Advantages of a smaller bodymass in humans when distance-running in warm, humid conditions

Using a 65-kg athlete running a 2 h 10 min marathon as an example, we estimated that imbalances between approximately 1400 W of heat production and dissipation would occur in ambient temperatures of 17 degrees C at 90% relative humidity (rh) to 37 degrees C at 50% rh. Because heat production during running depends on body mass and heat loss depends on surface area, intercepts between predicted heat production and maximal heat loss with increasing speeds depend on an athlete's body mass. At 35 degrees C and 60% rh, a 45-kg athlete could maintain thermal balance by running a 2 h 13 min marathon at 19.1 km x h(-1) but a 75-kg athlete would only be able run a 3 h 28 min marathon at 12.2 km x h(-1). In both cases, the production of 970-1020 W of heat would necessitate the evaporation of at least 1.5-1.6 l of sweat per hour. A lower metabolic heat production in lighter runners at any given speed may be one reason why smallness of stature is an asset in distance running.     

Individualized model of human thermoregulation for the simulation of heat stress response.

A population-based dynamic model of human thermoregulation was expanded with control equations incorporating the individual person's characteristics (body surface area, mass, fat%, maximal O(2) uptake, acclimation). These affect both the passive (heat capacity, insulation) and active systems (sweating and skin blood flow function). Model parameters were estimated from literature data. Other data, collected for the study of individual differences (working at relative or absolute workloads in hot-dry [45 degrees C, 20% relative humidity (rh)], warm-humid [35 degrees C, 80% rh], and cool [21 degrees C, 50% rh] environments), were used for validation. The individualized model provides an improved prediction [mean core temperature error, -0.21 --> -0.07 degrees C (P < 0.001); mean squared error, 0.40 --> 0.16 degrees C, (P < 0.001)]. The magnitude of improvement varies substantially with the climate and work type. Relative to an empirical multiple-regression model derived from these specific data sets, the analytical simulation model has between 54 and 89% of its predictive power, except for the cool climate, in which this ratio is zero. In conclusion, individualization of the model allows improved prediction of heat strain, although a substantial error remains.     

Hypohydration and exercise: effects of heat acclimation, gender, and environment

This study examined the effects of heat acclimation and subject gender on treadmill exercise in comfortable (20 degrees C, 40% rh), hot-dry (49 degrees C, 20% rh), and hot-wet (35 degrees C, 79% rh) environments while subjects were hypo- or euhydrated. Six male and six female subjects, matched for maximal aerobic power and percent body fat, completed two exercise tests in each environment both before and after a 10-day heat acclimation program. One exercise test was completed during euhydration and one during hypohydration (-5.0% from baseline body weight). In general, no significant (P greater than 0.05) differences were noted between men and women at the completion of exercise for rectal temperature (Tre), mean skin temperature (Tsk), or heat rate (HR) during any of the experimental conditions. Hypohydration generally increased Tre and HR values and decreased sweat rate values while not altering Tsk values. In the hypohydration experiments, heat acclimation significantly reduced Tre (0.19 degrees C) and HR (13 beats X min-1) values in the comfortable environment, but only HR values were reduced in hot-dry (21 beats X min-1) and hot-wet (21 beats X min-1) environments. The present findings indicated that men and women respond in a physiologically similar manner to hypohydration during exercise. They also indicated that for hypohydrated subjects heat acclimation decreased thermoregulatory and cardiovascular strain in a comfortable environment, but only cardiovascular strain decreased in hot environments.     

Control of sweating during the human menstrual cycle

Thermoregulatory responses were studied in seven women during two separate experimental protocols in the follicular (F, days 4-7) phase and during the luteal (L, days 19-22) phase of the menstrual cycle. Continuous measurements of esophageal temperature (Tes), mean skin temperature (Tsk), oxygen uptake and forearm sweating (ms) were made during all experiments. Protocol I involved both passive heat exposure (3 h) and cycle exercise at approximately 80% VO2 peak during which the environmental chamber was controlled at Ta = 50.0 degrees C, rh = 14% (Pw = 1.7 kPa). In protocol II subjects were tested during thirty-five minutes of exercise at approximately 85% VO2 peak at Ta = 35 degrees C and rh = 25% (Pw = 1.4 kPa). The normal L increase in resting Tes (approximately 0.3 degrees C) occurred in all seven subjects. Tsk was higher during L than F in all experiments conducted at 50 degrees C. During exercise and passive heat exposure, the Tes threshold for sweating was higher in L, with no change in the thermosensitivity (slope) of ms to Tes between menstrual cycle phases. This rightward or upward shift in Tes threshold for initiation of sweating averaged 0.5 degrees C for all experiments. The data indicate the luteal phase modulation in the control of sweating in healthy women is also apparent during severe exercise and/or heat stress.     

Effects of exercise detraining and deacclimation to the heat on plasma volume dynamics

The effects of the discontinuation (DET) of an endurance training/heat acclimation (T/A) program on vascular volumes were studied in 16 adult males. Resting and exercise blood volume dynamics were examined prior to and during an exercise task performed after completion of T/A (CT1) and again at the end of DET (CT2). T/A consisted of cycling at 60% of peak VO2 for 90 min per day, 6 days per week, for 4 weeks. Ambient temperature was 20 degrees C for the first 3 weeks and 40 degrees C for the last week (rh = 30-35%). Subjects were randomly assigned to one of the following DET conditions: 1) cycling one day per week at 40 degrees C, 2) cycling one day per week at 20 degrees C, 3) resting one day per week at 40 degrees C, 4) control. The exercise tasks consisted of 60 min of continuous cycle ergometer exercise at 50% of peak VO2 (Ta = 30 degrees C, rh = 35%). Although significant differences were found between CT1 and CT2, there were no interactions between the various DET conditions. Resting red cell volume decreased 98 ml and plasma volume decreased 248 ml following DET. A reduction in plasma protein content accounted for 97% of the decrease in plasma volume. Hemoconcentration occurred during exercise in both CT1 and CT2, while there were slight increases in plasma [Na+] and [Cl-] and a rapid rise in [K+]. It appears that a single exercise and/or heat exposure per week was not different from complete cessation of endurance exercise in the heat with regard to maintenance of the various vascular volumes.     

Control of local heat gain by vasomotor response of the hand

Finger blood flow (BF) was measured by venous occlusion plethysmography using mercury-in-Silastic strain gauges during immersion of one hand in hot water (raised by steps of 2 degrees C every 10 min from 35 to 43 degrees C), the other being a control (kept immersed in water at 35 degrees C). The measurements were made in three different thermal states on separate days: 1) cool-25 degrees C, 40% rh, esophageal temperature (Tes) = 36.64 +/- 0.10 degrees C; 2) warm-35 degrees C, 40% rh, Tes = 36.71 +/- 0.11 degrees C; and 3) hot-35 degrees C, 80% rh with the legs immersed in water at 42 degrees C, Tes = 37.26 +/- 0.11 degrees C. When water temperature was raised at 42 degrees C, Tes = 37.26 +/- 0.11 When water temperature was raised to 39-41 degrees C in the warm state, finger BF in the hand heated locally (BFw) decreased. When water temperature was raised to 43 degrees C, however, BFw returned to the control value. In the hot state, Tes rose steadily, reaching 37.90 +/- 0.12 degrees C at the end of the 50-min sessions. BF in the control finger also increased gradually during the session. BFw showed a tendency to decrease when water temperature was raised to 39 degrees C, but the change was not greater than that observed in the warm state. In the cool state, no such reduction in BFw was observed when water temperature was raised to 39-41 degrees C. On the contrary, BFw increased at water temperatures of 41-43 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inverse response of leukocyte heat shock proteins and DNA damage to exercise and heat

Elevated ambient temperature may exert an additional impact on the exercise-induced expression of heat shock proteins (HSP) and DNA damage in leukocytes. The protective functions of HSP include antioxidative and antiapoptotic effects and may prevent damage to DNA. Twelve athletes completed a continuous run (75% VO2max) on the treadmill, six at 28 degrees C and six at 18 degrees C room temperature. Leukocyte expression of HSP27 and inducible HSP70 was analyzed on mRNA- (RT-PCR) and protein-level (flow cytometry), while DNA damage was quantified by the comet assay. High ambient temperature induced an additional accumulation of HSP-mRNA and -protein in leukocytes compared with the exercise-induced expression at 18 degrees C. HSP27 showed a special heat sensitivity. Surprisingly, the increase of DNA damage was less pronounced after exercise at 28 degrees C compared to 18 degrees C although heat shock in vitro clearly induced DNA damage. The inverse relation between HSP and DNA damage may indicate functions of HSP which protect against exercise-induced DNA-damage in terms of thermotolerance or apoptosis.     

Untrained females: effects of submaximal exercise and heat on body fluids.

Five untrained females having no history of heat exposure worked in a cool (16-20 degrees C db, 28% rh) environment on day 1 and a warm environment on day 2 (45 degrees C db, 28% rh). Exercise level (bicycle ergometer) was 30% of individual Vo2 max values and work time on both days was 45 min. Venous blood samples were obtained at rest, after 40 min of exercise and 25 min after exercise ceased. Analysis of blood samples indicated an 8.3% increase in Hct during exercise on day 1 and a plasma volume reduction of 12.8% though total circulating protein increased 11.5%. Except for K+ all parameters approximated control values within 25 min postexercise. On day 2, exercise in heat caused a 12% increase in Hct and a plasma volume reduction of 17.7%. Mean total protein did not significantly change from resting values. These data indicated that for a given % Vo2 max, untrained females suffer considerably greater reductions in plasma volumes than do exercised males. Similar to males, dilatation of the cutaneous vascular bed in unacclimatized females resulted in loss of protein from the vascular volume.     

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.     

Effect of autonomic blockade on tracheobronchial blood flow

Tracheobronchial blood flow increases two to five times in response to cold and warm dry air hyperventilation in anesthetized tracheostomized dogs. In this series of experiments we have attempted to attenuate this increase by blockade of the autonomic nervous system. Four groups of anesthetized, tracheostomized, open-chest dogs were studied. Group 1 (n = 5) were hyperventilated for 30 min with 1) warm humid [approximately 26 degrees C, 100% relative humidity, (rh)] air followed by bilateral vagotomy, 2) warm humid air, 3) cold (-22 degrees C, 0% rh) dry air, and 4) warm humid air. Groups 2, 3, and 4 (n = 3/group) were hyperventilated for 30 min with 1) warm humid (approximately 41 degrees C, 100% rh) air, 2) warm dry (approximately 41 degrees C) air, 3) warm humid air, and 4) warm dry air. Group 2 were controls. Group 3 were given phentolamine, 0.6 mg/kg intravenously, as an alpha-blockade, and group 4 were given propranolol, 1 mg/kg, as a beta-blockade after warm dry air hyperventilation (period 2). Five minutes before the end of each 30-min period of hyperventilation, measurements of vascular pressures, cardiac output, arterial blood gases, and inspired, body, and tracheal temperatures were measured, and differently labeled radioactive microspheres were injected into the left atrium to make separate measurements of airway blood flow. After the last measurements had been made animals were killed and their lungs were excised. Blood flow to the airways and lung parenchyma was calculated.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of two cooling strategies on thermoregulatory responses of tetraplegic athletes during repeated intermittent exercise in the heat.

Athletes with spinal cord injury (SCI), and in particular tetraplegia, have an increased risk of heat strain and consequently heat illness relative to able-bodied individuals. Strategies that reduce the heat strain during exercise in a hot environment may reduce the risk of heat illness. To test the hypotheses that precooling or cooling during intermittent sprint exercise in a heated environment would attenuate the rise in core temperature in tetraplegic athletes, eight male subjects with SCI (lesions C(5)-C(7); 2 incomplete lesions) undertook four heat stress trials (32.0 +/- 0.1 degrees C, 50 +/- 0.1% relative humidity). After assessment of baseline thermoregulatory responses at rest for 80 min, subjects performed three intermittent sprint protocols for 28 min. All trials were undertaken on an arm crank ergometer and involved a no-cooling control (Con), 20 min of precooling (Pre), or cooling during exercise (Dur). Trials were administered in a randomized order. After the intermittent sprint protocols, mean core temperature was higher during Con (37.3 +/- 0.3 degrees C) compared with Pre and Dur (36.5 +/- 0.6 degrees C and 37.0 +/- 0.5 degrees C, respectively; P < 0.01). Moreover, perceived exertion was lower during Pre (13 +/- 2; P < 0.01) and Dur (12 +/- 1; P < 0.01) compared with Con (14 +/- 2). These results suggest that both precooling and cooling during intermittent sprint exercise in the heat reduces thermal strain in tetraplegic athletes. The cooling strategies also appear to show reduced perceived exertion at equivalent time points, which may translate into improved functional capacity.     

Thermoregulation during exercise in relation to sex and age

The thermoregulatory responses to 1 h exercise of 14 male (age range 18--65 year) and 7 female (age range 18--46 year) athletes and 4 (3 male and 1 female) non-athletic subjects have been investigated in a moderate environment (Tdb = 21 degrees C, Twb = 15 degrees C and rh less than 50%) and analysed in relation to age, sex, and maximum aerobic power output (VO2max). The maximal sweat loss (Msw max) under the given conditions was closely related (r = + 0.90) to VO2max and for a given relative work load (%VO2max), rectal (Tre) and mean skin (Tsk) temperatures was the same in all subjects. Sweat loss (Msw) was linearly related to total heat production (H) and to peripheral tissue heat conductance (K) and if expressed in relative terms (%Mswmax) was linearly related to Tre. For a given Tre relative sweat rate was identical in the groups studied. From these results it would seem that during exercise Tre rises to meet the requirements of heat dissipation by establishing a thermal gradient from core to skin and stimulating sweating in proportion to maximal capacity of the system. Thus provided the thermal responses to work were standardised using the appropriate physiological variables, there was no evidence to be found for differences in thermoregulatory function which could be ascribed to sex or age.     

Thermoregulation and heat balance in the dik-dik antelope (Rhynchotragus kirki): a field and laboratory study

Experiments were conducted in the field to study the physiological responses of dik-dik antelope to direct solar radiation and shade. The results were compared to those obtained in the laboratory. The rates of metabolic heat production when the animals were exposed either to the sun or the shade were identical. Dik-dik antelopes lost about 50% more heat evaporatively when exposed to the sun compared to the shade at an ambient temperature (Ta) of 28 degrees C or a Ta of 40 degrees C in a climatic chamber. Heat storage in the laboratory at Ta 40 degrees C or at Ta 28 degrees C in the shade accounted for between 30 and 35% of the total heat production. The corresponding value in the sun was 55%. The net rate of heat gain under the sun was four times greater than under shade at 28 degrees C or in the laboratory at 40 degrees C. Behavioural mechanisms for avoidance of high insolation must constitute important adaptations that the dik-dik uses to avoid dehydration and dependence on drinking water in their natural environment.     

Role of osmolality and plasma volume during rehydration in humans

To determine how the sodium content of ingested fluids affects drinking and the restoration of the body fluid compartments after dehydration, we studied six subjects during 4 h of recovery from 90-110 min of a heat [36 degrees C, less than 30% relative humidity (rh)] and exercise (40% maximal aerobic power) exposure, which caused body weight to decrease by 2.3%. During the 1st h, subjects rested seated without any fluids in a thermoneutral environment (28 degrees C, less than 30% rh) to allow the body fluid compartments to stabilize. Over the next 3 h, subjects rehydrated ad libitum using tap water and capsules containing either placebo (H2O-R) or 0.45 g NaCl (Na-R) per 100 ml water. During the 3-h rehydration period, subjects restored 68% of the lost water during H2O-R, whereas they restored 82% during Na-R (P less than 0.05). Urine volume was greater in H2O-R than in Na-R; thus only 51% of the lost water was retained during H2O-R, whereas 71% was retained during Na-R (P less than 0.05). Plasma osmolality was elevated throughout the rehydration period in Na-R, whereas it returned to the control level by 30 min in H2O-R (P less than 0.05). Changes in free water clearance followed changes in plasma osmolality. The restoration of plasma volume during Na-R was 174% of that lost. During H2O-R it was 78%, which seemed to be sufficient to diminish volume-dependent dipsogenic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of hypercapnia on thermoregulation at high ambient temperature

The reported investigations were carried out on rabbits exposed for three hours to ambient temperature of 25 degrees C or 35 degrees breathing athmospheric air (controls) or gas mixtures containing 4% or 7% of CO2. During the exposure to 35 degrees C in rabbits breathing the gas mixture with 7% of CO2 the rise of rectal temperature was significantly greater, heat elimination from the auricular surface was increased, whereas the oxygen uptake was increased insignificantly. In tracheostomized rabbits breathing the gas mixture with 7% of CO2 at 32 degrees C the respiratory rate decreased but the respiration volume increased as compared with the animals breathing atmospheric air. It seems that the hyperthermic effect of hypercapnia demonstrated in this work can be attributed to the impairment of heat elimination through the upper airways due to an inhibition of thermal panting.     

Suramin affects capsaicin responses and capsaicin-noxious heat interactions in rat dorsal root ganglia neurones

The effect of suramin, an inhibitor of G protein regulated signalling, was studied on the membrane currents induced by noxious heat and by capsaicin in cultured dorsal root ganglia neurones isolated from neonatal rats. Whole-cell responses induced by a heat ramp (24-52 degrees C) were little affected by suramin. The noxious heat-activated currents were synergistically facilitated in the presence of 0.3 microM capsaicin 13.2-fold and 6.3-fold at 40 degrees C and 50 degrees C, respectively. In 65% of neurones, the capsaicin-induced facilitation was inhibited by 10 microM suramin to 35 +/- 6% and 53 +/- 6% of control at 40 degrees C and 50 degrees C (S.E.M., n = 15). Suramin 30 microM caused a significant increase in the membrane current produced by a nearly maximal dose (1 microM) of capsaicin over the whole recorded temperature range (2.4-fold at 25 degrees C and 1.2-fold at 48 degrees C). The results demonstrate that suramin differentially affects the interaction between capsaicin and noxious heat in DRG neurones and thus suggest that distinct transduction pathways may participate in vanilloid receptor activation mechanisms.     

Genetic variation in fertility of heat-stressed male mice

The damaging effects of heat stress on male fertility are evident in developing spermatozoa expressed in ejaculates 18-28 days post-stress in mice. Our objectives were to: (1) assess genetic variation in fertility of heat-stressed male mice and (2) determine response to selection for fertility after heat stress in male mice. Mature male mice were exposed to heat stress (35+/-1 degrees C; n=50) or control (21+/-1 degrees C; n=10) conditions for 24h (day 0) and then hemicastrated for tissue collection. Two periods of mating tests followed, period 1 (from days 3 to 11) when no reductions in fertility were anticipated, and period 2 (days 18-26) when variation in fertility was expected. Period 2 pregnant females were sacrificed in late gestation. Males were indexed by multiplying overall mean ovulation rate by pre-implantation survival and number of pregnant period 2 mates. The five highest and five lowest ranking males were identified as heat stress resistant and susceptible, respectively. Resistant males were 61.2units superior in the index, 57.5% greater in pregnancy rate, and 57.6 total fetuses greater than susceptible males. Progeny of resistant sires were superior to progeny of susceptible sires in estimated breeding value by 4.5units for the index, 4.1% for pregnancy rate, and 5.2 fetuses (P<0.0001). Heritability estimates for the index, pregnancy rate, and number of fetuses ranged from 0.09 to 0.13, suggesting male fertility following heat stress is heritable and responds to selection.     

Human exposure to 2450 MHz CW energy at levels outside the IEEE C95.1 standard does not increase core temperature

Permission was received from the Brooks AFB Institutional Review Board and the AF Surgeon General's Office to exceed the peak power density (PD = 35 mW/cm(2)) we had previously studied during partial body exposure of human volunteers at 2450 MHz. Two additional peak PD were tested (50 and 70 mW/cm(2)). The higher of these PD (normalized peak local SAR = 15.4 W/kg) is well outside the IEEE C95.1 guidelines for partial body exposure, as is the estimated whole body SAR approximately 1.0 W/kg. Seven volunteers (four males, three females) were tested at each PD in three ambient temperatures (T(a) = 24, 28, and 31 degrees C) under our standard protocol (30 min baseline, 45 min RF exposure, 10 min baseline). The thermophysiological data (esophageal and six skin temperatures, metabolic heat production, local sweat rate, and local skin blood flow) were combined with comparable data at PD = 0, 27, and 35 mW/cm(2) from our 1999 study to generate response functions across PD. No change in esophageal temperature or metabolic heat production was recorded at any PD in any T(a). At PD = 70 mW/cm(2), skin temperature on the upper back (irradiated directly) increased 4.0 degrees C in T(a) = 24 degrees C, 2.6 degrees C in T(a) = 28 degrees C, and 1.8 degrees C in T(a) = 31 degrees C. These differences were primarily due to the increase in local sweat rate, which was greatest in T(a) = 31 degrees C. Also at PD = 70 mW/cm(2), local skin blood flow on the back increased 65% over baseline levels in T(a) = 31 degrees C, but only 40% in T(a) = 24 degrees C. Although T(a) becomes an important variable when RF exposure exceeds the C95.1 partial body exposure limits, vigorous heat loss responses of blood flow and sweating maintain thermal homeostasis efficiently. It is also clear that strong sensations of heat and thermal discomfort will motivate a timely retreat from a strong RF field, long before these physiological responses are exhausted. Published 2001 Wiley-Liss, Inc.     

Thermal, metabolic, and cardiovascular responses to various degrees of cold stress.

The metabolic, thermal, and cardiovascular responses of two male Caucasians to 1 2 h exposure to ambient temperature ranging between 28 degrees C and 5 degrees C were studied and related to the respective ambient temperatures. The metabolic heat production increased linearly with decreasing ambient temperature, where heat production (kcal times m- minus 2 times h- minus 1) = minus 2.79 Ta degrees C + 103.4, r = -0.97, P smaller than 0.001. During all exposures below 28 degrees C, the rate of decrease in mean skin temperature (Tsk) was found to be an exponential function dependent upon the ambient temperature (Ta) and the time of exposure. Reestablishment of Tsk steady state occurred at 90-120 min of exposure, and the time needed to attain steady state was linearly related to decreasing Ta. The net result was that a constant ratio of 1.5 of the external thermal gradient to the internal thermal gradient was obtained, and at all experimental temperatures, the whole body heat transfer coefficient remained constant. Cardiac output was inversely related to decreasing Ta, where cardiac output (Q) = minus 0.25 Ta degrees C + 14.0, r = minus 0.92, P smaller than 0.01. However, the primary reason for the increased Q, the stroke output, was also described as a third-order polynomial, although the increasing stroke volume throughout the Ta range (28-5 degrees C) was linearly related to decreasing ambients. The non-linear response of this parameter which occurred at 20 degrees C larger than or equal to Ta larger than or equal to 10 degrees C suggested that the organism's cardiac output response was an integration of the depressed heart rate response and the increasing stroke output at these temperatures.     

Mechanism for pressor response to nonexertional heating in the conscious rat

The purpose of this study was to determine the systemic hemodynamic mechanism(s) underlying the pressor response to nonexertional heat stress in the unrestrained conscious rat. After a 60-min control period [ambient temperature (Ta) 24 degrees C], male Sprague-Dawley rats (260-340 g) were exposed to a Ta of 42 degrees C until a colonic temperature (Tc) of 41 degrees C was attained. As Tc rose from control levels (38.1 +/- 0.1 degrees C) to 41 degrees C, mean arterial blood pressure (carotid artery catheter, n = 33) increased from 124 +/- 2 to 151 +/- 2 mmHg (P less than 0.05). During this period, heart rate increased (395 +/- 5 to 430 +/- 6 beats/min, P less than 0.05) and stroke volume remained unchanged. As a result, ascending aorta blood flow velocity (Doppler flow probe, n = 8), used as an index of cardiac output, did not change from control levels during heating, but there was a progressive Tc-dependent increase in systemic vascular resistance (+30% at end heating, P less than 0.05). This systemic vasoconstrictor response was associated with decreases in blood flow (-31 +/- 9 and -21 +/- 5%) and increases in vascular resistance (94 +/- 16 and 53 +/- 8%; all P less than 0.05) in the superior mesenteric and renal arteries (n = 8 each) and increases in plasma norepinephrine (303 +/- 37 to 1,237 +/- 262 pg/ml) and epinephrine (148 +/- 28 to 708 +/- 145 pg/ml) concentrations (n = 12, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)