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.

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.

The present study aims at investigating the physiological response and technical-tactical parameters in Brazilian jiu-jitsu competition.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.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.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.

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.