Hydration effects on thermoregulation and performance in the heat.

During exercise, sweat output often exceeds water intake, producing a water deficit or hypohydration. The water deficit lowers both intracellular and extracellular fluid volumes, and causes a hypotonic-hypovolemia of the blood. Aerobic exercise tasks are likely to be adversely effected by hypohydration (even in the absence of heat strain), with the potential affect being greater in hot environments. Hypohydration increases heat storage by reducing sweating rate and skin blood flow responses for a given core temperature. Hypertonicity and hypovolemia both contribute to reduced heat loss and increased heat storage. In addition, hypovolemia and the displacement of blood to the skin make it difficult to maintain central venous pressure and thus cardiac output to simultaneously support metabolism and thermoregulation. Hyperhydration provides no advantages over euhydration regarding thermoregulation and exercise performance in the heat.

Physiologic tolerance to uncompensable heat: intermittent exercise, field vs laboratory.

PURPOSE: This study determined whether exercise (30 min)-rest (10 min) cycles alter physiologic tolerance to uncompensable heat stress (UCHS) when outdoors in the desert. In addition, the relationship between core temperature and exhaustion from heat strain previously established in laboratory studies was compared with field studies. METHODS: Twelve men completed four trials: moderate intensity continuous exercise (MC), moderate intensity exercise with intermittent rest (MI), hard intensity continuous exercise (HC), and hard intensity exercise with intermittent rest (HI). UCHS was achieved by wearing protective clothing and exercising (estimated at 420 W or 610 W) outdoors in desert heat. RESULTS: Heat Stress Index values were 200%, 181%, 417%, and 283% for MC, MI, HC, and HI, respectively. Exhaustion from heat strain occurred in 36 of 48 trials. Core temperatures at exhaustion averaged 38.6 +/- 0.5 degrees, 38.9 +/- 0.6 degrees, 38.9 +/- 0.7 degrees, and 39.0 +/- 0.7 degrees C for MC, MI, HC, and HI, respectively. Core temperature at exhaustion was not altered (P > 0.05) by exercise intensity or exercise-rest cycles and 50% of subjects incurred exhaustion at core temperature of 39.4 degrees C. These field data were compared with laboratory and field data collected over the past 35 years. Aggregate data for 747 laboratory and 131 field trials indicated that 50% of subjects incurred exhaustion at core temperatures of 38.6 degrees and 39.5 degrees C, respectively. When heat intolerant subjects (exhaustion < 38.3 degrees C core temperature) were removed from the analysis, subjects from laboratory studies (who underwent short-term acclimation) still demonstrated less (0.8 degrees C) physiological tolerance than those from field studies (who underwent long-term acclimatization). CONCLUSION: Exercise-rest cycles did not alter physiologic tolerance to UCHS. In addition, subjects from field studies demonstrate greater physiologic tolerance than subjects from laboratory studies.

Hyperhydration and glycerol: thermoregulatory effects during exercise in hot climates.

Hyperhydration or increasing body water content above normal (euhydration) level was thought to have some benefit during exercise heat-stress; however, attempts to overdrink have been minimized by a rapid diuretic response. The perception that hyperhydration might be beneficial for exercise performance and for thermoregulation arose from the adverse consequences of hypohydration. Many studies had examined the effects of hyperhydration on thermoregulation in the heat; however, most of them suffer from design problems that confound their results. The design problems included control conditions not representing euhydration but hypohydration, control conditions not adequately described, cold fluid ingestion that reduced core temperature, and/or changing heat acclimation status. Several investigators reported lower core temperatures during exercise after hyperhydration, while other studies do not. Some investigators reported higher sweating rates with hyperhydration, while other studies do not. Recent research that controlled for these confounding variables reported that hyperhydration (water or glycerol) did not alter core temperature, skin temperature, whole body sweating rate, local sweating rate, sweating threshold temperature, sweating sensitivity, or heart rate responses compared to euhydration trial. If euhydration is maintained during exercise-heat stress then hyperhydration appears to have no meaningful advantage.

Impact of muscle injury and accompanying inflammatory response on thermoregulation during exercise in the heat.

This study examined whether muscle injury and the accompanying inflammatory responses alter thermoregulation during subsequent exercise-heat stress. Sixteen subjects performed 50 min of treadmill exercise (45-50% maximal O(2) consumption) in a hot room (40 degrees C, 20% relative humidity) before and at select times after eccentric upper body (UBE) and/or eccentric lower body (LBE) exercise. In experiment 1, eight subjects performed treadmill exercise before and 6, 25, and 30 h after UBE and then 6, 25, and 30 h after LBE. In experiment 2, eight subjects performed treadmill exercise before and 2, 7, and 26 h after LBE only. UBE and LBE produced marked soreness and significantly elevated creatine kinase levels (P < 0.05), but only LBE increased (P < 0.05) interleukin-6 levels. In experiment 1, core temperatures before and during exercise-heat stress were similar for control and after UBE, but some evidence for higher core temperatures was found after LBE. In experiment 2, core temperatures during exercise-heat stress were 0.2-0.3 degrees C (P < 0.05) above control values at 2 and 7 h after LBE. The added thermal strain after LBE (P < 0.05) was associated with higher metabolic rate (r = 0.70 and 0.68 at 2 and 6-7 h, respectively) but was not related (P > 0.05) to muscle soreness (r = 0.47 at 6-7 h), plasma interleukin-6 (r = 0.35 at 6-7 h), or peak creatine kinase levels (r = 0.22). Local sweating responses (threshold core temperature and slope) were not altered by UBE or LBE. The results suggest that profuse muscle injury can increase body core temperature during exercise-heat stress and that the added heat storage cannot be attributed solely to increased heat production.

Effects of dehydration, hypohydration, and hyperhydration on tolerance during uncompensable heat stress.

The present study examined the effects of dehydration from prior exercise on subsequent exercise tolerance time (TT) that involved wearing nuclear, biological, and chemical (NBC) protective clothing. It was hypothesised that TT would be reduced in the dehydrated state. Ten men undertook continuous treadmill walking at 4.8 km.h-1 at 35 degrees C and 50% relative humidity, wearing NBC clothing while euhydrated (EU) or dehydrated (D) by 2.3% of body weight. Hydration status had no impact on thermoregulatory or cardiovascular responses during exercise. Also rectal temperature at exhaustion did not differ between EU (38.52 +/- 0.39 degrees C) and D (38.43 +/- 0.45 degrees C). Exercise TT during this uncompensable heat stress was reduced significantly for D (47.7 +/- 15.3 min) compared with EU (59.0 +/- 13.6 min). It was concluded that prior exercise leading to levels of dehydration to 2.3% of body weight, together with subsequent fluid restriction during exposure to uncompensable heat stress, impaired TT while wearing the NBC protective clothing. The integration of these findings together with other comparable studies that have examined the influence of hypo- and hyperhydration on TT while wearing NBC protective clothing revealed that hydration status has less effect on TT as the severity of uncompensable heat stress increases.

Water and electrolyte requirements for exercise.

Exercise performance can be compromised by a body water deficit, particularly when exercise is performed in hot climates. It is recommended that individuals begin exercise when adequately hydrated. This can be facilitated by drinking 400 mL to 600 mL of fluid 2 hours before beginning exercise and drinking sufficient fluid during exercise to prevent dehydration from exceeding 2% body weight. A practical recommendation is to drink small amounts of fluid (150-300 mL) every 15 to 20 minutes of exercise, varying the volume depending on sweating rate. Core temperature, heart rate, and perceived effort remain lowest when fluid replacement comes closest to matching the rate of sweat loss. During exercise lasting less than 90 minutes, water alone is sufficient for fluid replacement. During prolonged exercise lasting longer than 90 minutes, commercially available carbohydrate electrolyte beverages should be considered to provide an exogenous carbohydrate source to sustain carbohydrate oxidation and endurance performance. Electrolyte supplementation is generally not necessary because dietary intake is adequate to offset electrolytes lost in sweat and urine; however, during initial days of hot-weather training or when meals are not calorically adequate, supplemental salt intake may be indicated to sustain sodium balance.

Fluid replacement recommendations for training in hot weather.

The U.S. Army's fluid replacement guidelines emphasize fluid replacement during hot weather training to prevent degradation of performance and minimize the risk of heat injury. Little consideration has been given, however, to possible overhydration and development of water intoxication. Sufficient epidemiological evidence is available to demonstrate an increasing incidence of water intoxication during military training. This article summarizes the development and validation of revised fluid replacement guidelines for hot weather training. The end product is an easy-to-read table that provides the user with the appropriate hourly work time and fluid intake to support work during hot weather training. The guidelines include the range of hot weather conditions likely to be encountered during military training and cover a broad range of military activities. It is expected that the revised guidelines will sustain hydration and minimize the number of heat injuries during military training while protecting the soldier from becoming sick from overdrinking.

Hydration effects on temperature regulation.

During exercise in the heat, sweat output often exceeds water intake which results in a body water deficit (hypohydration) and electrolyte losses. Daily water losses can be substantial and persons need to emphasize drinking during exercise as well as at mealtime. Aerobic exercise tasks are likely to be adversely affected by heat stress and hypohydration; and the warmer the climate the greater the potential for performance decrements. Hypohydration increases heat storage and reduces one's ability to tolerate heat strain. The increased heat storage is mediated by reduced sweating rate (evaporative heat loss) and reduced skin blood flow (dry heat loss) for a given core temperature. Hyperhydration (increased total body water) has been suggested to reduce physiologic strain during exercise heat stress, however, data supporting that notion are not robust.

Hyperhydration: tolerance and cardiovascular effects during uncompensable exercise-heat stress.

This study examined the efficacy of glycerol and water hyperhydration (1 h before exercise) on tolerance and cardiovascular strain during uncompensable exercise-heat stress. The approach was to determine whether 1-h preexercise hyperhydration (29.1 ml H2O/kg lean body mass with or without 1.2 g/kg lean body mass of glycerol) provided a physiological advantage over euhydration. Eight heat-acclimated men completed three trials (control euhydration before exercise, and glycerol and water hyperhydrations) consisting of treadmill exercise-heat stress (ratio of evaporative heat loss required to maximal capacity of climate = 416). During exercise ( approximately 55% maximal O2 uptake), there was no difference between glycerol and water hyperhydration methods for increasing (P < 0.05) total body water. Glycerol hyperhydration endurance time (33. 8 +/- 3.0 min) was longer (P < 0.05) than for control (29.5 +/- 3.5 min), but was not different (P > 0.05) from that of water hyperhydration (31.3 +/- 3.1 min). Hyperhydration did not alter (P > 0.05) core temperature, whole body sweating rate, cardiac output, blood pressure, total peripheral resistance, or core temperature tolerance. Exhaustion from heat strain occurred at similar core and skin temperatures and heart rates in each trial. Symptoms at exhaustion included syncope and ataxia, fatigue, dyspnea, and muscle cramps (n = 11, 10, 2, and 1 cases, respectively). We conclude that 1-h preexercise glycerol hyperhydration provides no meaningful physiological advantage over water hyperhydration and that hyperhydration per se only provides the advantage (over euhydration) of delaying hypohydration during uncompensble exercise-heat stress.

Thermal and cardiovascular strain from hypohydration: influence of exercise intensity.

This study determined the effects of exercise intensity on the physiologic (thermal and cardiovascular) strain induced from hypohydration during heat stress. We hypothesized that the added thermal and cardiovascular strain induced by hypohydration would be greater during high intensity than low intensity exercise. Nine heat-acclimated men completed a matrix of nine trials: three exercise intensities, 25%, 45% and 65% VO2 max; and three hydration levels, euhydration and hypohydration at 3% and 5% body weight loss (BWL). During each trial, subjects attempted 50 min of treadmill exercise in a hot room (30 degrees C db, 50% rh) while body temperatures and cardiac output were measured. Hypohydration was achieved by exercise and fluid restriction the day preceding the trials. Core temperature increased (P<0.05) 0.12 degrees C per%BWL at each hypohydration level and was not affected by exercise intensity. Cardiac output was reduced (P<0.05) compared to euhydration levels and was reduced more during high compared to low intensity exercise after 5% BWL. It was concluded that: a) the thermal penalty (core temperature increase) accompanying hypohydration is not altered by exercise intensity; and b) at severe hypohydration levels, the cardiovascular penalty (cardiac output reduction) increases with exercise intensity.

Hyperhydration: thermoregulatory effects during compensable exercise-heat stress.

This study examined the effects of hyperhydration on thermoregulatory responses during compensable exercise-heat stress. The general approach was to determine whether 1-h preexercise hyperhydration [29. 1 ml/kg lean body mass; with or without glycerol (1.2 g/kg lean body mass)] would improve sweating responses and reduce core temperature during exercise. During these experiments, the evaporative heat loss required (Ereq = 293 W/m2) to maintain steady-state core temperature was less than the maximal capacity (Emax = 462 W/m2) of the climate for evaporative heat loss (Ereq/Emax = 63%). Eight heat-acclimated men completed five trials: euhydration, glycerol hyperhydration, and water hyperhydration both with and without rehydration (replace sweat loss during exercise). During exercise in the heat (35 degrees C, 45% relative humidity), there was no difference between hyperhydration methods for increasing total body water (approximately 1.5 liters). Compared with euhydration, hyperhydration did not alter core temperature, skin temperature, whole body sweating rate, local sweating rate, sweating threshold temperature, sweating sensitivity, or heart rate responses. Similarly, no difference was found between water and glycerol hyperhydration for these physiological responses. These data demonstrate that hyperhydration provides no thermoregulatory advantage over the maintenance of euhydration during compensable exercise-heat stress.

Aldosterone and vasopressin responses in the heat: hydration level and exercise intensity effects.

We examined the separate and combined effects of hypohydration level and exercise intensity on aldosterone (ALD) and arginine vasopressin (AVP) responses during exercise-heat stress. Nine heat acclimated men performed 50 min of treadmill exercise in a warm room (30 degrees C dry bulb (DB), 50% relative humidity (RH) at 25%, 45% and 65% VO2max when euhydrated and when hypohydrated by 3% and 5% of body weight. Blood samples were drawn at rest and at 20 min of exercise. ALD and AVP increased (P < 0.05) in a graded manner with hypohydration level, and this effect persisted during exercise-heat stress. High intensity exercise produced greater ALD and AVP increases than low intensity exercise. ALD responses during exercise were independent of hypohydration level. AVP responses were closely related to osmolality (N = 6 of 7 subjects; r = 0.51 to r = 0.98; average r = 0.84) despite varying hydration, exercise intensity, or core temperature. We conclude that: 1) ALD and AVP increase in a graded manner with hypohydration, and this effect persists during exercise-heat stress; 2) ALD and AVP increases elicited by exercise are greater during high intensity than low intensity exercise; 3) Hypohydration and exercise intensity have additive effects on ALD: and 4) AVP responses are closely coupled to osmolality.

Inspiratory resistance effects on exercise breathing pattern relationships to chemoresponsiveness.

This study examined the effects of added inspiratory resistance (R5 5 cm H2O.L-1.S-1) on the relationship between exercise breathing pattern and resting hypercapnic ventilatory responsiveness (HCVR). Twelve men completed an HCVR test and two progressive intensity exercise tasks with minimal (R0) and elevated (R5) resistance. Peak oxygen uptake, and peak power output were not different, but peak VE was decreased with the R5 load. Exercise ventilation (VE was tightly coupled to VCO2 (r = 0.97) as was mean inspiratory flow rate (VT/TI, r = 0.95), but not duty cycle (TI/TTOT, r = 0.39). With imposition of R5, VT/TI was depressed (p < 0.05) at mild (approximately 40% VO2peak) to peak exercise intensities, whereas TI/TTOT was relatively unaffected. At both moderate (approximately 60% peak VO2) and peak exercise intensities, VE was positively correlated (r = 0.62, p < 0.05 and r = 0.82, p < 0.01, respectively) to subjects' HCVR. However, when normalized, VE.VCO2(-1) was significantly correlated to HCVR only at peak exercise ventilation during the R0 load. Analysis of the exercise breathing pattern revealed that at both moderate and peak exercise intensities, VT/TI was positively correlated to HCVR, but TI/TTOT was not. The imposition of R5 decreased the slope of the relationship between exercise VT/TI and HCVR at both moderate and peak exercise intensities, and weakened the positive correlation at the moderate exercise intensity. Our analysis indicates that: 1) the positive correlation between exercise hyperpnea and HCVR is mediated by the mean inspiratory flow rate rather than the duty cycle component of the breathing pattern and, 2) at moderate exercise the relationship between mean inspiratory flow rate and resting HCVR is more sensitive to added inspiratory resistance than minute ventilation per se. These findings suggest that the degree of influence resting HCVR has on exercise hyperpnea is dependent upon the magnitudes of both the ventilatory hyperpnea and mechanical loading placed on the ventilatory system.

Control of thermoregulatory sweating is altered by hydration level and exercise intensity.

The purpose of this study was to examine the thermoregulatory sweating control parameters of threshold temperature and sensitivity to determine whether 1) these variables were altered by hypohydration level and exercise intensity and 2) these alterations, if present, were additive and independent. Nine heat-acclimated men completed a matrix of nine trials: three exercise intensities of 25, 45, and 65% maximal O2 uptake and three hydration levels, i.e., euhydration and hypohydration (Hy) at 3 and 5% of body weight. During each trial, subjects attempted 50 min of treadmill exercise in a warm room (30 degrees C dry bulb, 50% relative humidity) while esophageal temperature and upper arm sweating rate were continuously measured. Hypohydration was achieved by exercise and fluid restriction the day preceding the trials. The following new findings were made: 1) threshold temperature increased in graded manner with hypohydration level (approximately 0.06 degree C/% Hy); 2) sensitivity decreased in a graded manner with hypohydration level (approximately 0.06 units/%Hy); 3) threshold temperature was not altered by exercise intensity; and 4) sensitivity increased from low- to moderate- and high-intensity exercise. We conclude that both hypohydration level and exercise intensity produce independent effects on control of thermoregulatory sweating.

Metabolic and thermal adaptations from endurance training in hot or cold water.

Metabolic and thermal adaptations resulting from endurance training in hot vs. cold water were compared. It was hypothesized that training in hot water would have greater effects on muscle glycogen use and blood lactate accumulation during exercise than training in cold water. Eighteen men exercised at 60% of maximal oxygen uptake while immersed in hot (n = 9) or cold water (n = 9) for 1 h, 5 days/wk, for 8 wk. Training in hot water (35 degrees C) potentiated body temperature increases during exercise, and training in cold water (20 degrees C) blunted body temperature increases during exercise. Before and after training, cardiorespiratory and thermoregulatory responses and muscle glycogen and blood lactate changes were assessed during a 1-h exercise trial in hot water and, on a separate day using the same intensity, in cold water. Oxygen uptake was similar for all trials, averaging 2.0 +/- 0.1 l/min. It was observed that 1) training reduced glycogen use and lactate accumulation during exercise, with no difference between cold and hot water training groups in the magnitude of this effect; 2) lactate accumulation during exercise was the same in hot water as in cold water; and 3) skin temperature decreased more rapidly during cold-water exercise after than before training, with no difference between cold and hot water training groups in the magnitude of this effect. Thus, exercise-induced body temperature increases are not an important stimulus for glycogen-sparing effects and blunted lactate accumulation associated with endurance training.

Human tolerance to heat strain during exercise: influence of hydration.

This study determined whether 1) exhaustion from heat strain occurs at the same body temperatures during exercise in the heat when subjects are euhydrated as when they are hypohydrated, 2) aerobic fitness influences the body temperature at which exhaustion from heat strain occurs, and 3) curves could be developed to estimate exhaustion rates at a given level of physiological strain. Seventeen heat-acclimated men [maximal oxygen uptake (VO2max) from 45 to 65 ml.kg-1.min-1] attempted two heat stress tests (HSTs): one when euhydrated and one when hypohydrated by 8% of total body water. The HSTs consisted of 180 min of rest and treadmill walking (45% VO2max) in a hot-dry (ambient temperature 49 degrees C, relative humidity 20%) environment. The required evaporative cooling (Ereq) exceeded the maximal evaporative cooling capacity of the environment (Emax); thus thermal equilibrium could not be achieved and 27 of 34 HSTs ended by exhaustion from heat strain. Our findings concerning exhaustion from heat strain are 1) hypohydration reduced the core temperature that could be tolerated; 2) aerobic fitness, per se, did not influence the magnitude of heat strain that could be tolerated; 3) curves can be developed to estimate exhaustion rates for a given level of physiological strain; and 4) exhaustion was rarely associated with a core temperature up to 38 degrees C, and it always occurred before a temperature of 40 degrees C was achieved. These findings are applicable to heat-acclimated individuals performing moderate-intensity exercise under conditions where Ereq approximates or exceeds Emax and who have high skin temperatures.

Human thermoregulatory responses during heat exposure after artificially induced sunburn.

Thermoregulatory responses in the heat (ambient temperature 49 degrees C, 20% relative humidity, 1 m/s wind) were investigated in 10 unacclimated men during 50 min of cycle ergometer exercise (approximately 53% of maximal aerobic power) after a 10-min rest before as well as 24 h and 1 wk after twice the minimal erythemal dose of UV-B radiation that covered approximately 85% of the body surface area. In 7 subjects esophageal temperature (Tes) was recorded while in all 10 subjects five-site skin and rectal temperatures, heart rate, and back, left forearm, and shielded (12 cm2 area) right forearm sweating rates (msw) were recorded at 15-s intervals. Venous blood was collected before and after exercise-heat stress. Mean skin temperature, Tes, rectal temperature, heart rate, and total body sweating rate were not significantly (P greater than 0.05) affected by sunburn. Pre- and postexercise values of hematocrit, hemoglobin, plasma protein, plasma volume, and plasma osmolality were also not affected (P greater than 0.05) by sunburn. Analysis of presunburn and post-sunburn data showed that the Tes intercept for sweating (degrees C) was unaffected (P greater than 0.05), but msw/Tes and final msw from the left forearm (msw/Tes 0.24 +/- 0.02 vs. 0.17 +/- 0.01 mg.cm-2.min-1. degrees C-1, P less than 0.05; msw 0.60 +/- 0.05 vs. 0.37 +/- 0.02, mg.cm-2.min-1, P less than 0.05) and back (msw/Tes 0.43 +/- 0.03 vs. 0.36 +/- 0.01 mg.cm-2.min-1. degrees C-1, P = 0.052; msw 1.08 +/- 0.09 vs. 0.74 +/- 0.05 mg.cm-2.min-1, P less than 0.05) were significantly reduced 24 h postsunburn.(ABSTRACT TRUNCATED AT 250 WORDS)

Human thermoregulatory responses during cold water immersion after artificially induced sunburn.

Thermoregulatory responses during cold-water immersion (water temperature 22 degrees C) were compared in 10 young men before as well as 24 h and 1 wk after twice the minimal erythemal dose of ultraviolet-B radiation that covered approximately 85% of the body surface area. After 10 min of seated rest in cold water, the mean exercised for 50 min on a cycle ergometer (approximately 51% of maximal aerobic power). Rectal temperature, regional and mean heat flow (hc), mean skin temperature from five sites, and hearrt rate were measured continuously for all volunteers while esophageal temperature was measured for six subjects. Venous blood samples were collected before and after cold water immersion. The mean skin temperature was higher (P less than 0.05) throughout the 60-min cold water exposure both 24 h and 1 wk after sunburn compared with before sunburn. Mean hc was higher (P less than 0.05) after 10 min resting immersion and during the first 10 min of exercise when 24 h postsunburn was compared with presunburn, with the difference attributed primarily to higher hc from the back and chest. While rectal temperature and heart rate did not differ between conditions, esophageal temperature before immersion and throughout the 60 min of cold water immersion was higher (P less than 0.05) when 24 h postsunburn was compared with presunburn. Plasma volume increased (P less than 0.05) after 1 wk postsunburn compared with presunburn, whereas plasma protein concentration was reduced (P less than 0.05). After exercise cortisol was greater (P less than 0.05) 24 h postsunburn compared with either presunburn or 1 wk postsunburn.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of pyridostigmine bromide on physiological responses to heat, exercise, and hypohydration.

Five men underwent eight heat stress tests (HSTs) at 35 degrees C, each consisting of four 25-min treadmill walks (35% Vo2max), separated by 5-min rests, in four conditions: 1) 20% relative humidity (rh), subjects euhydrated and drinking ad libitum; 2) 20% rh, euhydrated; 3) 75% rh, euhydrated; and 4) 20% rh, hypohydrated 3% of body weight. In Conditions 2-4 subjects drank during the walks to maintain their pre-HST weight. In each condition we tested subjects once after 30 mg pyridostigmine bromide (PB) by mouth and once after placebo. PB lowered heart rate a mean of 3 beats/min overall, most with hypohydration. PB did not significantly affect rectal temperature (Tre), but reduced the rise in Tre during hypohydrated exercise. In Condition 2, chest skin temperature decreased more during exercise with PB. PB had no significant effect on other skin temperatures, sweating, hematocrit, hemoglobin, total plasma protein, osmolality, ad libitum drinking, rate of O2 uptake, or subject ratings of temperature, discomfort, or exertion. PB thus had little effect on physiological responses to moderate exercise-heat stress.

Hypohydration does not impair skeletal muscle glycogen resynthesis after exercise.

The purpose of this investigation was to examine the effects of moderate hypohydration (HY) on skeletal muscle glycogen resynthesis after exhaustive exercise. On two occasions, eight males completed 2 h of intermittent cycle ergometer exercise (4 bouts of 17 min at 60% and 3 min at 80% of maximal O2 consumption/10 min rest) to reduce muscle glycogen concentrations (control values 711 +/- 41 mumol/g dry wt). During one trial, cycle exercise was followed by several hours of light upper body exercise in the heat without fluid replacement to induce HY (-5% body wt); in the second trial, sufficient water was ingested during the upper body exercise and heat exposure to maintain euhydration (EU). In both trials, 400 g of carbohydrate were ingested at the completion of exercise and followed by 15 h of rest while the desired hydration level was maintained. Muscle biopsy samples were obtained from the vastus lateralis immediately after intermittent cycle exercise (T1) and after 15 h of rest (T2). During the HY trial, the muscle water content was lower (P less than 0.05) at T1 and T2 (288 +/- 9 and 265 +/- 5 ml/100 g dry wt, respectively; NS) than during EU (313 +/- 8 and 301 +/- 4 ml/100 g dry wt, respectively; NS). Muscle glycogen concentration was not significantly different during EU and HY at T1 (200 +/- 35 vs. 251 +/- 50 mumol/g dry wt) or T2 (452 +/- 34 vs. 491 +/- 35 mumol/g dry wt). These data indicate that, despite reduced water content during the first 15 h after heavy exercise, skeletal muscle glycogen resynthesis is not impaired.