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

This study examined the efficacy of glycerol andwater hyperhydration (1 h before exercise) on tolerance andcardiovascular strain during uncompensable exercise-heat stress. Theapproach was to determine whether 1-h preexercise hyperhydration (29.1 ml H₂O/kg lean body mass with orwithout 1.2 g/kg lean body mass of glycerol) provided a physiologicaladvantage over euhydration. Eight heat-acclimated men completed threetrials (control euhydration before exercise, and glycerol and waterhyperhydrations) consisting of treadmill exercise-heat stress (ratio ofevaporative heat loss required to maximal capacity of climate = 416).During exercise (~55% maximalO₂ uptake), there was nodifference between glycerol and water hyperhydration methods forincreasing (P < 0.05) total bodywater. Glycerol hyperhydration endurance time (33.8 ± 3.0 min) waslonger (P < 0.05) than for control(29.5 ± 3.5 min), but was not different(P > 0.05) from that of waterhyperhydration (31.3 ± 3.1 min). Hyperhydration didnot 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 andheart rates in each trial. Symptoms at exhaustion included syncope andataxia, fatigue, dyspnea, and muscle cramps(n = 11, 10, 2, and 1 cases,respectively). We conclude that 1-h preexercise glycerolhyperhydration provides no meaningful physiological advantage overwater hyperhydration and that hyperhydration per se only provides theadvantage (over euhydration) of delaying hypohydration duringuncompensble exercise-heat stress.

     

Hydration effects on physiological strain of horses during exercise-heat stress

This study examined the effects ofhyperhydration, exercise-induced dehydration, and oral fluidreplacement on physiological strain of horses during exercise-heatstress. On three occasions, six horses completed a 90-min exerciseprotocol (50% maximal O₂ uptake,34.5°C, 48% relative humidity) divided into two 45-min periods(exercise I andexercise II) with a 15-min recoverybetween exercise bouts. In random order, horses receivedno fluid (NF), 10 liters of water (W), or a carbohydrate-electrolytesolution (CE) 2 h before exercise and between exercise bouts. Compared with NF, preexercise hyperhydration (W and CE) did not alter heart rate, cardiac output (), stroke volume (SV), corebody temperature, sweating rate (SR), or sweating sensitivity duringexercise I. In contrast, afterexercise II, exercise-induceddehydration in NF (decrease in body mass: NF, 5.6 ± 0.8%; W, 1.1 ± 0.4%; CE, 1.0 ± 0.2%) resulted in greater heat storage,with core body temperature ~1.0°C higher compared with W and CE.In exercise II, the greater thermalstrain in NF was associated with significant(P < 0.05) decreases in (10 ± 2%), SV (9 ± 3%), SR, and sweatingsensitivity. We concluded that 1)preexercise hyperhydration provided no thermoregulatory advantage;2) maintenance of euhydration byoral fluid replacement (~85% of sweat fluid loss) during exercise inthe heat was reflected in higher , SV, and SR withdecreased heat storage; and 3) W oran isotonic CE solution was equally effective in reducing physiological strain associated with exercise-induced dehydration and heat stress.

     

Endocrine responses during exercise-heat stress: effects of prior isotonic and hypotonic intravenous rehydration

Exercise following exercise-induced dehydration (EID) has been shown to elevate concentrations of plasma norepinephrine (NE) and hypothalamic-pituitary-adrenal axis hormones. However, it is not known how intravenous (i.v.) rehydration (Rh) with isotonic (ISO) or hypotonic (HYPO) saline affects these hormone concentrations. It was hypothesized that HYPO, versus ISO, would lead to lower plasma NE and cortisol concentrations ([CORT]) during subsequent exercise following EID due to a decrease in plasma sodium concentration [Na⁺]. Eight non-heat acclimated men completed three experimental treatments (counterbalanced design) immediately following EID (33°C) to −4% body mass loss. The Rh treatments were i.v. 0.9% NaCl (ISO, 25 ml · kg⁻¹), i.v. 0.45% NaCl (HYPO, 25 ml · kg⁻¹), and no fluid (NF). After Rh and rest (2 h total), the subjects walked at 53–54 percent of maximal O₂ uptake for 45 min at 36°C. After Rh, the following observations were made before/during exercise: percentage change in plasma volume (PV) was lower in NF compared to ISO and HYPO but similar between ISO and HYPO; Δ[Na⁺] was similar between ISO and NF and higher in ISO compared to HYPO; Δ plasma NE was higher in NF compared to ISO and HYPO, but similar between ISO and HYPO; Δ plasma [CORT] was higher in NF compared to ISO and HYPO and higher in ISO compared to HYPO; rectal temperature was higher in NF compared to ISO and HYPO. These data would suggest that sympathetic nervous activity and [CORT] during exercise, subsequent to EID and Rh, was affected by lower PV (probably through cardiopulmonary baroreflexes) as well as core temperature. Furthermore, [CORT] was affected by Δ[Na⁺] after Rh through an unknown mechanism. Accepted: 16 July 1997     

Intravenous vs. oral rehydration: effects on subsequent exercise-heat stress

Castellani, John W., Carl M. Maresh, Lawrence E. Armstrong,Robert W. Kenefick, Deborah Riebe, Marcos Echegaray, Douglas Casa, andV. Daniel Castracane. Intravenous vs. oral rehydration: effects onsubsequent exercise-heat stress. J. Appl.Physiol. 82(3): 799-806, 1997.This studycompared the influence of intravenous vs. oral rehydration afterexercise-induced dehydration during a subsequent 90-min exercisebout. It was hypothesized that cardiovascular, thermoregulatory, and hormonal variables would be the same between intravenous and oral rehydration because of similar restoration ofplasma volume (PV) and osmolality (Osmo). Eight non-heat-acclimated menreceived three experimental treatments (counterbalanced design) immediately after exercise-induced dehydration (33°C) to 4%body weight loss. Treatments were intravenous 0.45% NaCl (iv; 25 ml/kg), no fluid (NF), and oral saline (Oral; 25 ml/kg).After rehydration and rest (2 h total), subjects walked at 50% maximalO₂ consumption for up to 90 min at36°C. The following observations were made: 1) heart rate was higher(P < 0.05) in Oral vs. ivat minutes 45, 60, and75 of exercise;2) rectal temperature, sweat rate, percent change in PV, and change in plasma Osmo were similar between ivand Oral; 3) change in plasmanorepinephrine decreased less (P < 0.05) in Oral compared with iv at minute45; 4) changes in plasma adrenocorticotropic hormone and cortisol were similar between ivand Oral after exercise was initiated; and5) exercise time was similar betweeniv (77.4 ± 5.4 min) and Oral (84.2 ± 2.3 min). These datasuggest that after exercise-induced dehydration, iv and Oral wereequally effective as rehydration treatments. Thermoregulation, changein adrenocorticotropic hormone, and change in cortisol were notdifferent between iv and Oral after exercise began; this is likely dueto similar percent change in PV and change in Osmo.

     

Aging and assessment of physiological strain during exercise-heat stress

The purpose of this study was to evaluate the physiological strain index (PSI) for different age groups during exercise-heat stress (EHS). PSI was applied to three different databases. First, from young and middle-age men (21 +/- 2 and 46 +/- 5 yr, respectively) matched (n = 9 each, P > 0.05) for maximal aerobic power. Subjects were heat acclimated by daily treadmill walking for two 50-min bouts separated by 10-min rest for 10 days in a hot-dry environment [49 degrees C, 20% relative humidity (RH)]. The second database involved a group (n = 8) of young (YA) and a group (n = 7) of older (OA) men (26 +/- 1 and 69 +/- 1 yr, respectively) who underwent 16 wk of aerobic training and two control groups (n = 7 each) who were matched for age to YA and OA. These four groups performed EHS at 36 degrees C, 40% RH on a cycle ergometer for 60 min at 60% maximal aerobic power before and after training. The third database was obtained from three groups of postmenopausal women and a group of 10 men. Two groups of women (n = 8 each) were undergoing hormone replacement therapy, estrogen or estrogen plus progesterone, and the third group (n = 9) received no hormone replacement. Subjects were over 50 yr and performed the same EHS: exercising at 36 degrees C, 40% RH on a cycle ergometer for 60 min. PSI assessed the strain for all three databases and reported differences were significant at P < 0.05. This index rated the strain in rank order, whereas the postacclimation and posttraining groups were assessed as having less strain than the preacclimation and pretraining groups. Furthermore, middle-aged women on estrogen replacement therapy had less strain than estrogen + progesterone and no hormone therapy. PSI evaluation was extended for men and women of different ages (50-70 yr) during acute EHS, heat acclimation, after aerobic training, and inclusive of women undergoing hormone replacement therapy.     

Plasma hormonal responses at graded hypohydration levels during exercise-heat stress

The effects of graded levels of hypohydration (3, 5, and 7% of body weight) on hormonal responses to exercise in the heat were examined in six heat-acclimated male volunteers. On the day following dehydration, subjects performed light (approximately 25% maximal O2 consumption, 1.03 1 X min-1) exercise in a hot (49 degrees C, 20% relative humidity) environment for four consecutive 25-min intervals interspaced by 10-min rests; blood was obtained before exercise and at approximately 10 min before completion of each exercise period. During euhydration, plasma cortisol (PC) levels manifested significant decrements over time (e.g., time 0, 14.2 micrograms X 100 ml-1 vs. time 2, 8.9 micrograms X 100 ml-1), probably related to its diurnal periodicity. However, during hypohydration, levels of PC were increased and correlated with hypohydration intensity (e.g., time 0, 0, 3, 5, and 7% hypohydration, 14.2, 16.5, 19.8, and 36.2 micrograms X 100 ml-1, respectively). Plasma renin activity (PRA) was increased significantly by hypohydration (e.g., time 0, euhydrated vs. 3%, 3.7 vs. 6.2 units) but was unaffected by exercise in the heat. Plasma aldosterone (ALD) levels were generally increased by exercise in the heat (e.g., time 0 vs. time 4, 3% hypohydration, 12.1 vs. 18.7 ng X 100 ml-1). Regression analysis illustrated that graded intensities of hypohydration were correlated with incremented PRA and ALD through 5% hypohydration. Conversely, PC was incrementally elevated through 7% hypohydration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of polycythemia on blood volume and thermoregulation during exercise-heat stress

We studied the effects of autologous erythrocyte infusion on blood volume and thermoregulation during exercise in the heat. By use of a double-blind design, nine unacclimated male subjects were infused with either 600 ml of a NaCl-glucose-phosphate solution containing a approximately 50% hematocrit (n = 6, reinfusion) or 600 ml of this solution only (n = 3, saline). A heat stress test (HST) was attempted approximately 2-wk pre- and 48-h postinfusion during the late spring months. After 30 min of rest in a 20 degrees C antechamber, the HST consisted of a 120-min exposure (2 repeats of 15 min rest and 45 min treadmill walking) in a hot (35 degrees C, 45% rh) environment while euhydrated. Erythrocyte volume (RCV, 51Cr) and plasma volume (PV, 125I) were measured 24 h before each HST, and maximal O2 uptake (VO2max) was measured 24 h after each HST. Generally, no significant effects were found for the saline group. For the reinfusion group, RCV (11%, P less than 0.01) and VO2max (11%, P less than 0.05) increased after infusion, and the following observations were made: 1) the increased RCV was associated with a reduction in PV to maintain the same blood volume as during the preinfusion measurements; 2) polycythemia reduced total circulating protein but did not alter F-cell ratio, plasma osmolality, plasma protein content, or plasma lactate at rest or during exercise-heat stress; 3) polycythemia did not change the volume of fluid entering the intravascular space from rest to exercise-heat stress; and 4) polycythemia tended to reduce the rate of heat storage during exercise-heat stress.     

Physiological consequences of intermittent exercise during compensable and uncompensable heat stress.

Time-weighted averaging is a traditional method used in heat stress analyses to approximate, in terms of a single continuous level of heat production, the rate of heat production from complex intermittent exercise patterns. Physiological responses during intermittent and continuous exercise were studied in four subjects exposed to heat stress in which evaporation was either free or severely restricted. Intermittent work consisted of repeated 10-min exercise-rest patterns. Continuous work was at the time-weighted average of intermittent exercise: 3.3 mets. When heat stress was uncompensable, intermittent work induced more physiological strain than continuous work: endurance time was 14 min less (P less than 0.05); core temperature at 60 min was 0.40 degrees C higher (P less than 0.05); and, after 30 min of exposure, the rate of core temperature rise was 33% greater. The difference in the rate of heat storage was not satisfactorily explained by a discrepancy in the average rate of heat production or in the calculated rate of surface heat loss. Alternatively, the results may be partially explained by interruptions in the usual rate of heat transport via the cutaneous circulation. These interruptions may be caused by nonthermal factors associated with postural and work load transitions. Although the mechanisms are not totally understood, it is clear that application of the time-weighted averaging method can lead to erroneous overprediction of endurance time and should be applied with discretion.     

Varied and repeated atropine dosages and exercise-heat stress

Comparisons of physiological responses to 0, 0.5, 1, and 2 mg atropine (IM) were made in seven males (X +/- SD: age, 24 +/- 3 years; ht, 174 +/- 12 cm; wt, 76 +/- 3 kg) while they exercised (approximately 390 W) in a hot-dry (40 degrees C, 20% rh) environment. Responses to 4 mg, as well as repeatability of responses to 2 mg, were studied in two and six of these subjects, respectively. On 8 test days an intramuscular injection of atropine or saline control was administered 20 min before subjects walked on a treadmill for two 50-min bouts. Heart rate (HR) during exercise did not change in the control trial but by min 50 increased during all atropine trials (P less than 0.01). Rectal temperature (Tre) increased (P less than 0.01) in all trials by min 50 and continued increasing (P less than 0.01) in the 2-mg trial during the second exercise bout. For the two subjects tested with all dosages (0.5 - 4 mg atropine), the change in HR and Tre between the atropine and control trials at 50 min of exercise was regressed against the various atropine dosages. The relationship (r = 0.92) for HR was curvilinear while the relationship (r = 0.99) for Tre was linear. Mean weighted skin temperature (Tsk) was relatively constant during exercise and was warmer (P less than 0.05) with increasing atropine dosage. In a repeat 2 mg trial, HR was 6 bt . min-1 lower (P less than 0.05) on the second exposure but Tre was the same (P greater than 0.05) on both days. For subjects walking in the heat, three new observations were: 1) 0.5 mg of atropine resulted in increased HR and Tsk compared to control values; 2) HR was elevated but the magnitude of change decreased with increasing dosage, while the elevation in Tre was consistent with increasing dosage; and 3) rectal temperatures (in trials with and without atropine) were unaffected by previous days of atropine administration.     

Monte Carlo simulations of individual variability and their effects on simulated heat stress using thermoregulatory modeling

This paper addresses a variable-dependence (VD) MC method developed based on a previous attempt (VI-MC method) (J. Therm. Biol. 29 (2004), 515) to be incorporated in a thermoregulatory model. Simulated individuals with anthropometrics by VI- and VD-MC methods for US Army population were compared using principal component analysis and Fisher's exact tests. The results indicated that VD-MC data represented overall body size as the primary component and body shape as the secondary component that were more realistic and similar to the measured US Army data (p>0.05) rather than VI-MC data (p<0.05). Such differences consequently affected individual thermoregulatory responses to simulated heat stress. The VD-MC method provides a more realistic representation of individual variability and thus underpins more realistic predictions of individual thermoregulatory responses.     

Heat stress induces a biphasic thermoregulatory response in mice

Previous animal models of heat stress have been compromised by methodologies, such as restraint and anesthesia, that have confounded our understanding of the core temperature (T(c)) responses elicited by heat stress. Using biotelemetry, we developed a heat stress model to examine T(c) responses in conscious, unrestrained C57BL/6J male mice. Before heat stress, mice were acclimated for >4 wk to an ambient temperature (T(a)) of 25 degrees C. Mice were exposed to T(a) of 39.5 +/- 0.2 degrees C, in the absence of food and water, until they reached maximum T(c) of 42.4 (n = 11), 42.7 (n = 12), or 43.0 degrees C (n = 11), defined as mild, moderate, and extreme heat stress, respectively. Heat stress induced an approximately 13% body weight loss that did not differ by final group T(c); however, survival rate was affected by final T(c) (100% at 42.4 degrees C, 92% at 42.7 degrees C, and 46% at 43 degrees C). Hypothermia (T(c) < 34.5 degrees C) developed after heat stress, with the depth and duration of hypothermia significantly enhanced in the moderate and extreme compared with the mild group. Regardless of heat stress severity, every mouse that transitioned out of hypothermia (survivors only) developed a virtually identical elevation in T(c) the next day, but not night, compared with nonheated controls. To test the effect of the recovery T(a), a group of mice (n = 5) were acclimated for >4 wk and recovered at T(a) of 30 degrees C after moderate heat stress. Recovery at 30 degrees C resulted in 0% survival within approximately 2 h after cessation of heat stress. Using biotelemetry to monitor T(c) in the unrestrained mouse, we show that recovery from acute heat stress is associated with prolonged hypothermia followed by an elevation in daytime T(c) that is dependent on T(a). These thermoregulatory responses to heat stress are key biomarkers that may provide insight into heat stroke pathophysiology.     

Human thermoregulatory responses during serial cold-water immersions

This studyexamined whether serial cold-water immersions over a 10-h period wouldlead to fatigue of shivering and vasoconstriction. Eight men wereimmersed (2 h) in 20°C water three times (0700, 1100, and 1500) in1 day (Repeat). This trial was compared with single immersions(Control) conducted at the same times of day. Before Repeat exposuresat 1100 and 1500, rewarming was employed to standardize initial rectaltemperature. The following observations were made in the Repeatrelative to the Control trial: 1)rectal temperature was lower and heat debt was higher(P < 0.05) at 1100; 2) metabolic heat production waslower (P < 0.05) at 1100 and 1500;3) subjects perceived the Repeattrial as warmer at 1100. These data suggest that repeated coldexposures may impair the ability to maintain normal body temperaturebecause of a blunting of metabolic heat production, perhaps reflectinga fatigue mechanism. An alternative explanation is that shiveringhabituation develops rapidly during serially repeated cold exposures.

     

Hyperhydration induced by glycerol ingestion: hormonal and renal responses

The simultaneous time courses of hydromineral hormones (renin-aldosterone system, arginine vasopressin, and atrial natriuretic peptide) and renal responses were examined during and after the completion of hyperhydration induced by glycerol and fluid ingestion. Eight healthy young male Caucasian subjects participated in two separate trials, each including three consecutive phases in a thermoneutral environment. Phases 1 and 3 involved a 90-min period at rest, while phase 2 involved a 120-min period at rest designed to provide either (i) euhydration (control trial) or (ii) hyperhydration induced by ingestion of glycerol (1.1 g/kg body mass) and fluid (21.4 mL/kg body mass). During the 2-h time period of glycerol and fluid ingestion, urine flow, urine osmolality, and plasma levels of hydromineral hormones remained at basal values. In contrast, after hyperhydration completion during phase 3, the diuresis increased markedly together with a dilution of the urine (p < 0.05) while hormonal responses did not change. These results indicate significant differences in renal responses during and after hyperhydration completion and suggest that these changes are independent of fluid-regulating hormonal responses.     

Impaired thermoregulatory ability of oxytocin-deficient mice during cold-exposure

We analyzed temperature homeostasis in oxytocin-deficient (Oxt(-/-)) mice and found that Oxt(-/-) mice exhibited lower body temperatures than wild-type animals when they were exposed to cold. Oxt(-/-) mice also showed slightly more weight gain, but there were no obvious differences in the morphology of white and brown adipose tissues as between wild-type and Oxt(-/-) mice. In cold-exposed conditions, oxytocin neurons containing c-Fos immunoreactivity existed in the paraventricular nucleus of the hypothalamus. These results suggest that the central oxytocin neurons constitute part of the thermoregulatory system involved in maintaining body temperature in cold environments.     

Age-related thermoregulatory differences during core cooling in humans

The current study assessed sympathetic neuronal and vasomotor responses, total body oxygen consumption, and sensory thermal perception to identify thermoregulatory differences in younger and older human subjects during core cooling. Cold fluid (40 ml/kg, 4 degrees C) was given intravenously over 30 min to decrease core temperature (Tc) in eight younger (age 18-23) and eight older (age 55-71) individuals. Compared with younger subjects, the older subjects had significantly lower Tc thresholds for vasoconstriction (35.5 +/- 0.3 vs. 36.2 +/- 0.2 degrees C, P = 0.03), heat production (35.2 +/- 0.4 vs. 35.9 +/- 0.1 degrees C, P = 0.04), and plasma norepinephrine (NE) responses (35.0 vs. 36.0 degrees C, P < 0.05). Despite a lower Tc nadir during cooling, the maximum intensities of the vasoconstriction (P = 0.03) and heat production (P = 0.006) responses were less in the older compared with the younger subjects, whereas subjective thermal comfort scores were similar. Plasma NE concentrations increased fourfold in the younger but only twofold in the older subjects at maximal Tc cooling. The vasomotor response for a given change in plasma NE concentration was decreased in the older group (P = 0.01). In summary, aging is associated with 1) a decreased Tc threshold and maximum response intensity for vasoconstriction, total body oxygen consumption, and NE release, 2) decreased vasomotor responsiveness to NE, and 3) decreased subjective sensory thermal perception.     

Oxidative stress and its effects during dehydration

Water is usually thought to be required for the living state, but several organisms are capable of surviving complete dehydration (anhydrobiotes). Elucidation of the mechanisms of tolerance against dehydration may lead to development of new methods for preserving biological materials that do not normally support drying, which is of enormous practical importance in industry, in clinical medicine as well as in agriculture. One of the molecular mechanisms of damage leading to death in desiccation-sensitive cells upon drying is free-radical attack to phospholipids, DNA and proteins. This review aims to summarize the strategies used by anhydrobiotes to cope with the danger of oxygen toxicity and to present our recent results about the importance of some antioxidant defense systems in the dehydration tolerance of Saccharomyces cerevisiae, a usual model in the study of stress response.     

Distinctive stress effects on learning during puberty

Puberty is a time of significant change in preparation for adulthood. Here, we examined how stressful experience affects cognitive and related hormonal responses in male and female rats prior to, during and after puberty. Groups were exposed to an acute stressor of brief periodic tailshocks and tested 24 h later in an associative memory task of trace eyeblink conditioning. Exposure to the stressor did not alter conditioning in males or females prior to puberty but enhanced conditioning in both males and females during puberty. The enhancement occurred in pubescent females irrespective of the estrous cycle. In adulthood, sex differences in trace conditioning and the response to stress emerged: females outperformed males under unstressed conditions, but after stressor exposure, trace conditioning in females was impaired whereas that in males was enhanced. These differences were not related to changes in gross motor activity or other nonspecific measures of performance. The effects of acute stress on corticosterone, estradiol, progesterone, and testosterone were also measured. Stressor exposure increased the concentration of corticosterone in all age groups, although sex differences were only evident in adults. All reproductive hormones except estradiol increased with age in a predictable and sex dependent fashion and none were affected by stressor exposure. Estradiol decreased in male rats across age, and remained stable for female rats. Together, these data indicate that males and female respond similarly to learning opportunities and stressful experience before and during puberty; it is in adulthood that sex differences and the opposite responses to stress arise.     

Reduced tolerance to morphine thermoregulatory effects in senescent rats

Age-related differences in the thermoregulatory response to morphine have been shown in rats. To determine if these age-related differences would be reflected in the acquisition of tolerance, we studied morphine tolerance induced by either a single morphine dose or implantation of a morphine pellet. precipitated withdrawal was also analyzed by inducing withdrawal with naloxone in morphine-pelleted rats. Senescent (26 or 27 month old), mature (10 or 11 month old) and young (3 or 4 month old) male Fischer 344 rats were restrained and changes in rectal temperature were monitored for six hours after morphine administration. Only mature and young rats exhibited increased hyperthermic responses to a second low dose of morphine (5 mg/kg s.c.). Only young rats became tolerant after a single higher morphine dose (25 mg/kg s.c.). All age groups showed tolerance three days after morphine pellet implantation. Hypothermia was equivalent in all age groups when withdrawal was induced by naloxone in morphine-pelleted rats. These results indicate that older rats were more resistant to the acquisition of tolerance to the thermic effects of morphine; however; with continued morphine treatment, rats became tolerant regardless of age.     

Gastric emptying during exercise: effects of heat stress and hypohydration

To determine the effects of acute heat stress, heat acclimation and hypohydration on the gastric emptying rate of water (W) during treadmill exercise, ten physically fit men ingested 400 ml of W before each of three 15 min bouts of exercise (treadmill, approximately 50% VO2max) on five separate occasions. Stomach contents were aspirated after each exercise bout. Before heat acclimation (ACC), experiments were performed in a neutral (18 degrees C), hot (49 degrees C) and warm (35 degrees C) environment. Subjects were euhydrated for all experiments before ACC. After ACC, the subjects completed two more experiments in the warm (35 degrees C) environment; one while euhydrated and a final one while hypohydrated (-5% of body weight). The volume of ingested water emptied into the intestines at the completion of each exercise bout was inversely correlated (P less than 0.01) with the rectal temperature (r = -0.76). The following new observations were made: 1) exercise in a hot (49 degrees C) environment impairs gastric emptying rate as compared with a neutral (18 degrees C) environment, 2) exercise in a warm (35 degrees C) environment does not significantly reduce gastric emptying before or after heat acclimation, but 3) exercise in a warm environment (35 degrees C) when hypohydrated reduces gastric emptying rate and stomach secretions. Reductions in gastric emptying appear to be related to the severity of the thermal strain induced by an exercise/heat stress.