Evaluation of pre-game hydration status, heat stress, and fluid balance during professional soccer competition in the heat

This study evaluated initial hydration status (stadium arrival urine specific gravity), fluid balance (pre- and post-game nude body weight, fluid intake, urine collection), and core temperature changes (pre-game, half-time, post-game) during a professional soccer game. We monitored 17 male players (goalies included) between stadium arrival and game end (3h), playing at 34.9°C and 35.4% relative humidity, for an average Wet Bulb Globe Temperature (WBGT) heat stress index of 31.9°C. Data are mean ± SD (range). Initial urine specific gravity (USG) was 1.018 ± 0.008 (1.003-1.036); seven players showed USG ≥ 1.020. Over the three hours, body mass (BM) loss was 2.58 ± 0.88kg (1.08-4.17kg), a dehydration of 3.38 ± 1.11%BM (1.68-5.34%BM). Sweat loss was 4448 ± 1216mL (2950-6224mL), vs. fluid intake of 1948 ± 954mL (655-4288mL). Despite methodological problems with many players, core temperatures greater than or equal to 39.0°C were registered in four players by halftime, and in nine by game’s end. Many of these players incurred significant dehydration during the game, compounded by initial hypohydration; thermoregulation may have been impaired to an extent we were unable to measure accurately. We suggest some new recommendations for soccer players training and competing in the heat to help them avoid substantial dehydration.Gatorade Sports Science Institute//Universidad de Costa Rica VI-245-A4-303UCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias Sociales::Centro de Investigación en Ciencias del Movimiento Humano (CIMOHU

Comparative characterization of Shiga toxin type 2 and subtilase cytotoxin effects on human renal epithelial and endothelial cells grown in monolayer and bilayer conditions

Published: June 23, 2016Postdiarrheal hemolytic uremic syndrome (HUS) affects children under 5 years old and is responsible for the development of acute and chronic renal failure, particularly in Argentina. This pathology is a complication of Shiga toxin (Stx)-producing Escherichia coli infection and renal damage is attributed to Stx types 1 and 2 (Stx1, Stx2) produced by Escherichia coli O157:H7 and many other STEC serotypes. It has been reported the production of Subtilase cytotoxin (SubAB) by non-O157 STEC isolated from cases of childhood diarrhea. Therefore, it is proposed that SubAB may contribute to HUS pathogenesis. The human kidney is the most affected organ because very Stx-sensitive cells express high amounts of biologically active receptor. In this study, we investigated the effects of Stx2 and SubAB on primary cultures of human glomerular endothelial cells (HGEC) and on a human tubular epithelial cell line (HK-2) in monoculture and coculture conditions. We have established the coculture as a human renal proximal tubule model to study water absorption and cytotoxicity in the presence of Stx2 and SubAB. We obtained and characterized cocultures of HGEC and HK-2. Under basal conditions, HGEC monolayers exhibited the lowest electrical resistance (TEER) and the highest water permeability, while the HGEC/HK-2 bilayers showed the highest TEER and the lowest water permeability. In addition, at times as short as 20-30 minutes, Stx2 and SubAB caused the inhibition of water absorption across HK-2 and HGEC monolayers and this effect was not related to a decrease in cell viability. However, toxins did not have inhibitory effects on water movement across HGEC/HK-2 bilayers. After 72 h, Stx2 inhibited the cell viability of HGEC and HK-2 monolayers, but these effects were attenuated in HGEC/HK-2 bilayers. On the other hand, SubAB cytotoxicity shows a tendency to be attenuated by the bilayers. Our data provide evidence about the different effects of these toxins on the bilayers respect to the monolayers. This in vitro model of communication between human renal microvascular endothelial cells and human proximal tubular epithelial cells is a representative model of the human proximal tubule to study the effects of Stx2 and SubAB related to the development of HUS.Romina S. Álvarez, Flavia Sacerdoti, Carolina Jancic, Adrienne W. Paton, James C. Paton, Cristina Ibarra, María M. Amara

Chemical and dimensional characterization of the renal countercurrent system in mice.

Chemical and dimensional characterization of the renal countercurrent system in mice.This study sought to identify the mechanisms leading to vasopressin (ADH)-resistant urinary concentrating defects in several genotypes of mice by analyzing the chemical composition as well as the dimensions of their countercurrent systems.As an aid to the analysis, a method was developed for estimating solute concentrations at the papillary tip by extrapolating from measurements of papillary solute concentration.The results indicate that the mechanisms causing decreased urinary concentration vary with the genotypes.In some, decreased water permeability appears to be the primary defect, leading secondarily to diminished cortico-papillary gradients for sodium and urea.In other genotypes a foreshortened countercurrent system and osmotic diuresis per nephron diminish the cortico-papillary urea gradient.And in still others, a combination of these causes appears to be involved.The study shows again that various diuretic states selectively wash out the medullary urea, probably because they curtail the medullary source of urea but not that of sodium.Characteres chimiques et importance du systeme de contre-courant renal chez la souris.Le but de cette étude était d'identifier les mécanismes responsables du défaut de concentration des urines résistant à la vasopressine (ADH) observé dans plusieurs génotypes de souris.Le moyen utilisé a été l'analyse de la composition chimique et des dimensions de leurs systèmes à contre-courant.Pour facilites cette analyse, une méthode a été élaborée qui perment calculer, pas extrapolation, la concentration à la pointe de la papille des substances dissoutes dont les concentrations ont été mesurées dans la papille.Les résultats montrent que les mécanismes responsables de la diminution de concentration urinaire diffèrent avec les génotypes.Dans certains cas, la diminution de perméabilité à l'eau semble être le défaut primaire, responsable d'une diminution secondaire des gradients cortico-papillaires du sodium et de l'urée.Dans d'autres cas, un raccourcissement du système de contre-courant et une diurèse osmotique par nephron diminuent le gradient cortico-papillaire de l'urée.Enfin dans d'autres cas ces différents mécanismes paraissent combinés.L'étude montre à nouveau que différents états diurétiques evacuent d'une façon sélective l'urée médullaire, sans doute en tarissant la source medullaire d'urée, mais non alle du sodium