD and highlights the pharmacological inhibition of SGLTs as a useful approach not only for controlling glycemia but also for mitigating development and/or progression of NAFLD.Keywords: GLUT2, PEPCK, G6Pase, phlorizin, NASH

Metabolic diseases, notably obesity and type 2 diabetes (T2D), have reached alarming proportions and constitute a significant global health challenge, emphasizing the urgent need for effective preventive and therapeutic strategies. In contrast, exercise training emerges as a potent intervention, exerting numerous positive effects on metabolic health through adaptations to the metabolic tissues. Here, we reviewed the major features of our current understanding with respect to the intricate interplay between metabolic diseases and key metabolic tissues, including adipose tissue, skeletal muscle, and liver, describing some of the main underlying mechanisms driving pathogenesis, as well as the role of exercise to combat and treat obesity and metabolic disease.

Objective: The intrauterine environment during pregnancy is a critical factor in the development of obesity, diabetes, and cardiovascular disease in offspring. Maternal exercise prevents the detrimental effects of a maternal high fat diet on the metabolic health in adult offspring, but the effects of maternal exercise on offspring cardiovascular health have not been thoroughly investigated., Methods: To determine the effects of maternal exercise on offspring cardiovascular health, female mice were fed a chow (C; 21% kcal from fat) or high-fat (H; 60% kcal from fat) diet and further subdivided into sedentary (CS, HS) or wheel exercised (CW, HW) prior to pregnancy and throughout gestation. Offspring were maintained in a sedentary state and chow-fed throughout 52 weeks of age and subjected to serial echocardiography and cardiomyocyte isolation for functional and mechanistic studies., Results: High-fat fed sedentary dams (HS) produced female offspring with reduced ejection fraction (EF) compared to offspring from chow-fed dams (CS), but EF was preserved in offspring from high-fat fed exercised dams (HW) throughout 52 weeks of age. Cardiomyocytes from HW female offspring had increased kinetics, calcium cycling, and respiration compared to CS and HS offspring. HS offspring had increased oxidation of the RyR2 in cardiomyocytes coupled with increased baseline sarcomere length, resulting in RyR2 overactivity, which was negated in female HW offspring., Conclusions: These data suggest a role for maternal exercise to protect against the detrimental effects of a maternal high-fat diet on female offspring cardiac health. Maternal exercise improved female offspring cardiomyocyte contraction, calcium cycling, respiration, RyR2 oxidation, and RyR2 activity. These data present an important, translatable role for maternal exercise to preserve cardiac health of female offspring and provide insight on mechanisms to prevent the transmission of cardiovascular diseases to subsequent generations., Competing Interests: Declaration of competing interest The authors declare no conflicts of interest., (Copyright © 2024 The Author(s). Published by Elsevier GmbH.. All rights reserved.)

Expression of the glucose transporter GLUT4, encoded by Slc2a4 gene, is reduced in both type 1 and type 2 diabetes (T1D and T2D), contributing to glycemic impairment. The present study investigated epigenetic regulations at the Slc2a4 promoter in skeletal muscle of T1D- and T2D-like experimental models. Slc2a4/GLUT4 repression was observed in T1D and T2D and that was reversed by insulin and resveratrol treatments, respectively. In both T1D-like and T2D-like animals, tri-methylation at lysine 9 of histone 3 (H3K9me3) increased in the Slc2a4 enhancer segment, whereas MEF2A/D binding into this segment was reduced; all effects were reversed by respective treatments. This study reveals that increased H3K9me3 in the Slc2a4 promoter enhancer segment contributes to reduce GLUT4 expression in skeletal muscle and to worse glycemic control in diabetes, pointing to the H3K9me3 of Slc2a4 promoter as a potential target for development of new approaches for treating diabetes., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Objective: The goal of this study was to evaluate the influence of high-intensity interval training (HIIT) on anthropometric variables in adults afflicted with overweight or obesity and to compare the effects with those of moderate-intensity continuous training., Methods: A computer literature search was performed for HIIT intervention studies that evaluated anthropometric variables in adults afflicted with overweight or obesity., Results: Of the 857 articles retrieved in the electronic search, 48 met the inclusion criteria. The analyses demonstrated that HIIT was effective in decreasing body mass (-1.45 kg [95% CI: -1.85 to -1.05 kg]), body mass index (-0.44 kg m -2 [95% CI: -0.59 to -0.30 kg m -2 ]), waist circumference (-2.3 cm [95% CI: -3.1 to -1.4 cm]), waist/hip ratio (-0.01 [95% CI: -0.02 to -0.00]), body fat percentage (-1.29% [95% CI: -1.70% to -0.87%]) and abdominal visceral fat area (-6.83 cm 2 [95% CI: -11.95 to -1.71 cm 2 ]). When considering equalization between the two methods (energy expenditure or workload matched), no differences were found in any measure except body mass (for which HIIT was superior)., Conclusions: High-intensity interval training and moderate-intensity continuous training results were similar, particularly when equalization between the two methods was considered. Thus, HIIT can be used as a secondary method for the treatment of obesity in adults., (© 2018 World Obesity Federation.)

Aims/hypothesis: The discovery of osteocalcin, a protein synthetized by osteoblasts, as a hormone that has positive effects on insulin resistance, contributed to support the concept of bone as an endocrine organ. However, very little is known about the molecular pathways involved in osteocalcin improved-insulin resistance. The present study aimed to investigate the mechanisms of action of osteocalcin on insulin resistance and inflammation in obese mice and 3T3-L1 adipocytes., Methods and Results: Lean control, saline-treated obese and uncarboxylated osteocalcin (uOC)-treated obese mice were subjected to insulin tolerance test in vivo. Blood was collect for biochemical/metabolic profile analysis; and, skeletal muscle, white adipose tissue (WAT) and bone were collected for protein (Western blotting) and mRNA (RT-qPCR) analysis. uOC effects on insulin resistance and inflammation were also investigated in 3T3-L1 adipocytes challenged with tumor necrosis factor. Osteocalcin treatment improved in vivo insulin resistance in obese mice. In WAT, osteocalcin had positive effects such as (1) WAT weight reduction; (2) upregulation of glucose transporter (GLUT) 4 protein and its mRNA (Slc2a4); (3) improved insulin-induced AKT phosphorylation; (4) downregulation of several genes involved in inflammation and inflammassome transcriptional machinery, and (5) reduction of the density of macrophage in crown-like structures (histomorphometrical analysis). Notably, in 3T3-L1 adipocytes, osteocalcin restored Slc2a4/GLUT4 content and reduced the expression of inflammatory genes after TNF-a challenge; moreover, osteocalcin treatment increased AKT phosphorylation induced by insulin. Finally, it was observed that in bone, osteocalcin improves insulin resistance by increasing insulin-induced AKT phosphorylation and reducing the expression of genes involved in bone insulin resistance, resulting in increased secretion of uncarboxylated osteocalcin in circulation., Conclusion: We provided some mechanisms of action for osteocalcin in the amelioration of insulin resistance in obesity: in WAT, osteocalcin improves insulin resistance by decreasing inflammation, and increasing insulin signaling and the expression of Slc2a4/GLUT4; and, in bone, osteocalcin increases the secretion of uncarboxylated osteocalcin by improving insulin resistance., (Copyright © 2017 Elsevier Inc. All rights reserved.)

The reduced expression of solute carrier family 2, facilitated glucose transporter member 4 (GLUT4) and hexokinase-2 (HK2) in skeletal muscle participates in insulin resistance of diabetes mellitus (DM). MicroRNAs (miRNAs) have emerged as important modulators of mRNA/protein expression, but their role in DM is unclear. We investigated miRNAs hypothetically involved in GLUT4/HK2 expression in soleus muscle of type 1 diabetes-like rats. In silico analysis revealed 651 miRNAs predicted to regulate solute carrier family 2 member 4 ( Slc2a4 ) mRNA, several of them also predicted to regulate Hk2 mRNA, and 16 miRNAs were selected for quantification. Diabetes reduced Slc2a4 /GLUT4 and Hk2 /HK2 expression (50-77%), upregulated miR-29b-3p and miR-29c-3p (50-100%), and downregulated miR-93-5p, miR-150-5p, miR-199a-5p, miR-345-3p, and miR-532-3p (~30%) expression. Besides, GLUT4 and HK2 proteins correlated ( P < 0.05) negatively with miR-29b-3p and miR-29c-3p and positively with miR-199a-5p and miR-532-3p, suggesting that these miRNAs could be markers of alterations in GLUT4 and HK2 expression. Additionally, diabetes increased the nuclear factor kappa B subunit 1 protein (p50) expression, a repressor of Slc2a4 , which was also predicted as a target for miR-199a-5p and miR-532-3p. Correlations were also detected between these miRNAs and blood glucose, 24-h glycosuria and plasma fructosamine, and insulin therapy reversed most of the alterations. In sum, we report that diabetes altered miR-29b-3p, miR-29c-3p, miR-199a-5p and miR-532-3p expression in muscle of male rats, where their predicted targets Slc2a4 /GLUT4 and Hk2 /HK2 are repressed. These data shed light on these miRNAs as a markers of impaired skeletal muscle glucose disposal, and, consequently, glycemic control in diabetes.

Little is known about advanced glycation end products (AGEs) participation in glucose homeostasis, a process in which skeletal muscle glucose transporter GLUT4 (Scl2a4 gene) plays a key role. This study investigated (1) the in vivo and in vitro effects of AGEs on Slc2a4/GLUT4 expression in skeletal muscle of healthy rats, and (2) the potential involvement of endoplasmic reticulum and inflammatory stress in the observed regulations. For in vivo analysis, rats were treated with advanced glycated rat albumin (AGE-albumin) for 12 weeks; for in vitro analysis, soleus muscles from normal rats were incubated with bovine AGE-albumin for 2.5 to 7.5 hours. In vivo, AGE-albumin induced whole-body insulin resistance; decreased (~30%) Slc2a4 mRNA and GLUT4 protein content; and increased (~30%) the nuclear content of nuclear factor NF-kappa-B p50 subunit (NFKB1), and cellular content of 78 kDa glucose-regulated protein (GRP78). In vitro, incubation with AGE-albumin decreased (~50%) the Slc2a4/GLUT4 content; and increased cellular content of GRP78/94, phosphorylated-IKK-alpha/beta, nuclear content of NFKB1 and RELA, and the nuclear protein binding into Slc2a4 promoter NFKB-binding site. The data reveal that AGEs impair glucose homeostasis in non-diabetic states of increased AGEs concentration; an effect that involves activation of endoplasmic reticulum- and inflammatory-stress and repression of Slc2a4/GLUT4 expression.

Insulin resistance participates in the glycaemic control disruption in type 2 diabetes mellitus (T2DM), by reducing muscle glucose influx and increasing liver glucose efflux. GLUT4 ( Slc2a4 gene) and GLUT2 ( Slc2a2 gene) proteins play a fundamental role in the muscle and liver glucose fluxes, respectively. Resveratrol is a polyphenol suggested to have an insulin sensitizer effect; however, this effect, and related mechanisms, have not been clearly demonstrated in T2DM. We hypothesized that resveratrol can improve glycaemic control by restoring GLUT4 and GLUT2 expression in muscle and liver. Mice were rendered obese T2DM in adult life by neonatal injection of monosodium glutamate. Then, T2DM mice were treated with resveratrol for 60 days or not. Glycaemic homeostasis, GLUT4, GLUT2, and SIRT1 (sirtuin 1) proteins (Western blotting); Slc2a4 , Slc2a2 , and Pck1 (key gluconeogenic enzyme codifier) mRNAs (RT-qPCR); and hepatic glucose efflux were analysed. T2DM mice revealed: high plasma concentration of glucose, fructosamine, and insulin; insulin resistance (insulin tolerance test); decreased Slc2a4 /GLUT4 content in gastrocnemius and increased Slc2a2 /GLUT2 content in liver; and increased Pck1 mRNA and gluconeogenic activity (pyruvate tolerance test) in liver. All alterations were restored by resveratrol treatment. Additionally, in both muscle and liver, resveratrol increased SIRT1 nuclear content, which must participate in gene expression regulations. In sum, the results indisputably reveals that resveratrol improves glycaemic control in T2DM, and that involves an increase in muscle Slc2a4 /GLUT4 and a decrease in liver Slc2a2 /GLUT2 expression. This study contributes to our understanding how resveratrol might be prescribed for T2DM according to the principles of evidence-based medicine., Competing Interests: The authors have nothing to disclose.

Purpose: To estimate the contribution of the 3 energy systems to simulated judo matches., Methods: Twelve judo athletes (18 ± 1 y, 175.1 ± 5.3 cm, 74.3 ± 10.5 kg, 11.7% ± 1.5% body fat, 8 ± 2 y of practice) performed 5 combats with different durations (1, 2, 3, 4, and 5 min), against the same opponent, on different days and blinded to the duration. The estimated energy contributions for the oxidative, glycolytic, and ATP-PCr systems were calculated based on oxygen uptake (V̇O2) during activity, Delta of lactate, and the fast phase of excess V ̇ O2, respectively. Analysis of mixed models for repeated measures was used to compare the contribution of the 3 energy systems and different durations of judo matches, followed by a post hoc Bonferroni test., Results: The oxidative system's contribution (70%) was higher than those of the glycolytic (8%; P < .001) and ATP-PCr (21%; P < .001) energy systems (in all durations), and the ATP-PCr contribution was higher than that of the glycolytic energy system (up to 3 min). In addition, during the match there was an increase in the oxidative (from 50% to 81%; P < .001), a decrease in the ATP-PCr (from 40% to 12%; P < .001), and maintenance of the glycolytic contributions (between 6% and 10%)., Conclusions: There is a predominance of the oxidative system to supply the energy cost of judo matches from the first minute of combat up to the end, compared with the anaerobic systems.

Diabetes mellitus (DM) induces a variable degree of muscle sarcopenia, which may be related to protein degradation and to the expression of both E3 ubiquitin ligases and some specific microRNAs (miRNAs). The present study investigated the effect of diabetes and acute muscle contraction upon the TRIM63 and FBXO32 expression as well as the potential involvement of some miRNAs. Diabetes was induced by streptozotocin and studied after 30 days. Soleus muscles were harvested, stimulated to contract in vitro for twitch tension analysis (0.5 Hz), 30 min later for tetanic analysis (100 Hz), and 30 min later were frozen. TRIM63 and FBXO32 proteins were quantified by western blotting; Trim63 mRNA, Fbxo32 mRNA, miR-1-3p, miR-29a-3p, miR-29b-3p, miR-133a-3p, and miR-133b-3p were quantified by qPCR. Diabetes induced sarcopenia by decreasing (P < 0.05) muscle weight/tibia length index, maximum tetanic contraction and relaxation rates, and absolute twitch and tetanic forces (P < 0.05). Diabetes decreased (P < 0.05) the Trim63 and Fbxo32 mRNAs (30%) and respective proteins (60%), and increased (P < 0.01) the miR-29b-3p (2.5-fold). In muscle from diabetic rats, acute contractile stimulus increased TRIM63 protein, miR-1-3p, miR-29a-3p, and miR-133a/b-3p, but decreased miR-29b-3p (P < 0.05). Independent of the metabolic condition, after muscle contraction, both TRIM63 and FBXO32 proteins correlated significantly with miR-1-3p, miR-29a/b-3p, and miR-133a/b-3p. All diabetes-induced regulations were reversed by insulin treatment. Concluding, the results depict that muscle wasting in long-term insulinopenic condition may not be accompanied by increased proteolysis, pointing out the protein synthesis as an important modulator of muscle sarcopenia in DM.

The solute carrier family 2 facilitated glucose transporter member 4 (GLUT4) plays a key role in the insulin-induced glucose uptake by muscle and adipose tissues. In prediabetes and diabetes, GLUT4 expression/translocation has been detected as reduced, participating in mechanisms that impair glycemic control. Recently, a class of short endogenous noncoding RNAs named microRNAs (miRNAs) has been increasingly described as involved in the posttranscriptional epigenetic regulation of gene expression. The present review focuses on miRNAs potentially involved in the expression of GLUT4 expression, and proteins related to GLUT4 and translocation in skeletal muscle, seeking to correlate them with insulin resistance and diabetes. So far, miR-21a-5p, miR-29a-3p, miR-29c-3p, miR-93-5p, miR-106b-5p, miR-133a-3p, miR-133b-3p, miR-222-3p, and miR-223-3p have been reported to directly and/or indirectly regulate the GLUT4 expression; and their expression is altered under diabetes-related conditions. Besides, some miRNAs that have been linked to the expression of proteins involved in GLUT4 translocation machinery in muscle could also impact glucose uptake. That makes these miRNAs promising targets for preventive and/or therapeutic approaches, which could improve glycemic control, thus deserving future new investigations.

This study analysed the physiological, nutritional and performance profiles of athletes practicing Brazilian jiu-jitsu. To this end, 15 athletes that practiced Brazilian jiu-jitsu (aged: 28 ± 5 years; 8 brown belts and 7 black belts; training experience: 11 ± 4 years) underwent anthropometric measurements (body composition and somatotype), dietary evaluation (24 h recall) and physical fitness tests (movement time, dynamometer handgrip, kimono grip strength, vertical jump and sit-and-reach tests). The athletes had 12.7 ± 4.8% of body fat, 59.2 ± 5.0% of muscle mass and their somatotype was dominated by the mesomorphic component (5.3 ± 2.0), followed by endomorphic (3.7 ± 1.5) and ectomorphic (1.4 ± 0.9) components. Nutritional assessment suggested a diet consisting of 54 ± 7% of carbohydrates, 19 ± 4% of protein and 27 ± 6% of lipids. Movement time on the handgrip tests was 0.42 ± 0.05 s, for handgrip strength, 53 ± 7 kgf was found for the dominant hand and 50 ± 9 kgf for the non-dominant hand. For the countermovement jump, the jiu-jitsu athletes reached 41 ± 5 cm. Athletes remained 30 ± 14 s in the maximum static suspension test gripping a kimono, and reached 27 ± 8 cm in the sit-and-reach test. Overall the sample presented average levels of body fat, elevated muscle mass and a predominantly mesomorphic somatotype. Diet was generally poor, with low carbohydrate intake, high protein intake and adequate lipid intake. Maximum isometric handgrip strength was consistent with observations of other athletes in this sport discipline. However, the performance in the maximum static suspension test gripping a kimono was lower than in other Brazilian jiu-jitsu athletes. Movement time was comparable and lower body muscle power was worse compared to athletes in similar sports. Additionally, flexibility was rated as poor.

Objectives: The present study aimed to evaluate the effects of using hyperbaric oxygen therapy during post-training recovery in jiu-jitsu athletes., Methods: Eleven experienced Brazilian jiu-jitsu athletes were investigated during and following two training sessions of 1h30min. Using a cross-over design, the athletes were randomly assigned to passive recovery for 2 hours or to hyperbaric oxygen therapy (OHB) for the same duration. After a 7-day period, the interventions were reversed. Before, immediately after, post 2 hours and post 24 hours, blood samples were collected to examine hormone concentrations (cortisol and total testosterone) and cellular damage markers [creatine kinase (CK), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH)]. Moreover, the rating of perceived exertion (RPE) and recovery (RPR) scales were applied., Results: Final lactate [La] values (control: 11.9 ± 1.4 mmol/L, OHB: 10.2 ± 1.4 mmol/L) and RPE [control: 14 (13-17 a.u.), OHB: 18 (17-20 a.u.)] were not significantly different following the training sessions. Furthermore, there was no difference between any time points for blood lactate and RPE in the two experimental conditions (P>0.05). There was no effect of experimental conditions on cortisol (F1,20 = 0.1, P = 0.793, η2 = 0.00, small), total testosterone (F1,20 = 0.03, P = 0.877, η2 = 0.00, small), CK (F1,20 = 0.1, P = 0.759, η2 = 0.01, small), AST (F1,20 = 0.1, P = 0.761, η2 = 0.01, small), ALT (F1,20 = 0.0, P = 0.845, η2 = 0.00, small) or LDH (F1,20 = 0.7, P = 0.413, η2 = 0.03, small). However, there was a difference between the two experimental conditions in RPR with higher values at post 2 h and 24 h in OHB when compared to the control condition (P<0.05)., Conclusions: Thus, it can be concluded that OHB exerts no influence on the recovery of hormonal status or cellular damage markers. Nonetheless, greater perceived recovery, potentially due to the placebo effect, was evident following the OHB condition.

The aim of this study was to analyze physiological responses in Brazilian jiu-jitsu athletes during simulated competition. To this end, 10 athletes (age: 28 ± 4 years, body mass: 81.8 ± 7.4 kg, body fat: 13.0 ± 4.8%, systematic practice: 11 ± 4 years) were analyzed in simulated competition (4 matches of 10 minutes). Blood samples were taken to assess energy demand, hormonal responses, and cell damage. Additionally, the heart rate variability (HRV) response was analyzed. The main results show that in simulated competition, during the last matches, athletes had lower lactate (p < 0.001), epinephrine (p < 0.001), norepinephrine (p < 0.001), and insulin (p = 0.002) concentrations. Increases observed in creatine kinase (p < 0.001), aspartate aminotransferase (p < 0.001), alanine aminotransferase (p = 0.007), and creatinine (p < 0.001) seen, especially, in the last matches are indicative of possible cell damage. The HRV reflected a decrease in the RR medium (average of the normal R-R intervals) (p = 0.001) during the competition. Thus, it is concluded that successive matches from competition generate a gradual decrease of adrenergic and glycolytic activities, which is accompanied by a gradual increase in cell damage markers and decrease in the RR medium of the HRV.

The aim of this study was to analyze performance, time structure, technical actions, and perceptual responses in Brazilian jiu-jitsu athletes during a simulated competition. For this purpose, 10 athletes were analyzed in a simulated competition (4 matches of 10 minutes). Physical tests and scales of the perception of effort and recovery were applied. The matches were recorded for the purpose of technical-tactical analysis and to determine the time structure. The main results show that in the simulated competition, reaction time (F(2.5,17.6) = 2.7; p = 0.087; η² = 0.28) and flexibility (F(7,63) = 1.5; p = 0.172; η² = 0.15) were unchanged across the matches. An analysis of variance showed a significant difference for grip endurance using the kimono (F(2.0,15.9) = 8.1; p = 0.004; η² = 0.50), which was not confirmed by the Bonferroni test. Jump height indicated postactivation potentiation after match 2 (F(7,63) = 3.5; p = 0.003; η² = 0.28). The maximal isometric handgrip strength in the dominant hand (F(3.2,28.6) = 2.9; p = 0.049; η² = 0.24) and in the nondominant hand (F(7,63) = 3.8; p = 0.002; η² = 0.30) showed a decline after matches 3 and 4. Although these data indicate the onset of fatigue, the effort/pause ratio of the matches was not altered (F(3,12) = 0.6; p = 0.624; η² = 0.13). The perceptions of effort (F(3,27) = 0.9; p = 0.469; η² = 0.09) and recovery (F(1.9,17.0) = 2.4; p = 0.125; η² = 0.21) and the degree of fatigue reported (F(1.5,13.8) = 0.5; p = 0.588; η² = 0.05) did not change during the simulated competition. Thus, it may be concluded that the execution of successive matches causes a decline in maximal isometric handgrip strength. No changes in the time structure of the matches or in the perceptual responses were observed.

Aims: The insulin-sensitive glucose transporter protein GLUT4 (solute carrier family 2 member 4 (Slc2a4) gene) plays a key role in glycemic homeostasis. Decreased GLUT4 expression is a current feature in insulin resistant conditions such as diabetes, and the restoration of GLUT4 content improves glycemic control. This study investigated the effect of insulin upon Slc2a4/GLUT4 expression, focusing on the AT-rich element, E-box and nuclear factor NF-kappa-B (NFKB) site., Main Methods: Rat soleus muscles were incubated during 180 min with insulin, added or not with wortmannin (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma isoform (PI3K)-inhibitor), ML9 (serine/threonine protein kinase (AKT) inhibitor) and tumor necrosis factor (TNF, GLUT4 repressor), and processed for analysis of GLUT4 protein (Western blotting); Slc2a4, myocyte enhancer factor 2a/d (Mef2a/d), hypoxia inducible factor 1a (Hif1a), myogenic differentiation 1 (Myod1) and nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (Nfkb1) messenger ribonucleic acids (mRNAs) (polymerase chain reaction (PCR)); and AT-rich- (myocyte-specific enhancer factor 2 (MEF2)-binding site), E-box- (hypoxia inducible factor 1 alpha (HIF1A)- and myoblast determination protein 1 (MYOD1)-binding site), and NFKB-binding activity (electrophoretic mobility assay)., Key Findings: Insulin increased Slc2a4 mRNA expression (140%) and nuclear proteins binding to AT-rich and E-box elements (~90%), all effects were prevented by wortmannin and ML9. Insulin also increased Mef2a/d and Myod1 mRNA expression, suggesting the participation of these transcriptional factors in the Slc2a4 enhancing effect. Conversely, insulin decreased Nfkb1 mRNA expression and protein binding to the NFKB-site (~50%). Furthermore, TNF-induced inhibition of GLUT4 expression (~40%) was prevented by insulin in an NFKB-binding repressing mechanism. GLUT4 protein paralleled the Slc2a4 mRNA regulations., Significance: Insulin enhances the Slc2a4/GLUT4 expression in the skeletal muscle by activating AT-rich and E-box elements, in a PI3K/AKT-dependent mechanism, and repressing NFKB-site activity as well. These results unravel how post-prandial increase of insulin may guarantee GLUT4 expression, and how the insulin signaling impairment can participate in insulin resistance-induced repression of GLUT4., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Purpose: The present study aims at investigating the physiological response and technical-tactical parameters in Brazilian jiu-jitsu competition., Methods: The study included 35 male Brazilian jiu-jitsu athletes (adult category, body mass: 80.2 ± 13.0 kg), graded from white to brown belt, during combats fought at regional level. Twenty-two fights were analyzed in terms of technique and time structure. Blood glucose, lactate and maximal isometric grip strength were determined before and after the fights. The rate of perceived exertion was also assessed after the fight, using the 6-20 Borg rating. The fights were recorded and the following variables were determined: the exertion/pause ratio and subjective intensity of actions, categorized between low and high intensity., Results: The results indicated that during Brazilian jiu-jitsu fights, the glycolytic pathway is only moderately activated (lactate before: 4.4 (4.0 - 4.6) mmol/L, after: 10.1 (8.0 - 11.3) mmol/L; glucose before: 112.4 ± 22.3 mg/dL, after: 130.5 ± 31.0 mg/dL). The exertion during the fight resulted in significant reductions in handgrip strength (right hand grip before: 45.9 ± 10.3 kgf, after: 40.1 ± 9.5 kgf; left hand grip before: 44.2 ± 11.1 kgf, after: 37.0 ± 10.2 kgf). The athletes rated the fight as hard: 15 (13 - 15). Effort/pause ratio was 6:1, while high-intensity actions lasted approximately 4 s, resulting in a low/high intensity? ratio of 8:1., Conclusion: It is recommended that coaches direct the training loads to simulate the energy demand imposed by the competitive matches, activating moderately the glycolytic pathway. Moreover, the time structure of combats can be used to prescribe both physical and technical-tactical training.