Estado de hidratação em atletas de esportes de combate durante a perda de peso corporal

Introduction: Combat sports increasingly infiltrate society, stimulating strategies for preserving the physical integrity of fighters, such as the division of categories by weight. During the Weight Cycling, some athletes use the acute water loss for insertion into lower categories. Objective: To verify the state of hydration in combat sports athletes during the loss of body weight. Materials and methods: The sample consisted of nine MMA fighters and seven Muay Thai fighters. The data were collected 30 days before the fight, on the weighing day and on the day of the fight. The hydration status was verified from the body weight (%), color and density of the urine. Discussion: Even with organizations 'intent to protect athletes' physical integrity, some fighters manipulate body weight. Decreased glomerular filtration rate induced by dehydration may trigger a network of future health problems for these individuals. One of the main complications is Chronic Kidney Disease. Results: According to urine staining, 88.8% (MMA) and 100% (Muay Thai) were found to have some level of dehydration, 100% (MMA) and 62.5% (Muay Thai) were not hydrated according to urine density, and 88.8% (MMA) and 85.7% (Muay Thai) were also dehydrated. Conclusion: We demonstrate the high rate of fighters in some state of dehydration, evidencing the emerging need for attention and care through the professionals responsible for the Weight Cycling.Introdução: Os esportes de combate cada vez mais se infiltram na sociedade, estimulando estratégias para preservação da integridade física dos lutadores, como a divisão de categorias por peso. Durante o Weight Cycling, alguns atletas utilizam a perda hídrica aguda para inserção em categorias inferiores.  Objetivo: verificar o estado de hidratação em atletas de esportes de combate durante a perda de peso corporal. Materiais e métodos: A amostra foi composta por nove lutadores de MMA e sete Muay Thai. Os dados foram coletados 30 dias antes da luta, no dia da pesagem e no dia da luta. O estado de hidratação foi verificado a partir do peso corporal (%), coloração e densidade da urina. Discussão: Mesmo com a intenção das organizações de proteger a integridade física dos atletas, alguns lutadores manipulam o peso corporal. A diminuição da taxa de filtração glomerular induzida pela desidratação pode desencadear uma rede de problemas futuros de saúde para estes indivíduos. Uma das principais complicações é a Doença Renal Crônica. Resultados: De acordo com a coloração da urina, 88,8% (MMA) e 100% (Muay Thai) se encontravam com algum nível de desidratação, 100% (MMA) e 62,5% (Muay Thai) não estavam hidratados de acordo com a densidade da urina, e 88,8% (MMA) e 85,7% (Muay Thai) também se apresentaram desidratados. Conclusão: Demonstramos a alta taxa de lutadores em algum estado de desidratação, ficando evidente a necessidade emergente de atenção e cuidado por meio dos profissionais responsáveis pelo o Weight Cycling

Pharmacokinetic profile of glucosamine and chondroitin sulfate association in healthy male individuals

Osteoarthrosis is a chronic joint disease that, once patent, leads to a progressive functional disability. As proteochondroitin sulfates are the major contents of the cartilage, it is expected that the ingestion of glucosamine and chondroitin might improve the biological status of that tissue. As we could not find any studies on the pharmacokinetic profile of this association by oral administration route in human beings, the objective of this study was to evaluate it by using the association of glucosamine sulfate (GS) and chondroitin sulfate (CS) given to two groups of twelve healthy male volunteers (group I: one capsule containing 500 mg of GS and 400 mg of CS; group II: four capsules with the same content). Blood samples were collected at pre-determined time intervals up to 48 hours post-dosing. GS and CS were measured in plasma by the DMMB (1,9,dimethyl-dimethilene blue) method. Maximum concentration was achieved within 2 hours (average ± SE; 0.893±0.093 µg/ml, group I; and 2.222±0.313 µg/ml, group II). Areas under curve up to 48 hours were 10.803±0.965 µg-hr/ml and 38.776±2.981 µg-hr/ml for groups I and II, respectively. Both groups showed a second peak after 18 hours, indicating an enterohepatic flow. Our results indicate that this association is absorbed through the oral route by a saturable mechanism, which can enable its use in clinical treatments.A osteoartrose é uma doença crônica das articulações que, uma vez instalada, leva seus portadores a uma incapacidade funcional progressiva. Como os proteocondroitins sulfato são os maiores constituintes das cartilagens, espera-se que com a ingestão de glucosamina e condroitina haja uma melhora das condições biológicas desse tecido. Uma vez que não temos conhecimento de estudo da farmacocinética da administração oral dessa associação em seres humanos, o objetivo deste trabalho foi avaliá-la utilizando a associação entre o sulfato de glucosamina (SG) e o sulfato de condroitina (SC) administrada a dois grupos de doze voluntários sadios do sexo masculino (grupo I uma cápsula de (500 mg SG; 400 mg SC) e grupo II quatro cápsulas). Amostras de sangue foram retiradas a intervalos de tempo pré-definidos até 48 horas pós-dose. O SG e o SC foram dosados no plasma pelo método de DMMB (azul de 1,9,dimetildimetileno). A concentração máxima foi atingida em 2 horas (média ±SE; 0,893±0,093 µg/mL, grupo I e 2,222±0,313 µg/mL, grupo II). As áreas sob a curva até 48 horas foram de 10,803±0,965 µg-hr/mL e 38,776±2,981 µg-hr/mL, respectivamente para os grupos I e II. Os dois grupos apresentaram um segundo pico após 18 horas, indicando circulação êntero-hepática. Os nossos resultados indicam que essa associação é absorvida por via oral por mecanismo saturável, o que pode facilitar o seu uso em tratamentos clínicos.Fundação Oswaldo Ramos Hospital do Rim e HipertensãoUNIFESP-EPMUNIFESP, EPMSciEL

Molecular bases of diabetic nephropathy

The determinant of the diabetic nephropathy is hyperglycemia, but hypertension and other genetic factors are also involved. Glomerulus is the focus of the injury, where mesangial cell proliferation and extracellular matrix occur because of the increase of the intra- and extracellular glucose concentration and overexpression of GLUT1. Sequentially, there are increases in the flow by the poliol pathway, oxidative stress, increased intracellular production of advanced glycation end products (AGEs), activation of the PKC pathway, increase of the activity of the hexosamine pathway, and activation of TGF-beta1. High glucose concentrations also increase angiotensin II (AII) levels. Therefore, glucose and AII exert similar effects in inducing extracellular matrix formation in the mesangial cells, using similar transductional signal, which increases TGF-beta1 levels. In this review we focus in the effect of glucose and AII in the mesangial cells in causing the events related to the genesis of diabetic nephropathy. The alterations in the signal pathways discussed in this review give support to the observational studies and clinical assays, where metabolic and antihypertensive controls obtained with angiotensin-converting inhibitors have shown important and additive effect in the prevention of the beginning and progression of diabetic nephropathy. New therapeutic strategies directed to the described intracellular events may give future additional benefits.O principal determinante da nefropatia diabética é a hiperglicemia, mas hipertensão e fatores genéticos também estão envolvidos. O glomérulo é o foco de lesão, onde proliferação celular mesangial e produção excessiva de matriz extracelular decorrem do aumento da glicose intracelular, por excesso de glicose extracelular e hiperexpressão de GLUT1. Seguem-se aumento do fluxo pela via dos polióis, estresse oxidativo intracelular, produção intracelular aumentada de produtos avançados da glicação não enzimática (AGEs), ativação da via da PKC, aumento da atividade da via das hexosaminas e ativação de TGF-beta1. Altas concentrações de glicose também aumentam angiotensina II (AII) nas células mesangiais por aumento intracelular da atividade da renina (ações intrácrinas, mediando efeitos proliferativos e inflamatórios diretamente). Portanto, glicose e AII exercem efeitos proliferativos celulares e de matriz extracelular nas células mesangiais, utilizando vias de transdução de sinais semelhantes, que levam a aumento de TGF-beta1. Nesse estudo são revisadas as vias que sinalizam os efeitos da glicose e AII nas células mesangiais em causar os eventos-chaves relacionados à gênese da glomerulopatia diabética. As alterações das vias de sinalização implicadas na glomerulopatia, aqui revisadas, suportam dados de estudos observacionais/ensaios clínicos, onde controle metabólico e anti-hipertensivo, especificamente com inibidores do sistema renina-angiotensina, têm-se mostrado importantes - e aditivos - na prevenção do início e progressão da nefropatia. Novas estratégias terapêuticas dirigidas aos eventos intracelulares descritos deverão futuramente promover benefício adicional.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)HC Instituto do Coração Unidade de HipertensãoUSP FMUniversidade Federal de São Paulo (UNIFESP), Escola Paulista de Medicina (EPM) Laboratório de NefrologiaFundação Universitária de Cardiologia Instituto de Cardiologia Laboratório de Cardiologia Molecular e CelularUNIFESP, EPM, Laboratório de NefrologiaSciEL

NADPH oxidase and enhanced superoxide generation in intrauterine undernourished rats: involvement of the renin-angiotensin system

Objective: We previously reported that intrauterine undernutrition increased the oxidative stress by decreasing superoxide dismutase activity. in the present study, we tested whether NADPH oxidase, xanthine oxidase, cyclooxygenase or nitric oxide synthase are responsible for the increased O-2(-) generation observed in rats submitted to intrauterine undernutrition. in addition, we investigated the 2 effect of angiotensin II (ANG II on O-2(-) production via activation of NADPH oxidase. Methods: Female pregnant Wistar rats were fed either normal or 50% of the normal intake diets, during the whole gestational period. At 16 weeks of age, the rats were used for the study of intravital fluorescence microscopy; microvascular reactivity, local ANG II concentration and AT(1), p22(phox) and gp91(phox) gene expression. in this study only the male offspring was used. Results: Treatment of mesenteric arterioles with the xanthine oxidase inhibitor oxypurinol, the nitric oxide synthase inhibitor L-NAME or the cyclooxygenase, inhibitor diclofenac did not significantly change superoxide production. Thus, these vascular sources of superoxide were not responsible for the increased superoxide concentration. in contrast, treatment with the NADPH oxidase inhibitor apocynin significantly decreased superoxide generation and improved vascular function. On the other hand, intrauterine undernutrition did not alter the gene expression for p22(phox) and gp91(phox). the fact that the local ANG II concentration was increased and the attenuation of oxidative stress by blocking AT, receptor with losartan, led us to suggest that ANG II induces O-2 generation in intrauterine undernourished rats. Conclusion: Our study shows that NADPH oxidase inhibition attenuated superoxide anion generation and ameliorated vascular function in rats submitted to intrauterine undernutrition. Although it is not clear which mechanisms are responsible for the increase in NADPH oxidase activity, a role for ANG II-mediated superoxide production via activation of NADPH oxidase is suggested. (C) 2003 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.Univ São Paulo, Inst Biomed Sci, Dept Pharmacol, Lab Hypertens, BR-05508900 São Paulo, SP, BrazilUNIFESP, Lab Nephrol, São Paulo, SP, BrazilUNIFESP, Lab Nephrol, São Paulo, SP, BrazilWeb of Scienc

Effect of Time of Day on Performance, Hormonal and Metabolic Response during a 1000-M Cycling Time Trial

The aim of this study was to determine the effect of time of day on performance, pacing, and hormonal and metabolic responses during a 1000-m cycling time-trial. Nine male, recreational cyclists visited the laboratory four times. During the 1st visit the participants performed an incremental test and during the 2nd visit they performed a 1000-m cycling familiarization trial. On the 3rd and 4th visits, the participants performed a 1000-m TT at either 8 am or 6 pm, in randomized, repeated-measures, crossover design. the time to complete the time trial was lower in the evening than in the morning (88.2 +/- 8.7 versus 94.7 +/- 10.9 s, respectively, p<0.05), but there was no significant different in pacing. However, oxygen uptake and aerobic mechanical power output at 600 and 1000 m tended to be higher in the evening (p<0.07 and 0.09, respectively). There was also a main effect of time of day for insulin, cortisol, and total and free testosterone concentration, which were all higher in the morning (+60%, +26%, +31% and +22%, respectively, p<0.05). the growth hormone, was twofold higher in the evening (p<0.05). the plasma glucose was similar to 11% lower in the morning (p<0.05). Glucagon, norepinephrine, epinephrine and lactate were similar for the morning and evening trials (p<0.05), but the norepinephrine response to the exercise was increased in the morning (+46%, p<0.05), and it was accompanied by a 5-fold increase in the response of glucose. Muscle recruitment, as measured by electromyography, was similar between morning and evening trials (p<0.05). Our findings suggest that performance was improved in the evening, and it was accompanied by an improved hormonal and metabolic milieu.Alagoas Research Foundation (FAPEAL)Univ Fed Alagoas, Sports Sci Res Grp, Maceio, Alagoas, BrazilUniv Fed Pernambuco, CAV, Dept Phys Educ & Sports Sci, Vitoria de Santo Anta, PE, BrazilUniv São Paulo, Sch Phys Educ & Sport, Endurance Performance Res Grp, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Med, Div Nephrol, São Paulo, BrazilVictoria Univ, Inst Sport Exercise & Act Living, Melbourne, Vic 8001, AustraliaUniversidade Federal de São Paulo, Dept Med, Div Nephrol, São Paulo, BrazilAlagoas Research Foundation (FAPEAL): 20110825-011-0025-0004Web of Scienc

Upregulation of ERK1/2-eNOS via AT2 Receptors Decreases the Contractile Response to Angiotensin II in Resistance Mesenteric Arteries from Obese Rats

It has been clearly established that mitogen-activated protein kinases (MAPKS) are important mediators of angiotensin II (Ang II) signaling via AT1 receptors in the vasculature. However, evidence for a role of these kinases in changes of Ang II-induced vasoconstriction in obesity is still lacking. Here we sought to determine whether vascular MAPKs are differentially activated by Ang II in obese animals. the role of AT2 receptors was also evaluated. Male monosodium glutamate-induced obese (obese) and non-obese Wistar rats (control) were used. the circulating concentrations of Ang I and Ang II, determined by HPLC, were increased in obese rats. Ang II-induced isometric contraction was decreased in endothelium-intact resistance mesenteric arteries from obese compared with control rats and exhibited a retarded AT1 receptor antagonist response. Blocking of AT2 receptors and inhibition of either endothelial nitric oxide synthase (eNOS) or extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) restored Ang II-induced contraction in obese rats. Western blot analysis revealed increased protein expression of AT2 receptors in arteries from obese rats. Basal and Ang II-induced ERK1/2 phosphorylation was also increased in obese rats. Blockade of either AT1 or AT2 receptors corrected the increased ERK1/2 phosphorylation in arteries from obese rats to levels observed in control preparations. Phosphorylation of eNOS was increased in obese rats. Incubation with the ERK1/2 inhibitor before Ang II stimulation did not affect eNOS phosphorylation in control rats; however, it corrected the increased phosphorylation of eNOS in obese rats. These results clearly demonstrate that enhanced AT2 receptor and ERK1/2-induced, NO-mediated vasodilation reduces Ang II-induced contraction in an endothelium-dependent manner in obese rats.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Univ São Paulo, Inst Biomed Sci, Dept Pharmacol, São Paulo, BrazilUniv Fed Goias, Div Cardiovasc Physiol, Dept Biol Sci, Jatai, BrazilUniversidade Federal de São Paulo, Div Nephrol, Dept Med, Escola Paulista Med, São Paulo, BrazilUniversidade Federal de São Paulo, Div Nephrol, Dept Med, Escola Paulista Med, São Paulo, BrazilFAPESP: 2007/58311-0FAPESP: 2008/51622-3FAPESP: 2010/03642-5Web of Scienc