Thermoregulatory, cardiovascular, and psychophysical response to alcohol in men in 40 degrees C water.

The goals of the study were to test the hypotheses that ethyl alcohol (ETOH) in low-to-moderate doses would alter thermo-regulation and/or disrupt the normal relationship between physiological and psychophysical indexes of heat stress during 40 degrees C water immersion and to characterize the cardiovascular response to the combined stimuli of heat, water immersion, and ETOH. Six healthy men underwent three trials of 21 min of immersion in water at 40.0 +/- 0.1 degrees C after consuming 0, 0.27, or 0.54 g ETOH/kg. Esophageal temperature (Tes) rose by approximately 1.0 degrees C during immersion for each trial. Per unit of Tes rise, changes during immersion in skin temperature, sweat rate, heart rate, systolic and diastolic blood pressure, and psychophysical assessments of comfort and overheating did not differ significantly by trial. Across trials, there was an apparent threshold for activation of thermoregulatory responses at an approximately 0.5 degrees C increase in Tes occurring after approximately 9 min of immersion. This threshold was identified psychophysically by increased ratings of overheating and decreased comfort. Above the threshold, there was an attenuation of the rate of increase of Tes. Cardiovascular stress was mild (rate-pressure product approximately 12,000) and not significantly increased by ETOH. Hypotension and tachycardia when subjects stood to exit the tub were observed. The data suggest that ETOH at the doses administered does not affect thermoregulatory, cardiovascular, or psychophysical indexes of heat stress during 40 degrees C water immersion.     

Thermoregulatory responses of rats exposed to 9.3-GHz microwaves: a comparison of E and H orientation.

The purpose of this study was to determine the effects of exposure orientation relative to electric and magnetic fields (E and H fields) on the thermal, cardiovascular, and respiratory changes in ketamine-anesthetized rats exposed to far-field, continuous-wave, 9.3-GHz radiofrequency radiation (RFR). Irradiation (specific absorption rate = 12.5 W/kg in both orientations; power levels of 79 and 59 mW/cm2 in E and H orientations, respectively) was conducted to produce 1 degree C colonic temperature changes (38.5 to 39.5 degrees C). During experimentation, arterial blood pressure and respiratory rate, colonic (Tc) tympanic (Tt) left and right subcutaneous (Tsl & Tsr) (sides toward and away from RFR source), and tail temperatures (Tta) were continuously recorded. The Tsr change during E-orientation exposure was considerably less than the Tc change; the Tt and Tsr (H-orientation) changes approximated the Tc increase; and the Tsl and Tta changes (both orientations) were considerably greater than the Tc increase. The Tt and Tsl increases were virtually equal under the two exposure conditions; however, the Tsr increase was significantly greater during H-orientation irradiation, and the Tta increase was significantly greater during E-orientation exposure. Heart rate and mean arterial pressure increased significantly during irradiation; however the cardiovascular responses were not affected by exposure orientation. The latter findings at 9.3 GHz contrast with the marked cardiovascular response differences between E- and H-orientation exposure noted during previous studies at 0.7 to 2.45 GHz.     

Thermoregulatory, cardiovascular, and muscular factors related to exercise after precooling

The effect of slightly lowered body temperature on endurance time and possibly related physiological factors was studied in seven male volunteers exercising on a cycle ergometer at an ambient temperature (Ta) of 18 degrees C. Work load was increased to 40% in a stepwise manner (phase I, min 0-16) followed by a period at 80% of peak oxygen consumption (VO2) sustained to exhaustion. On one day, exercise was preceded by a double cold exposure (precooling test, PRET), resulting in a 204-kJ/m2 negative heat storage and a 4 and 0.2 degrees C lower mean skin and core temperature at the start of exercise compared with the control test (CONT). Core temperature dropped further during exercise in PRET. Endurance time at 80% of peak VO2 was increased by 12% (P less than 0.05) in PRET. Heart rate (HR) was decreased throughout PRET (P less than 0.05); oxygen pulse and arteriovenous O2 difference were significantly increased in phase I of PRET, whereas the PRET-CONT differences in stroke volume and cardiac output were not significant. In phase II of PRET (min 16-28, heavy exercise) sweat rate (SR) and heat conductivity, indicating forearm blood flow, were lower (-39%, P less than 0.001; -37%). Pedal rate (PR) was 9% lower (P less than 0.01) in phase II of PRET. At the termination of exercise, PRET-CONT differences in HR, SR, and PR had disappeared.     

Thermoregulatory and metabolic changes during fever in young and old rats

We injected old and young rats with lipopolysaccharide (LPS; 50 microg/kg ip) at two ambient temperatures (Ta; 21 and 31 degrees C). Young rats mounted equivalent fevers at both Tas [peak body temperatures (Tb) of 38.3 and 38.7 degrees C, respectively]. The Tb of old rats was not different from baseline (37.3 degrees C) after LPS at Ta 21 degrees C, whereas, at 31 degrees C, their Tb rose to a mean peak of 38.4 degrees C. We also measured the associated thermoregulatory responses by use of calorimetry. At 21 degrees C, young rats developed a fever by increasing both O2 consumption and heat conservation. Old rats did not become febrile, and O2 consumption fell by 15%. Heat loss was the same in old and young rats. At 31 degrees C, young and old rats developed similar fevers with similar increases in heat production and conservation. Our results suggest that the lack of LPS fever in old rats at 21 degrees C is due mainly to the lowered metabolic rate.     

Thermoregulatory adjustments in squirrel monkeys exposed to microwaves at high power densities

The present study was undertaken to investigate the thermal adjustments of squirrel monkeys exposed in a cold environment to relatively high energy levels of microwave fields. The animals (Saimiri sciureus) were equilibrated for 90 min to a cool environment (Ta = 20 degrees C) to elevate metabolic heat production (M). They were then exposed for brief (10-min) or long (30-min) periods to 2,450-MHz continuous-wave microwaves. Power densities (MPD) were 10, 14, 19, and 25 mW/cm2 during brief exposures and 30, 35, 40, and 45 mW/cm2 during long exposures (rate of energy absorption: SAR = 0.15 [W/kg]/[mW/cm2]). Individual exposures were separated by enough time to allow physiological variables to return to baseline levels. The results confirm that each microwave exposure induced a rapid decrease in M. In a 20 degree C environment, the power density of a 10-min exposure required to lower M to approximate the resting level was 35 mW/cm2 (SAR = 5.3 W/kg). During the long exposures, 20 min was needed to decrease M to its lowest level. Cessation of irradiation was associated with persistence of low levels of M for periods that depended on the power density of the preceding microwave exposure. Vasodilation, as indexed by changes in local skin temperature, occurred at a high rate of energy absorption (SAR = 4.5 W/kg) and was sufficient to prevent a dramatic increase in storage of thermal energy by the body; vasoconstriction was reinstated after termination of irradiation. Patterns of thermophysiological responses confirm the influence both of peripheral and of internal inputs to thermoregulation in squirrel monkeys exposed to microwaves in a cool environment.     

Thermoregulatory and metabolic responses of Japanese quail to hypoxia

Common responses to hypoxia include decreased body temperature (T_b) and decreased energy metabolism. In this study, the effects of hypoxia and hypercapnia on T_b and metabolic oxygen consumption (V.O₂) were investigated in Japanese quail (Coturnix japonica). When exposed to hypoxia (15, 13, 11 and 9% O₂), T_b decreased only at 11% and 9% O₂ compared to normoxia; quail were better able to maintain T_b during acute hypoxia after a one-week acclimation to 10% O₂. V.O₂ also decreased during hypoxia, but at 9% O₂ this was partially offset by increased anaerobic metabolism. T_b and V.O₂ responses to 9% O₂ were exaggerated at lower ambient temperature (T_a), reflecting a decreased lower critical temperature during hypoxia. Conversely, hypoxia had little effect on T_b or V.O₂ at higher T_a (36 °C). We conclude that Japanese quail respond to hypoxia in much the same way as mammals, by reducing both T_b and V.O₂. No relationship was found between the magnitudes of decreases in T_b and V.O₂ during 9% O₂, however. Since metabolism is the source of heat generation, this suggests that Japanese quail increase thermolysis to reduce T_b. During hypercapnia (3, 6 and 9% CO₂), T_b was reduced only at 9% CO₂ while V.O₂ was unchanged.     

Thermoregulatory responses of the immature rat following repeated postnatal exposures to 2,450-MHz microwaves

This study was designed to determine the changes that occur in the thermoregulatory ability of the immature rat repeatedly exposed to low-level microwave radiation. Beginning at 6-7 days of age, previously untreated rats were exposed to 2,450-MHz continuous-wave microwaves at a power density of 5 mW/cm2 for 10 days (4 h/day). Microwave and sham (control) exposures were conducted at ambient temperatures (Ta) which represent different levels of cold stress for the immature rat (ie, "exposure" Ta = 20 and 30 degrees C). Physiological tests were conducted at 5-6 and 16-17 days of age, in the absence of microwaves, to determine pre- and postexposure responses, respectively. Measurements of metabolic rate, colonic temperature, and tail skin temperature were made at "test" Ta = 25.0, 30.0, 32.5, and 35.0 degrees C. Mean growth rates were lower for rats exposed to Ta = 20 degrees C than for those exposed to Ta = 30 degrees C, but microwave exposure exerted no effect at either exposure Ta. Metabolic rates and body temperatures of all exposure groups were similar to values for untreated animals at test Ta of 32.5 degrees C and 35.0 degrees C. Colonic temperatures of rats repeatedly exposed to sham or microwave conditions at exposure Ta = 20 degrees C or to sham conditions at exposure Ta = 30 degrees C were approximately 1 degrees C below the level for untreated animals at test Ta of 25.0 degrees C and 30.0 degrees C. However, when the exposure Ta was warmer, rats exhibited a higher colonic temperature at these cold test Ta, indicating that the effectiveness of low-level microwave treatment to alter thermoregulatory responses depends on the magnitude of the cold stress.     

Thermoregulatory (core, surface and metabolic) responses of unrestrained rats to repeated POAH injections of beta-endorphin or adrenocorticotropin

Repeated preoptic-anterior hypothalamic (POAH) injections of saline and 10 or 25 micrograms/microliters of beta-endorphin or ACTH were given to groups of male Sprague-Dawley rats. One hr after the fifth injection of beta-endorphin or ACTH, each rat received a POAH injection of naloxone HCl (10 micrograms/microliters). Core (Tre-rectal) and surface (Tt-tail) temperatures, metabolic (VO2) and behavioral responses were recorded 30 min before and 60 min after each drug injection. The initial POAH injection of either dose of beta-endorphin produced a hyperthermia. Peak hyperthermia was reduced in the group given 10 micrograms/microliters of beta-endorphin repeatedly. TtS rose after each beta-endorphin injection but temporally lagged Tre increases. Metabolic rate (VO2) was increased with repeated POAH injections of beta-endorphin. Naloxone reduced the elevated Tre seen with beta-endorphin by increasing Tt's further and reducing VO2. POAH administration of ACTH evoked only a slight hyperthermic Tre response, but elevated TtS and VO2S, due to enhanced grooming and explorative behavior. With repeated ACTH injections, TreS did not change from those on the first day as TtS and VO2 remained enhanced. Naloxone reduced VO2 and TtS of the ACTH-treated rats but TreS still were unchanged. Results suggest that the hyperthermia of unrestrained rats given an acute as opposed to repeated POAH beta-endorphin injections is mediated by different effector mechanisms. With the doses used, the slight and unchanging TreS seen with ACTH occurred because this peptide increased heat production due to locomotor activation yet also exaggerated heat loss by vasodilating the peripheral vasculature.     

Thermoregulatory and metabolic responses to a half-marathon run in hot,humid conditions

This study describes the thermoregulatory and metabolic responses during a simulated half-marathon (21 km) run performed outdoors in a hot, humid environment. Ten male runners were recruited for the study, The run was carried out individually under solar radiation on a predetermined path in the following environmental conditions (ambient temperature: 27.96 ± 1.70 °C, globe temperature: 28.52 ± 2.51 °C, relative humidity: 76.88 ± 7.49%, wet bulb globe temperature: 25.80 ± 1.18 °C). Core temperature, skin temperature, head temperature, heat storage, heart rate, expired gases, rating of perceived exertion, and speed were measured or calculated before the start, every 3 km, and immediately following the run. Comparisons were made for each dependent variable using one-way repeated measures analysis of variance tests, and a Bonferroni test. Average run time and pace were 101:00 ± 9:52 min and 4:48 ± 00:16 min km^-1, respectively. Participants significantly reduced their running speed, oxygen consumption, and heat storage at 9 km (p < 0.05). While core temperature was significantly increased at 6 km (p < 0.05) before plateauing for the remainder of the run. The key finding was that most of the runners reduced their pace when a T_core of 39 °C was reached which occurred between 6 and 9 km of the run, yet runners were able to increase their speed demonstrating an “end-spurt” near the end of the run.     

Opposite metabolic response to fenofibrate treatment in pregnant and virgin rats.

The level of maternal circulating triglycerides during late pregnancy has been correlated to newborns' weight in humans. To investigate the response to fenofibrate, a hypotriglyceridemic agent, in pregnant rats, 0, 100, or 200 mg of fenofibrate/kg body weight as oral doses were given twice a day from day 16 of gestation and studied at day 20. Virgin rats were studied in parallel. Liver weight was higher in pregnant than in virgin rats, and either dose of fenofibrate increased this variable in both groups. The highest dose of fenofibrate decreased fetal weight. Although plasma triglycerides decreased during the first 2 days of fenofibrate treatment in pregnant rats, the effect disappeared on day 3, and plasma triglycerides were even enhanced at day 4. In virgin rats, fenofibrate decreased plasma triglycerides throughout the experiment. Plasma cholesterol levels in pregnant rats decreased during the first 3 days of treatment, and the effect disappeared on day 4, whereas in virgin rats, values remained decreased. Changes in plasma triglycerides paralleled those of VLDL triglycerides. In pregnant rats, VLDL cholesterol levels increased while LDL cholesterol decreased with the treatment, whereas in virgin rats, cholesterol levels decreased in all lipoprotein fractions. Only in virgin rats did liver triglyceride concentration increase with fenofibrate treatment. Lumbar adipose tissue LPL was lower in pregnant than in virgin rats, and fenofibrate treatment decreased this variable in both groups. Maternal fenofibrate treatment increased fetal plasma and liver triglyceride and cholesterol concentrations.It is proposed that the opposite effects of fenofibrate treatment in virgin and pregnant rats are a consequence of both the enhanced liver capability for VLDL triglyceride production and a rebound response to the drug in the latter.     

Thermoregulatory, motor, behavioural, and nociceptive responses of rats to 3 long-acting neuroleptics

We investigated physiological effects of intramuscular injections of the following 3 long-acting neuroleptics commonly used in wildlife management: haloperidol (0.05, 0.1, and 0.5 mg/kg body mass), zuclopenthixol acetate (0.5, 1, and 5 mg/kg), and perphenazine enanthate (1, 3, and 10 mg/kg), in a rat model. Body temperature and cage activity were measured by intra-abdominal telemeters. Nociceptive responses were assessed by challenges to noxious heat and pressure. Haloperidol (0.5 mg/kg) produced a significant nocturnal hypothermia (p < 0.05) and decreased nighttime cage activity and food intake. Zuclopenthixol (5 mg/kg) significantly decreased nighttime body temperature and cage activity and, at 1 mg/kg and 5 mg/kg, significantly decreased food intake 5-17 h after injection (p < 0.05). Perphenazine (10 mg/kg) significantly decreased nighttime body temperature and cage activity and, at all doses, significantly decreased food intake 5-17 h after injection (p < 0.05). Significant analgesic activity was evident in rats given 5 mg/kg zuclopenthixol up to 40 h after injection, and 10 mg/kg perphenazine from 48 to 96 h after injection (p < 0.0001). Zuclopenthixol (5 mg/kg) and perphenazine (10 mg/kg) had significant antihyperalgesic activities at 16 h postinjection and 24-48 h postinjection, respectively (p < 0.0001). Haloperidol had no significant antinociceptive activity at doses tested. Motor function was impaired in rats given 0.5 mg/kg haloperidol, 5 mg/kg zuclopenthixol and 10 mg/kg perphenazine. Effects of long-acting neuroleptics on body temperature, feeding, and activity were short-lasted and should not preclude their use in wildlife. Antinociceptive actions were longer-lasting, but were nonspecific, and we recommend additional analgesics for painful procedures during wildlife management.     

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.     

Thermoregulatory responses of diabetic rats

1. Thermal responses and skin microcirculation were measured in streptozotocin-induced diabetic (SD) rats during acute and chronic exposure to ambient (Ta) temperatures ranging from about 5 to 35 degrees C. 2. At 28 degrees C, SD rats had higher rate of oxygen consumptions (VO2), tail skin blood flow (SKBF), but lower rectal temperatures (Tre) than saline-injected controls. 3. Chronic exposure of the SD rats to 35 and 5 degrees C caused a sharp rise and decline in Tre, respectively. 4. At 35 degrees C, hyperthermia in the SD rats was associated with greater increase in VO2 than controls, but changes in SKBF were similar in both groups. 5. At 5 degrees C, VO2 changed similarly in both the SD and control rats, but vasoconstriction was greater in the controls. 6. The data suggest that hypothermia in SD rats may be associated with impairment of vasoconstriction and hyperthermia may be related to an increase VO2 not accompanied by greater vasodilation.     

Thermoregulatory and metabolic responses to repeated bouts of prolonged cycle-ergometer exercise in man

Changes in body temperature, oxygen uptake (VO2), heart rate (HR), sweating rate and plasma osmolarity were examined in 10 human subjects, performing four successive 30 min exercise-bouts of the same intensity (50% VO2 max) separated by 30 min rest periods. In spite of the rest intervals and replacement of body fluid loss there was a progressive increase in VO2. HR, rectal (Tre) and mean body (Tb) temperatures in consecutive exercise bouts. The thermoregulatory efficiency showed an increasing tendency, and a delay in the sweating response at the beginning of each exercise was shortened. It is concluded that a drift in metabolic and temperature responses to exercise, reported throughout a long-term continuous work, occurs also in the euhydrated subjects performing a prolonged intermittent exercise. It is not caused by an impaired thermoregulation during exercise but rather by insufficient restitution of metabolic processes during rest intervals.     

Chronic high-carbohydrate, high-fat feeding in rats induces reversible metabolic, cardiovascular, and liver changes

Age-related physiological changes develop at the same time as the increase in metabolic syndrome in humans after young adulthood. There is a paucity of data in models mimicking chronic diet-induced changes in human middle age and interventions to reverse these changes. This study measured the changes during chronic consumption of a high-carbohydrate (as cornstarch), low-fat (C) diet and a high-carbohydrate (as fructose and sucrose), high-fat (H) diet in rats for 32 wk. C diet feeding induced changes without metabolic syndrome, such as disproportionate increases in total body lean and fat mass, reduced bone mineral content, cardiovascular remodeling with increased systolic blood pressure, left ventricular and arterial stiffness, and increased plasma markers of liver injury. H diet feeding induced visceral adiposity with reduced lean mass, increased lipid infiltration in the skeletal muscle, impaired glucose and insulin tolerance, cardiovascular remodeling, hepatic steatosis, and increased infiltration of inflammatory cells in the heart and the liver. Chia seed supplementation for 24 wk attenuated most structural and functional modifications induced by age or H diet, including increased whole body lean mass and lipid redistribution from the abdominal area, and normalized the chronic low-grade inflammation induced by H diet feeding; these effects may be mediated by increased metabolism of anti-inflammatory n-3 fatty acids from chia seed. These results suggest that chronic H diet feeding for 32 wk mimics the diet-induced cardiovascular and metabolic changes in middle age and that chia seed may serve as an alternative dietary strategy in the management of these changes.