A comprehensive evaluation of heat stress and heat strain in a sample of sugarcane cutters in Brazil.

Sugarcane cutters are vulnerable to extreme heat and are at risk for heat-related illness and chronic kidney disease, potentially due to high heat strain. We performed a comprehensive assessment of the physiological demands of sugarcane cutters via measurements of metabolic, thermal, and cardiovascular responses. In addition, we assessed cross-shift changes in markers of kidney function. Nine male sugarcane cutters were monitored while working during the spring harvest season in Brazil. Core temperature (Tcore) and heart rate (HR) were continuously recorded, and oxygen consumption was measured during the work shift. Urine and blood samples were collected pre- and postwork shifts. Total sweat loss was calculated using body weight changes and adjusting for water ingestion and urine output. A wet-bulb globe temperature (WBGT) station was used to monitor environmental heat stress. WBGT was ≥30°C on 7 of the 8 study days. Mean and peak Tcore during the work shift were 37.96 ± 0.47°C and 38.60 ± 0.41°C, respectively, with all participants surpassing a Tcore of 38°C. Mean and peak HR during the work shift were 137 ± 14 and 164 ± 11 beats/min, respectively. Percent of maximal oxygen consumption was, on average, 53 ± 11%. Workers had a total sweat loss of 7.63 ± 2.31 L and ingested 6.04 ± 1.95 L of fluid. Kidney function (estimated glomerular filtration rate) was reduced from pre- to postwork shift (Δ -20 ± 18 mL·min·1.73 m2). We demonstrated that sugarcane cutters performing prolonged work during a period of high environmental heat stress display high levels of heat strain, high water turnover, and reduced kidney function.NEW & NOTEWORTHY We demonstrate that a shift of sugarcane cutting performed outdoors during the spring harvest season results in a high level of heat strain. In fact, all the studied workers sustained core temperatures above 38°C and heart rates above 75% of the measured maximum heart rate. Additionally, workers displayed a high water turnover with sweat loss close to 10% of their body weight. Finally, we report elevated muscle damage and reductions in kidney function following the work shift.

A Preliminary Evaluation of the Kidney Function of Sugarcane Cutters From Brazil.

OBJECTIVE: To evaluate clinical parameters, markers of kidney function, and skeletal muscle damage in a group of sugarcane cutters during harvesting season. METHODS: Seventeen volunteers were assessed for anthropometrics and cardiorespiratory fitness. Blood and urine samples were collected 48-hours after the last work session. Blood was analyzed for glucose, creatine kinase, cholesterol, and a complete hemogram. Urine and blood samples were also analyzed for markers related to kidney function. RESULTS: Volunteers were young (26 ±â€Š6 y), had low body fat (13 ±â€Š5%), and good cardiorespiratory fitness (41 ±â€Š6 mL/kg/min). Classical markers of kidney function (eGFR, creatinine, cystatin C) were within the normal range. However, ten volunteers presented elevated resting serum creatine kinase (221 ±â€Š68 U/L). CONCLUSION: Manual sugarcane harvesting is associated with sustained skeletal muscle damage which may increase the risk for kidney injury in Brazilian sugarcane cutters.

The magnitude of physical exercise-induced hyperthermia is associated with changes in the intestinal permeability and expression of tight junction genes in rats.

We investigated whether the magnitude of exercise-induced hyperthermia influences intestinal permeability and tight junction gene expression. Twenty-nine male Wistar rats were divided into four groups: rest at 24 °C and exercise at 13 °C, 24 °C or 31 °C. The exercise consisted of a 90-min treadmill run at 15 m/min, and different ambient temperatures were used to produce distinct levels of exercise-induced hyperthermia. Before the experimental trials, the rats were treated by gavage with diethylenetriaminepentaacetic acid labeled with technetium-99 metastable as a radioactive probe. The rats' core body temperature (TCORE) was measured by telemetry. Immediately after the trials, the rats were euthanized, and the intestinal permeability was assessed by measuring the radioactivity of blood samples. The mRNA levels of occludin and zonula occludens-1 (ZO-1) genes were determined in duodenum samples. Exercise at 24 °C increased TCORE to values close to 39 °C, without changing permeability compared with the resting trial at the same environment. Meanwhile, rats' TCORE exceeded 40 °C during exercise at 31 °C, leading to greater permeability relative to those observed after exercise in the other ambient temperatures (e.g., 0.0037%/g at 31 °C vs. 0.0005%/g at 13 °C; data expressed as medians; p < 0.05). Likewise, the rats exercised at 31 °C exhibited higher mRNA levels of ZO-1 and occludin genes than the rats exercised at 24 °C or 13 °C. The changes in permeability and gene expression were positively and significantly associated with the magnitude of hyperthermia. We conclude that marked hyperthermia caused by exercise in the warmer environment increases intestinal permeability and mRNA levels of tight junction genes.

Thermogenic and psychogenic sweating in humans: Identifying eccrine glandular recruitment patterns from glabrous and non-glabrous skin surfaces.

In this experiment, psychogenic (mental arithmetic), thermogenic (mean body temperature elevation of 0.6 °C) and combined thermo-psychogenic treatments were used to explore eccrine sweat-gland recruitment from glabrous (volar hand and forehead) and non-glabrous skin surfaces (chest). It was hypothesised that each treatment would activate the same glands, and that glandular activity would be intermittent. Nine individuals participated in a single trial with normothermic and mildly hyperthermic phases. When normothermic, a 10-min arithmetical challenge was administered, during which sudomotor activity was recorded. Following passive heating and thermal clamping, sweating responses were again evaluated (10 min). A second arithmetical challenge (10 min) was administered during clamped hyperthermia, with its sudorific impact recorded. The activity of individual sweat glands was recorded at 60-s intervals, using precisely positioned, and uniformly applied, starch-iodide papers. Those imprints were digitised and analysed. Peak activity typically occurred during the thermo-psychogenic treatment, revealing physiologically active densities of 128 (volar hand), 165 (forehead) and 77 glands.cm-2 (chest). Except for the hand (46%), glands uniquely activated by one treatment were consistently <10% of the total glands identified. Glandular activations were most commonly of an intermittent nature, particularly during the thermogenic treatment. Accordingly, we accepted the hypothesis that psychogenic, thermogenic and thermo-psychogenic stimuli activate the same sweat glands in both the glabrous and non-glabrous regions. In addition, this investigation has provided detailed descriptions of the intermittent nature of sweat-gland activity, revealing that a consistent proportion of the physiologically active glands are recruited during these thermal and non-thermal stimuli.

Thermogenic and psychogenic recruitment of human eccrine sweat glands: Variations between glabrous and non-glabrous skin surfaces.

Human eccrine sweat-gland recruitment and secretion rates were investigated from the glabrous (volar) and non-glabrous hand surfaces during psychogenic (mental arithmetic) and thermogenic stimuli (mild hyperthermia). It was hypothesised that these treatments would activate glands from both skin surfaces, with the non-thermal stimulus increasing secretion rates primarily by recruiting more sweat glands. Ten healthy men participated in two seated, resting trials in temperate conditions (25-26°C). Trials commenced under normothermic conditions during which the first psychogenic stress was applied. That was followed by passive heating (0.5°C mean body temperature elevation) and thermal clamping, with a second cognitive challenge then applied. Sudomotor activity was evaluated from both hands, with colourimetry used to identify activated sweat glands, skin conductance to determine the onset of precursor sweating and ventilated sweat capsules to measure rates of discharged sweating. From glandular activation and sweat rate data, sweat-gland outputs were derived. These psychogenic and thermogenic stimuli activated sweat glands from both the glabrous and non-glabrous skin surfaces, with the former dominating at the glabrous skin and the latter at the non-glabrous surface. Indeed, those stimuli individually accounted for ~90% of the site-specific maximal number of activated sweat glands observed when both stimuli were simultaneously applied. During the normothermic psychological stimulation, sweating from the glabrous surface was elevated via a 185% increase in the number of activated glands within the first 60s. The hypothetical mechanism for this response may involve the serial activation of additional eccrine sweat glands during the progressive evolution of psychogenic sweating.

Insights into the role of heat shock protein 72 to whole-body heat acclimation in humans.

Heat acclimation results in systemic and cellular adaptions that reduce the negative effect of heat and, consequently, the risk of heat illness. Although the classical changes observed with heat acclimation lead to increased tolerance to exercise in the heat by reducing heat storage (reflected in reduced core and skin temperatures) and increasing whole-body capacity for heat dissipation (greater plasma volume, sweat output, and skin blood flow), it appears that heat acclimation also induces changes at the cellular level that might increase tolerance of the whole organism to a higher core temperature for the development of fatigue. Thermotolerance is a process that involves increased resilience to an otherwise lethal heat stress that follows a sublethal exposure to heat. Thermotolerance is believed to be the result of increased content of heat shock proteins (Hsp), specially a member of the 70 kDa family, Hsp72 kDa. In humans, we and others have reported that heat acclimation increases intracellular Hsp72 levels. This increase in intracellular Hsp72 could improve whole-body organism thermotolerance by maintaining intestinal epithelial tight junction barriers, by increasing resistance to gut-associated endotoxin translocation, or by reducing the inflammatory response. In this review, we will initially provide an overview of the physiological adaptations induced by heat acclimation and emphasize the main cellular changes that occur with heat acclimation associated with intracellular accumulation of Hsp72. Finally, we will present an argument for a role of whole-body heat acclimation in augmenting cellular thermotolerance, which may protect vital organs from deleterious effects of heat stress in humans.

Temporal and thermal variations in site-specific thermoregulatory sudomotor thresholds: precursor versus discharged sweat production.

Temporal and thermal differences between the initiation of precursor, eccrine sweat and its surface discharge were investigated during passive heating. Sudomotor activity was evaluated using electrodermal (precursor) and ventilated sweat capsule measurements (dorsal fingers, dorsal hand, forehead, forearm). Passive heating significantly elevated auditory canal (0.5 degrees C) and mean body temperatures (0.9 degrees C). At each site, the precursor sudomotor thresholds occurred at a lower mean body temperature (P < .05), with an average elevation of 0.35 degrees C (SD 0.04). However, discharged thresholds were delayed until this temperature had risen 0.53 degrees C (SD 0.04), producing significant phase delays across sites (mean: 4.1 min [SD 0.5]; P < .05). It is concluded that precise sudomotor threshold determinations require methods that respond to sweat accumulating within the secretory coil, and not discharged secretions, reinforcing the importance of electrodermal techniques.

Hands and feet: physiological insulators, radiators and evaporators.

The purpose of this review is to describe the unique anatomical and physiological features of the hands and feet that support heat conservation and dissipation, and in so doing, highlight the importance of these appendages in human thermoregulation. For instance, the surface area to mass ratio of each hand is 4-5 times greater than that of the body, whilst for each foot, it is ~3 times larger. This characteristic is supported by vascular responses that permit a theoretical maximal mass flow of thermal energy of 6.0 W (136 W m(2)) to each hand for a 1 °C thermal gradient. For each foot, this is 8.5 W (119 W m(2)). In an air temperature of 27 °C, the hands and feet of resting individuals can each dissipate 150-220 W m(2) (male-female) of heat through radiation and convection. During hypothermia, the extremities are physiologically isolated, restricting heat flow to <0.1 W. When the core temperature increases ~0.5 °C above thermoneutral (rest), each hand and foot can sweat at 22-33 mL h(-1), with complete evaporation dissipating 15-22 W (respectively). During heated exercise, sweat flows increase (one hand: 99 mL h(-1); one foot: 68 mL h(-1)), with evaporative heat losses of 67-46 W (respectively). It is concluded that these attributes allow the hands and feet to behave as excellent radiators, insulators and evaporators.

Regional variations in transepidermal water loss, eccrine sweat gland density, sweat secretion rates and electrolyte composition in resting and exercising humans.

Literature from the past 168 years has been filtered to provide a unified summary of the regional distribution of cutaneous water and electrolyte losses. The former occurs via transepidermal water vapour diffusion and secretion from the eccrine sweat glands. Daily insensible water losses for a standardised individual (surface area 1.8 m2) will be 0.6-2.3 L, with the hands (80-160 g.h-1) and feet (50-150 g.h-1) losing the most, the head and neck losing intermediate amounts (40-75 g.h-1) and all remaining sites losing 15-60 g.h-1. Whilst sweat gland densities vary widely across the skin surface, this same individual would possess some 2.03 million functional glands, with the highest density on the volar surfaces of the fingers (530 glands.cm-2) and the lowest on the upper lip (16 glands.cm-2). During passive heating that results in a resting whole-body sweat rate of approximately 0.4 L.min-1, the forehead (0.99 mg.cm-2.min-1), dorsal fingers (0.62 mg.cm-2.min-1) and upper back (0.59 mg.cm-2.min-1) would display the highest sweat flows, whilst the medial thighs and anterior legs will secrete the least (both 0.12 mg.cm-2.min-1). Since sweat glands selectively reabsorb electrolytes, the sodium and chloride composition of discharged sweat varies with secretion rate. Across whole-body sweat rates from 0.72 to 3.65 mg.cm-2.min-1, sodium losses of 26.5-49.7 mmol.L-1 could be expected, with the corresponding chloride loss being 26.8-36.7 mmol.L-1. Nevertheless, there can be threefold differences in electrolyte losses across skin regions. When exercising in the heat, local sweat rates increase dramatically, with regional glandular flows becoming more homogeneous. However, intra-regional evaporative potential remains proportional to each local surface area. Thus, there is little evidence that regional sudomotor variations reflect an hierarchical distribution of sweating either at rest or during exercise.

The cholinergic blockade of both thermally and non-thermally induced human eccrine sweating.

Thermally induced eccrine sweating is cholinergically mediated, but other neurotransmitters have been postulated for psychological (emotional) sweating. However, we hypothesized that such sweating is not noradrenergically driven in passively heated, resting humans. To test this, nine supine subjects were exposed to non-thermal stimuli (palmar pain, mental arithmetic and static exercise) known to evoke sweating. Trials consisted of the following four sequential phases: thermoneutral rest; passive heating to elevate (by ~1.0°C) and clamp mean body temperature and steady-state sweating (perfusion garment and footbath); an atropine sulphate infusion (0.04 mg kg(-1)) with thermal clamping sustained; and following clamp removal. Sudomotor responses from glabrous (hairless) and non-glabrous skin surfaces were measured simultaneously (precursor and discharged sweating). When thermoneutral, these non-thermal stimuli elicited significant sweating only from the palm (P < 0.05). Passive heating induced steady-state sweating ranging from 0.20 ± 0.04 (volar hand) to 1.40 ± 0.14 mg cm(-2) min(-1) (forehead), with each non-thermal stimulus provoking greater secretion (P < 0.05). Atropine suppressed thermal sweating, and it also eliminated the sudomotor responses to these non-thermal stimuli when body temperatures were prevented from rising (P > 0.05). However, when the thermal clamp was removed, core and skin temperatures became further elevated and sweating was restored (P < 0.05), indicating that the blockade had been overcome, presumably through elevated receptor competition. These observations establish the dependence of both thermal and non-thermal eccrine sweating from glabrous and non-glabrous surfaces on acetylcholine release, and challenge theories concerning the psychological modulation of sweating. Furthermore, no evidence existed for the significant participation of non-cholinergic neurotransmitters during any of these stimulations.

Psychological sweating from glabrous and nonglabrous skin surfaces under thermoneutral conditions.

Recent experiments revealed psychological sweating to be a ubiquitous phenomenon in passively heated individuals. Since heating potentiates sweating, and since most research into psychological sweating was not conducted in this thermal state, these observations required thermoneutral verification. Thermoneutral subjects performed mental arithmetic (at 26(o) C) with psychological sweating evaluated from nine sites (ventilated capsules, skin conductance). Discharged sweating was evident from three glabrous sites (P < .05). However, significant sweating was evident from two nonglabrous surfaces (P < .05), and skin conductance increased at the volar and dorsal finger surfaces (P < .05). Each of these changes occurred while core and skin temperatures remained stable (P > .05). These thermoneutral observations further refute the proposition that psychological sweating in humans is restricted to the glabrous skin surfaces.

Sex-related differences in sweat gland cholinergic sensitivity exist irrespective of differences in aerobic capacity.

Mechanisms accounting for sex-related differences in the sweat response remain to be elucidated. In the present study, we focused on differences in sweat gland cholinergic sensitivity between males and females. Since, males usually possess higher aerobic capacity than females, we investigated sweating in males and females grouped according to aerobic capacity (.VO(2peak)). Forty-four subjects were assigned to four groups: males with higher (MH) and lower (ML), and females with higher (FH) and lower (FL) .VO(2peak). Forearm sweating was induced by iontophoretic administration (1.5 mA, 60 muA cm(-2), 5 min) of pure water or varying concentrations of pilocarpine hydrochloride (0.125, 0.250, 0.5, 1.0 and 2.0%). Local sweat rate (absorbent paper) and the number of activated sweat glands (iodine impregnated paper) were computed. Maximal pilocarpine-induced sweat rate (SR(max)) and the pilocarpine concentration which elicited 50% of maximal sweating response (K (m)) were calculated. Sweat rate and active gland density increased in response to greater doses of pilocarpine (p < 0.05). Inter-group differences were evident: SR(max) was greatest for MH and lowest for FL (p < 0.05), but no significant differences were observed between ML and FH (p = 0.24). Higher SR(max) were observed, within-sex, for those with greater aerobic capacity (p < 0.05). Furthermore, males' K (m) values were higher than females', indicating greater sweat gland affinity for pilocarpine even for groups having similar aerobic capacity (p < 0.05). In summary, we confirmed that the human sudomotor response is affected by aerobic capacity but, also, that sex-related differences in sweat gland cholinergic sensitivity exist and are not necessarily associated with the typical differences in .VO(2peak) observed between sexes.

Sweat secretion from palmar and dorsal surfaces of the hands during passive and active heating.

INTRODUCTION: It is generally accepted that the palmar (volar) and dorsal surfaces of human hands display different sudomotor responses to mental or thermal stimuli. We tested the hypothesis that, during thermal stimulation, secretion from the dorsal surfaces would always exceed that from the volar aspect of the hand. METHODS: Sweat secretion from 10 hand sites and the forehead was examined (ventilated capsules) in 10 subjects during passive heating (climate chamber: 36 degrees C, 60% relative humidity, water-perfusion suit: 40 degrees C) immediately followed by incremental cycling to volitional fatigue. RESULTS: This treatment significantly increased core temperature (39.3 degrees C), heart rate (178 bpm), and sweat rate at all sites. Mean sweat secretion during exercise was greater at the forehead (2.90 mg x cm(-2) x min(-1); +/- 0.19) than the hand (1.49 mg x cm(-2) min(-1); +/- 0.27). While no significant differences in sweating were observed among dorsal sites, a nonuniform secretion pattern was observed across the volar surface, with sweating at the palm being the lowest, and that from the volar aspect of the distal phalanges being equivalent to the dorsal hand. These differences became more evident as exercise progressed. Mean hand sweat rate during exercise was 41.7 ml x h(-1), with sweating from the palm accounting for only about 6% of sweat secretion. CONCLUSION: Sweat secretion from both the palmar and dorsal surfaces of the hand increases during exercise in the heat, although this occurs in a nonuniform fashion. It is possible that a greater sweat gland density on the fingers may account for variations across the volar surface. However, higher dorsal sweating with lower gland counts (high glandular flow) may be attributable to either larger sweat glands, or to a greater cholinergic sensitivity of these glands.

Local differences in sweat secretion from the head during rest and exercise in the heat.

The importance of the head in dissipating body heat under hot conditions is well recognised, although very little is known about local differences in sweat secretion across the surface of the head. In this study, we focused on the intra-segmental distribution of head sweating. Ten healthy males were exposed to passive heating and exercise-induced hyperthermia (36 degrees C, 60% relative humidity, water-perfusion suit: 46 degrees C), with ventilated sweat capsules (3.16 cm(2)) used to measure sweat rates from the forehead and nine sites inside the hairline. Sweat secretion from both non-hairy (glabrous) and hairy areas of the head increased linearly with increments in work rate and core temperature, with heart rate and core temperature peaking at 175 b min(-1) (+/-6) b min(-1) and 39.2 degrees C (+/-0.1). The mean sweat rate during exercise for sites within the hairline was 1.95 mg cm(-2) min(-1). However, the evolution of this secretion pattern was not uniformly distributed within the head, with the average sweat rate for the top of the head being significantly lower than at the anterior lateral aspect of the head (P < 0.05), and representing only 30% of the forehead sweat rate (P < 0.05). It is hypothesised that these intra-segmental observations may reflect variations in the local adaptation of eccrine glands to differences in local evaporation associated either with bipedal locomotion, which will influence forehead sweating, or the hidromeiotic suppression of sweating, which impacts upon sweat glands within the hairline.

Sweat secretion from the torso during passively-induced and exercise-related hyperthermia.

Thermal sweating from the human torso accounts for about half of the whole-body sweat secretion, yet its intra-segmental distribution has not been thoroughly examined. Therefore, the aim of the current study was to provide a detailed description of the distribution of eccrine sweating within the torso during passively-induced (water-perfusion garment: 40 degrees C) and progressively increasing, exercise-related thermal strain (36 degrees C, 60% relative humidity). Sudomotor function was measured in ten males using ventilated sweat capsules (3.16 cm(2)) attached to twelve sites on the ventral (four), lateral (three) and dorsal (four) torso, and upper shoulder surfaces. Sweating increased asymptotically in all sites, with the final core temperature averaging 39.7 degrees C (+/-0.1) and heart rates being 181 b min(-1) (+/-2). During exercise, the mean torso sweat rate averaged 1.35 mgcm(-2)min(-1), with sweating from the lateral torso surfaces generally being the lowest. Each of the between-site comparisons with the lateral torso differed significantly (P < 0.05), except for comparisons with the chest (P = 0.051) and shoulder (P > 0.05). The intra-segmental differences between the lateral torso and the chest, abdomen, upper- and lower-back areas were significantly accentuated during exercise. From these data, it is evident that the torso is another region that does not have a uniform distribution of thermally-induced sweating. Thus, it is no longer acceptable for researchers, modellers, sweating manikins engineers or clothing manufacturers to assume that the sweat rates for all local sites within any body segment are equivalent.

Hidratação durante o exercício: a sede é suficiente? / Hidratación durante el ejercicio: ¿la sed es suficiente? / Exercise fluid replacement: is thirst enough?

O objetivo deste trabalho é fazer uma revisão sobre a hidratação e discutir se, durante o exercício, a reposição de líquidos de acordo com a sede é suficiente para hidratar o indivíduo. A perda hídrica pela sudorese induzida pelo exercício, especialmente realizado em ambientes quentes, pode levar à desidratação, pode alterar o equilíbrio hidroeletrolítico, dificultar a termorregulação e, assim, representar um risco para a saúde e/ou provocar uma diminuição no desempenho esportivo. Tem sido citado que os atletas não ingerem voluntariamente água suficiente para prevenir a desidratação durante uma atividade física. Em função disso, têm sido propostas recomendações internacionais sobre a hidratação. Segundo o American College of Sports Medicine (ACSM), deve-se ingerir aproximadamente 500mL de líquidos nas duas horas antecedentes ao exercício. Durante o exercício, os atletas devem começar a beber desde o início e em intervalos regulares, em volume suficiente para repor as perdas pela sudorese ou o máximo tolerado. A National Athletic Trainer's Association (NATA) faz as seguintes recomendações: ingerir 500 a 600mL de água ou outra bebida esportiva duas a três horas antes do exercício e 200 a 300mL 10 a 20 minutos antes do exercício; durante o exercício, a reposição deve aproximar as perdas pelo suor e pela urina e pelo menos manter a hidratação, com perdas máximas correspondentes a 2 por cento de perda de peso corporal; após o exercício a hidratação deve ter como objetivo corrigir quaisquer perdas líquidas acumuladas. Além disso, o ACSM e o NATA fazem referências sobre temperatura e palatabilidade do líquido, adição de carboidratos e eletrólitos de acordo com a intensidade e duração do exercício e estratégias de hidratação para facilitar a acessibilidade do atleta ao líquido. No entanto, outros autores questionam o uso da reidratação em volumes predeterminados e sugerem que a ingestão de líquidos de acordo com a sede seja capaz de manter a homeostase.

The present work proposes a review about exercise fluid replacement and a discussion whether, during exercise, the fluid ingested according to thirst is sufficient to maintain hydration. Exercise sweat loss, mainly in the heat, can cause dehydration, can alter the hidroelectrolyte balance, disturb thermoregulation, presenting a health risk and/or impairing the athletic performance. It has been asserted that athletes do not drink, spontaneously, the sufficient fluid volume to prevent dehydration during the physical activity. Thus, international recommendations to fluid replacement during physical activities have been proposed. According to the American College of Sports Medicine (ACSM), about 500 mL of fluid on the two hours before the exercise must be ingested. During exercise, they propose that athletes should start fluid replacement since the beginning in regular periods and should drink enough fluid to restore all the sweating losses or ingest the maximal volume tolerated. The National Athletic Trainer's Association (NATA) proposes the following recommendations: ingestion of 500 to 600 mL of water two or three hours before exercise or other sport drink and ingestion of 200 to 300 mL 10 to 20 minutes before exercise starting. During exercise, the fluid replacement should match the sweating and urine losses and at least should maintain hydration status reaching maximal body weight losses of 2 percent. After the exercise, fluid replacement must restore all the fluid losses accumulated. In addition, ACSM and NATA asserted about fluid temperature and palatability, beverage carbohydrate and electrolyte additions according to exercise duration and intensity and recommended hydration schedules to provide easier access to fluid ingestion. However, other authors contest the use of hydration schedules based on predetermined fluid volumes and suggest that fluid replacement according to thirst is enough to maintain body homeostasis.

El objetivo de este trabajo es hacer una revisión sobre la hidratación y discutir si, durante el ejercicio, la reposición de líquidos de acuerdo con la sed es suficiente para hidratar al individuo. La pérdida hídrica por la sudoración inducida por el ejercicio, especialmente realizado en ambientes calurosos, puede llevar a la deshidratación, puede alterar el equilibrio hidroelectrolítico, dificultar la termorregulación y, así, representar un riesgo para la salud y/o provocar una disminución en el desempeño deportivo. Ha sido citado que los atletas no ingieren voluntariamente agua suficiente para prevenir la deshidratación durante una actividad física. En función de eso, han sido propuestas recomendaciones internacionales sobre la hidratación. Según American College of Sports Medicine (ACSM), se debe ingerir aproximadamente 500 ml de líquidos durante las dos horas antecedentes al ejercicio. Durante el ejercicio, los atletas deben comenzar a beber desde el inicio y a intervalos regulares, en volumen suficiente para reponer las pérdidas por la sudoración o el máximo tolerado. La National Athletic Trainer's Association (NATA) hace las siguientes recomendaciones: ingerir 500 a 600 ml de agua u otra bebida deportiva dos a tres horas antes del ejercicio y 200 a 300 ml de 10 a 20 minutos antes del ejercicio; durante el ejercicio, la reposición debe aproximarse a las pérdidas por el sudor y por la orina y por lo menos mantener la hidratación, con pérdidas máximas correspondientes a 2 por ciento de pérdida de peso corporal; después del ejercicio la hidratación debe tener como objetivo corregir cualesquier pérdidas líquidas acumuladas. Además de esto, la ACSM y la NATA hacen referencias sobre temperatura y palatabilidad del líquido, adición de carbohidratos y electrólitos de acuerdo con la intensidad y duración del ejercicio y estrategias de hidratación para facilitar la accesibilidad del atleta al líquido. A pesar de esto, otros autores cuestionan...

Possible biphasic sweating response during short-term heat acclimation protocol for tropical natives.

The aim of the present study was to evaluate the sweat loss response during short-term heat acclimation in tropical natives. Six healthy young male subjects, inhabitants of a tropical region, were heat acclimated by means of nine days of one-hour heat-exercise treatments (40+/-0 degrees C and 32+/-1% relative humidity; 50% (.)VO(2peak) on a cycle ergometer). On days 1 to 9 of heat acclimation whole-body sweat loss was calculated by body weight variation corrected for body surface area. On days 1 and 9 rectal temperature (T(re)) and heart rate (HR) were measured continuously, and rating of perceived exertion (RPE) every 4 minutes. Heat acclimation was confirmed by reduced HR (day 1 rest: 77+/-5 b.min(-1); day 9 rest: 68+/-3 b.min(-1); day 1 final exercise: 161+/-15 b.min(-1); day 9 final exercise: 145+/-11 b.min(-1), p<0.05), RPE (13 vs. 11, p<0.05) and T(re) (day 1 rest: 37.2+/-0.2 degrees C; day 9 rest: 37.0+/-0.2 degrees C; day 1 final exercise: 38.2+/-0.2 degrees C; day 9 final exercise: 37.9+/-0.1 degrees C, p<0.05). The main finding was that whole-body sweat loss increased in days 5 and 7 (9.49+/-1.84 and 9.56+/-1.86 g.m(-2).min(-1), respectively) compared to day 1 (8.31+/-1.31 g.m(-2).min(-1), p<0.05) and was not different in day 9 (8.48+/-1.02 g.m(-2).min(-1)) compared to day 1 (p>0.05) of the protocol. These findings are consistent with the heat acclimation induced adaptations and suggest a biphasic sweat response (an increase in the sweat rate in the middle of the protocol followed by return to initial values by the end of it) during short-term heat acclimation in tropical natives.