Evaluation of a temperate-environment test of heat tolerance in prior heatstroke patients and controls

It has been reported that scores from a temperate-environment step test describe the heat-tolerance status of prior heatstroke patients (HP). This investigation evaluated the ability of this temperate-environment heat-tolerance test (HTT) to indicate altered heart rate (HR) and rectal temperature (Tre) responses of HP, after 7 days of heat acclimation. On day 1, ten male HP (61 +/- 7 days post-heatstroke) and five control subjects (C) bench-stepped (0.30 m high, 27 steps.min-1) for 15 min (25.8 degrees C dry bulb, 16.2 degrees C wet bulb). On days 2-8, subjects underwent heat acclimation (40.1 degrees C dry bulb, 23.8 degrees C wet bulb; treadmill, 90 min.day-1). Heat acclimation resulted in significant decreases in final HR (152 +/- 5 vs 130 +/- 3 beats.min-1, P less than 0.025) and final Tre (38.62 +/- 0.11 vs 38.13 +/- 0.07 degrees C, p less than 0.01) in HP. One HP but no C was defined heat intolerant, exhibiting inability to adapt to daily exercise in the heat. On day 9, HP repeated HTT, exactly as performed on day 1; mean group HTT scores did not change (day 1 = 39 +/- 6; day 9 = 48 +/- 6, P greater than 0.05). All physical characteristics and physiological responses of HP (days 1, 2, 7, 9) were statistically similar (P greater than 0.05) to those of C. In contrast to heat-acclimation data, HTT scores (score less than or equal to 30) indicated that four HP were heat intolerant on day 1 and two HP were heat intolerant on day 9.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

The physiological strain index applied to heat-stressed rats.

A physiological strain index (PSI) based on heart rate (HR) and rectal temperature (Tre) was recently suggested to evaluate exercise-heat stress in humans. The purpose of this study was to adjust PSI for rats and to evaluate this index at different levels of heat acclimation and training. The corrections of HR and Tre to modify the index for rats are as follows: PSI = 5 (Tre t - Tre 0). (41.5 - Tre 0)-1 + 5 (HRt - HR0). (550 - HR0)-1, where HRt and Tre t are simultaneous measurements taken at any time during the exposure and HR0 and Tre 0 are the initial measurements. The adjusted PSI was applied to five groups (n = 11-14 per group) of acclimated rats (control and 2, 5, 10, and 30 days) exposed for 70 min to a hot climate [40 degrees C, 20% relative humidity (RH)]. A separate database representing two groups of acclimated or trained rats was also used and involved 20 min of low-intensity exercise (O2 consumption approximately 50 ml. min-1. kg-1) at three different climates: normothermic (24 degrees C, 40% RH), hot-wet (35 degrees C, 70% RH), and hot-dry (40 degrees C, 20% RH). In normothermia, rats also performed moderate exercise (O2 consumption approximately 60 ml. min-1. kg-1). The adjusted PSI differentiated among acclimation levels and significantly discriminated among all exposures during low-intensity exercise (P < 0.05). Furthermore, this index was able to assess the individual roles played by heat acclimation and exercise training.     

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

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

Thermoregulation in the meerkat (Suricata suricatta Schreber, 1776)

Tre of the suricates exhibits a marked diurnal rhythm (mean Tre at night 36.3 +/- 0.6 degrees C and 38.3 +/- 0.5 degrees C during the day). Oxygen consumption is lowest at Ta 30-32.5 degrees C (mean 0.365 +/- 0.022 ml O2 g-1 hr-1); this is 42% below the value expected from body mass. At Ta below the TNZ, oxygen uptake rises rapidly, minimal thermal conductance (0.040 ml O2 g-1 h-1 degrees C-1) being 18% above the mass-specific level. Lowest heart rates occur at Ta 30 degrees C (mean 109.6 +/- 9.8 beats min-1) and oxygen pulse is minimal at Ta 30-35 degrees C with 40-45 microliter O2 beat-1. At Ta 15-32.5 degrees C total evaporative water loss is between 0.46-0.63 ml H2O kg-1 hr-1 and increases markedly during heat stress (to a mean of 5.35 ml H2O kg-1 hr-1 at Ta 40 degrees C). This rise of TEWL is mainly attributable to the onset of panting at Ta above 35 degrees C.     

Effects of short-term exercise in the heat on thermoregulation, blood parameters, sweat secretion and sweat composition of tropic-dwelling subjects

This study investigates the effects of a short-term aerobic training program in a hot environment on thermoregulation, blood parameters, sweat secretion and composition in tropic-dwellers who have been exposed to passive heat. Sixteen healthy Malaysian-Malay male volunteers underwent heat acclimation (HA) by exercising on a bicycle ergometer at 60% of VO2max for 60 min each day in a hot environment (Ta: 31.1+/-0.1 degrees C, rh: 70.0+/-4.4%) for 14 days. All parameters mentioned above were recorded on Day 1 and at the end of HA (Day 16). On these two days, subjects rested for 10 min, then cycled at 60% of VO2max for 60 min and rested again for 20 min (recovery) in an improvised heat chamber. Rectal temperature (Tre), mean skin temperature (Tsk) heart rate (HR), ratings of perceived exertion (RPE), thermal sensation (TS), local sweat rate and percent dehydration were recorded during the test. Sweat concentration was analysed for sodium [Na+]sweat and potassium. Blood samples were analysed for biochemical changes, electrolytes and hematologic indices. Urine samples were collected before and after each test and analysed for electrolytes.After the period of acclimation the percent dehydration during exercise significantly increased from 1.77+/-0.09% (Day 1) to 2.14+/-0.07% (Day 16). Resting levels of hemoglobin, hematocrit and red blood cells decreased significantly while [Na+]sweat increased significantly. For Tre and Tsk there were no differences at rest. Tre, HR, RPE, TS, plasma lactate concentration, hemoglobin and hematocrit at the 40th min of exercise were significantly lower after the period of acclimation but mean corpuscular hemoglobin and serum osmolality were significantly higher while no difference was seen in [Na+]sweat and Tsk. It can be concluded that tropic-dwelling subjects, although exposed to prolonged passive heat exposure, were not fully heat acclimatized. To achieve further HA, they should gradually expose themselves to exercise-heat stress in a hot environment.     

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.     

Control of heat-induced cutaneous vasodilatation in relation to age

Well matched unacclimatised older (age 55-68, 4 women, 2 men) and younger (age 19-30, 4 women, 2 men) subjects performed 75 min cycle exercise (approximately 40% VO2max) in a hot environment (37 degrees C, 60% rh). Rectal temperature (Tre), mean skin temperature (Tsk), arm blood flow (ABF, strain gauge plethysmography), and cardiac output (Q, CO2 rebreathing) were measured to examine age-related differences in heat-induced vasodilatation. Tre and Tsk rose to the same extent in each group during the exposure. There was no significant intergroup difference in sweat rate (older: 332 +/- 43 ml.m-2.h-1, younger: 435 +/- 49 ml.m-2.h-1; mean +/- SEM). However, the older subjects responded to exercise in the heat with a lower ABF response which could be attributed to a lower Q for the same exercise intensity. The slope of the ABF-Tre relationship was attenuated in the older subjects (9.3 +/- 1.3 vs 17.9 +/- 3.3 ml.100 ml-1.min-1.degrees C-1, p less than 0.05), but the Tre threshold for vasodilatation was about 37.0 degrees C for both groups. These results suggest an altered control of skin vasodilatation during exercise in the heat in older individuals. This attenuated ABF response appears to be unrelated to VO2max, and may reflect an age-related change in thermoregulatory cardiovascular function.     

Rectal and rectal vs. esophageal temperatures in paraplegic men during prolonged exercise

This study investigated the rectal (Tre), esophageal (Tes), and skin (Tsk) temperature changes in a group of trained traumatic paraplegic men pushing their own wheelchairs on a motor-driven treadmill for a prolonged period in a neutral environment. There were two experiments. The first experiment (Tre and Tsk) involved a homogeneous group (T10-T12/L3) of highly trained paraplegic men [maximum O2 uptake (VO2max) 47.5 +/- 1.8 ml.kg-1.min-1] exercising for 80 min at 60-65% VO2max.Tre and Tsk (head, arm, thigh, and calf) and heart rate (HR) were recorded throughout. O2 uptake (VO2), minute ventilation (VE), CO2 production (VCO2), and heart rate (HR) were recorded at four intervals. During experiment 1 significant changes in HR and insignificant changes in VCO2, VE, and VO2 occurred throughout prolonged exercise. Tre increased significantly from 37.1 +/- 0.1 degrees C (rest) to 37.8 +/- 0.1 degrees C after 80 min of exercise. There were only significant changes in arm Tsk. Experiment 2 involved a nonhomogeneous group (T5-T10/T11) of active paraplegics (VO2max 39.9 +/- 4.3 ml.kg-1.min-1) exercising at 60-65% VO2max for up to 45 min on the treadmill while Tre and Tes were simultaneously recorded. Tes rose significantly faster than Tre during exercise (dT/dt 20 min: Tes 0.050 +/- 0.003 degrees C/min and Tre 0.019 +/- 0.005 degrees C/min), and Tes declined significantly faster than Tre at the end of exercise. Tes was significantly higher than Tre at the end of exercise. Our results suggest that during wheelchair propulsion by paraplegics, Tes may be a better estimate of core temperature than Tre.     

Effects of modafinil on heat thermoregulatory responses in humans at rest

The effects of modafinil on heat thermoregulatory responses were studied in 10 male subjects submitted to a sweating test after taking 200 mg of modafinil or placebo. Sweating tests were performed in a hot climatic chamber (45 degrees C, relative humidity <15%, wind speed = 0.8 m x s(-1), duration 1.5 h). Body temperatures (rectal (Tre) and 10 skin temperatures (Tsk)), sweat rate, and metabolic heat production (M) were studied as well as heart rate (HR). Results showed that modafinil induced at the end of the sweating test higher body temperatures increases (0.50 +/- 0.04 versus 0.24 +/- 0.05 degrees C (P < 0.01) for deltaTre and 3.64 +/- 0.16 versus 3.32 +/- 0.16 degrees C (P < 0.05) for deltaTsk (mean skin temperature)) and a decrease in sweating rate throughout the heat exposure (P < 0.05) without change in M, leading to a higher body heat storage (P < 0.05). AHR was also increased, especially at the end of the sweating test (17.95 +/- 1.49 versus 12.52 +/- 1.24 beats/min (P < 0.01)). In conclusion, modafinil induced a slight hyperthermic effect during passive dry heat exposure related to a lower sweat rate, probably by its action on the central nervous system, and this could impair heat tolerance.     

Physiological responses to fire fighting activities

Eight professional fire fighters participated in six fire fighting scenarios at a training facility. Data on heart rate (HR), rectal temperature (Tre), and skin temperatures at the chest and thigh were collected using a portable data acquisition system. Average HR ranged from 122 to 151 beats.min-1 during the six scenarios. Detailed analyses indicated that HR and Tre increases are related to both the physical and environmental stresses of the various activities carried out. The most demanding activity, that of building search and victim rescue, resulted in an average HR of 153 beats.min-1 and Tre rise of 1.3 degree C, while the least demanding activity, that of the crew captain who directs the fire fighting, resulted in an average HR of only 122 beats.min-1 and a Tre rise of only 0.3 degree C. This study shows that fire fighting is strenuous work for those directly entering a building and performing related duties, but that the physical demands of other activities are considerably less. The results further suggest that heat strain injuries in fire fighters could perhaps be reduced by rotating duties frequently with other crew members performing less stressful work.     

Overexpression of eNOS prevents the development of renovascular hypertension in mice

Gene therapy has become an important tool for understanding several cardiovascular diseases. In the present study we investigated the effects of endothelial nitric oxide synthase (eNOS) overexpression on renovascular hypertension. Experiments were carried out in C57BL/6 mice randomly assigned to either a two-kidney one-clip (2K1C) hypertension group or a sham-operated group. At the same time surgery was carried out, both 2K1C and sham mice received an intravenous injection of recombinant adenovirus expressing the functional gene eNOS or the reporter gene beta-galactosidase (beta-gal). Fourteen days later, arterial pressure, baroreflex sensitivity, and cardiac sympathetic and parasympathetic tone were evaluated in conscious mice. Measurement of mean arterial pressure showed arterial hypertension in 2K1C-betagal mice compared with sham-betagal mice (121 +/- 3 vs. 96 +/- 2 mm Hg, p < 0.01), which was prevented by eNOS overexpression (2K1C-eNOS 100 +/- 4 vs. sham-eNOS 99 +/- 3 mm Hg). Linear regression analysis of the reflex tachycardia response to sodium nitroprusside-induced hypotension showed that baroreflex sensitivity was significantly attenuated in 2K1C-betagal mice (5.8 +/- 0.5 vs. sham-betagal 8.0 +/- 0.8 beats.min-1 x mm Hg-1, p < 0.05), but this decrease was not prevented by eNOS overexpression (2K1C-eNOS 7.2 +/- 0.5 vs. sham-eNOS 8.8 +/- 0.7 beats x min-1 x mm Hg-1, p < 0.05). The cardiac sympathetic tone was augmented and the vagal tone was reduced in 2K1C-betagal (152 +/- 17 and 45 +/- 12 beats.min-1, respectively) compared with sham-betagal mice (112 +/- 6 and 89 +/- 7 beats.min-1, respectively), and similar results were observed in 2K1C-eNOS mice compared with sham-eNOS. The data indicate that eNOS overexpression was able to prevent the development of 2K1C renovascular hypertension in mice, without affecting other characteristic cardiovascular dysfunctions.     

Effect of pyridostigmine on the exercise-heat response of man

The effect of pyridostigmine on thermoregulatory responses was evaluated during exercise and heat stress. Eight heat acclimated, young adult male subjects received four doses of pyridostigmine (30 mg) or identical placebo tablets every 8 h, in a double blind, randomized, cross-over trial. A 30.3%, SD 4.6% inhibition of the circulating cholinesterase (ChE) activity was induced in the pyridostigmine-treated group. The subjects were exposed to 170-min exercise and heat-stress (dry bulb temperature, 33 degrees C; relative humidity 60%) consisting of 60 min in a sitting position and two bouts of 50-min walking (1.39 m.s-1, 5% gradient) which were separated by 10-min rest periods. No differences were found between treatments in the physiological responses and heat balance parameters at the end of exposure: heart rate (fc) was 141 beats.min-1, SD 16 and 150 beats.min-1, SD 12, rectal temperature (Tre) was 38.5 degrees C, SD 0.4 degrees and 38.6 degrees C, SD 0.3 degrees, heat storage was 60 W.m-2, SD 16 and 59 W.m-2, SD 15 and sweat rate was 678 g.h-1, SD 184 and 661 g.h-1, SD 133, in the pyridostigmine and placebo treatments, respectively. The changes in Tre and fc over the heat-exercise period were parallel in both study and control groups. Pyridostigmine caused a slight slowing of fc (5 beats.min-1) which was consistent throughout the entire exposure (P less than 0.001) but was of no clinical significance. The overall change in fc was similar for both groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Heat acclimation increases skin vasodilation and sweating but not cardiac baroreflex responses in heat-stressed humans.

In the present study, to test the hypothesis that exercise-heat acclimation increases orthostatic tolerance via the improvement of cardiac baroreflex control in heated humans, we examined cardiac baroreflex and thermoregulatory responses, including cutaneous vasomotor and sudomotor responses, during whole body heating before and after a 6-day exercise-heat acclimation program [4 bouts of 20-min exercise at 50% peak rate of oxygen uptake separated by 10-min rest in the heat (36 degrees C; 50% relative humidity)]. Ten healthy young volunteers participated in the study. On the test days before and after the heat acclimation program, subjects underwent whole body heat stress produced by a hot water-perfused suit during supine rest for 45 min and 75 degrees head-up tilt (HUT) for 6 min. The sensitivity of the arterial baroreflex control of heart rate (HR) was calculated from the spontaneous changes in beat-to-beat arterial pressure and HR. The HUT induced a presyncopal sign in seven subjects in the preacclimation test and in six subjects in the postacclimation test, and the tilting time did not differ significantly between the pre- (241 +/- 33 s) and postacclimation (283 +/- 24 s) tests. Heat acclimation did not change the slope in the HR-esophageal temperature (Tes) relation and the cardiac baroreflex sensitivity during heating. Heat acclimation decreased (P < 0.05) the Tes thresholds for cutaneous vasodilation in the forearm and dorsal hand and for sweating in the forearm and chest. These findings suggest that short-term heat acclimation does not alter the spontaneous baroreflex control of HR during heat stress, although it induces adaptive change of the heat dissipation response in nonglabrous skin.     

Unstable heart rate and temperature regulation predict mortality in AKR/J mice

Elderly populations face greater risks of mortality when exposed to changes in environmental stress. The purpose of the following study was to develop an age-dependent susceptibility model that achieved the following three goals: 1) to operationally define homeostasis by assessing the stability and periodicity in physical activity, heart rate (HR), and deep body temperature (T(db)), 2) to specify alterations in activity, HR, and T(db) regulation that signal imminent death, and 3) to test the hypothesis that the decay in homeostasis associated with imminent death incorporates the coincident disintegration of multiple physiological systems. To achieve these goals, the circadian regulation of activity, HR, and T(db) was assessed using radiotelemeters implanted in AKR/J (n = 17) inbred mice at approximately 190 days of age. During a 12:12-h light-dark cycle, weekly measurements were obtained at 30-min intervals for 48-h periods until each animal's natural death. The average (+/-SE) life span of surgically treated animals did not differ from untreated controls (319 +/- 12 vs. 319 +/- 14 days). Cardiac and thermal stability were characterized by a circadian periodicity, which oscillated around stable daily averages of 640 +/- 14 beats/min in HR and 36.6 +/- 0.1 degrees C in T(db). Stable HR and T(db) responses were compared with extreme conditions 3 days before death, during which a disintegration of circadian periodicity was coincident with a fall in the daily average HR and T(db) of approximately 29 and approximately 13% lower (i.e., 456 +/- 22 beats/min and 31.7 +/- 0.6 degrees C), respectively. The results further suggested that multiple predictors of cardiac and thermal instability in AK mice, including significant bradycardia, hypothermia, and a loss of circadian periodicity, forecast life span 5-6 wk before expiration.     

Influence of skeletal muscle glycogen on passive rewarming after hypothermia

To examine the influence of muscle glycogen on the thermal responses to passive rewarming subsequent to mild hypothermia, eight subjects completed two cold-water immersions (18 degrees C), followed by 75 min of passive rewarming (24 degrees C air, resting in blanket). The experiments followed several days of different exercise-diet regimens eliciting either low (LMG; 141.0 +/- 10.5 mmol.kg.dry wt-1) or normal (NMG; 526.2 +/- 44.2 mmol.kg.dry wt-1) prewarming muscle glycogen levels. Cold-water immersion was performed for 180 min or to a rectal temperature (Tre) of 35.5 degrees C. In four subjects (group A, body fat = 20 +/- 1%), postimmersion Tre was similar to preimmersion Tre for both trials (36.73 +/- 0.18 vs. 37.26 +/- 0.18 degrees C, respectively). Passive rewarming in group A resulted in an increase in Tre of only 0.13 +/- 0.08 degrees C. Conversely, initial rewarming Tre for the other four subjects (group B, body fat = 12 +/- 1%) averaged 35.50 +/- 0.05 degrees C for both trials. Rewarming increased Tre similarly in group B during both LMG (0.76 +/- 0.25 degrees C) and NMG (0.89 +/- 0.13 degrees C). Afterdrop responses, evident only in those individuals whose body core cooled during immersion (group B), were not different between LMG and NMG. These data support the contention that Tre responses during passive rewarming are related to body insulation. Furthermore these results indicate that low muscle glycogen levels do not impair rewarming time nor alter after-drop responses during passive rewarming after mild-to-moderate hypothermia.     

Heat debt as an index for cold adaptation in men

Several types of cold adaptation in men have been described in the literature (metabolic, insulative, hypothermic). The aim of this study is to show that the decrease of heat debt can be considered as a new index for cold adaptation. Ten male subjects were acclimated by water immersions (temperature 10-15 degrees C, 4 immersions/wk over 2 mo). Thermoregulatory responses before and after acclimation were tested by a standard cold test in a climatic chamber for 2 h at rest [dry bulb temperature (Tdb): 10 degrees C; relative humidity (rh): 25%]. After adaptation, four thermoregulatory modifications were observed: an increase in the delay for the onset of shivering (32.7 +/- 7.99 instead of 14.1 +/- 5.25 min); a decrease of body temperature levels for the onset of shivering [rectal temperature (Tre): 37.06 +/- 0.08 instead of 37.31 +/- 0.06 degrees C; mean skin temperature (Tsk): 24.83 +/- 0.56 instead of 26.86 +/- 0.46 degrees C; mean body temperature (Tb): 33.03 +/- 0.20 instead of 34.16 +/- 0.37 degrees C); a lower level of body temperatures in thermoneutrality (Tre = 37.16 +/- 0.08 instead of 37.39 +/- 0.06 degrees C; Tsk = 31.29 +/- 0.21 instead of 32.01 +/- 0.22 degrees C; Tb = 35.92 +/- 0.08 instead of 36.22 +/- 0.05 degrees C); a decrease of heat debt calculated from the difference between heat gains and heat losses (5.66 +/- 0.08 instead of 8.33 +/- 0.38 kJ/kg). The different types of cold adaptation observed are related to the physical characteristics of the subjects (percent body fat content) and the level of physical fitness (VO2max).(ABSTRACT TRUNCATED AT 250 WORDS)     

Responses of plasma human atrial natriuretic factor to high intensity submaximal exercise in the heat

No data exists regarding responses of human atrial natriuretic factor (ANF) to exercise in the heat. The purpose of this study was to examine the responses of plasma ANF to high intensity submaximal (71% +/- 0.9 VO2max) exercise in the heat over an eight day acclimation period. Fourteen healthy males volunteered to participate in the study. Subjects performed intermittent exercises on a treadmill (0% grade) during 50 min of each 100 min trial in an environmental chamber maintained at 41.2 +/- 0.5 degrees C, 39.0 +/- 1.7% relative humidity. Blood was obtained from an antecubital vein after standing 20 min in the heat prior to exercise, and immediately after exercise. Measures were compared on days 1, 4 and 8. ANF did not change pre- to post-exercise nor did it change over the eight day heat acclimation period despite other heat acclimation adaptations. Conversely, plasma aldosterone (ALDO), renin activity (PRA) and cortisol (COR) all increased (p less than 0.05) pre- to post-exercise on each day but again no changes were observed over the eight day period. These data support that ANF may not increase when ALDO and PRA increases are observed.     

Changes in thermal insulation during underwater exercise in Korean female wet-suit divers

The present work was undertaken to examine the effect of wet suits on the pattern of heat exchange during immersion in cold water. Four Korean women divers wearing wet suits were immersed to the neck in water of critical temperature (Tcw) while resting for 3 h or exercising (2-3 met on a bicycle ergometer) for 2 h. During immersion both rectal (Tre) and skin temperatures and O2 consumption (VO2) were measured, from which heat production (M = 4.83 VO2), skin heat loss (Hsk = 0.92 M +/- heat store change based on delta Tre), and thermal insulation were calculated. The average Tcw of the subjects with wet suits was 16.5 +/- 1.2 degrees C (SE), which was 12.3 degrees C lower than that of the same subjects with swim suits (28.8 +/- 0.4 degrees C). During the 3rd h of immersion, Tre and mean skin temperatures (Tsk) averaged 37.3 +/- 0.1 and 28.0 +/- 0.5 degrees C, and skin heat loss per unit surface area 42.3 +/- 2.66 kcal X m-2 X h. The calculated body insulation [Ibody = Tre - Tsk/Hsk] and the total shell insulation [Itotal = (Tre - TW)/Hsk] were 0.23 +/- 0.02 and 0.5 +/- 0.04 degrees C X kcal-1 X m2 X h, respectively. During immersion exercise, both Itotal and Ibody declined exponentially as the exercise intensity increased. Surprisingly, the insulation due to wet suit (Isuit = Itotal - Ibody) also decreased with exercise intensity, from 0.28 degrees C X kcal-1 X m2 X h at rest to 0.12 degrees C X kcal-1 X m2 X h at exercise levels of 2-3 met.(ABSTRACT TRUNCATED AT 250 WORDS)     

Atrial natriuretic peptide inhibits compensatory responses when cardiac performance is depressed.

We tested the hypothesis that the atrial natriuretic peptide (ANP) mediated decrease in baroreceptor sensitivity that is seen in normal rats is more pronounced in a state of depressed cardiac performance. Holtzman rats (n = 15) were injected with Adriamycin (1 mg/kg i.p. 3 times/week for 8-10 weeks). Control rats (n = 17) were injected with 0.9% saline. Experiments were done in conscious animals that had been catheterized for i.v. infusions and for measurement of arterial blood pressure (ABP) and heart rate (HR). ANP (250 ng.kg-1.min-1) or saline vehicle was infused i.v. Graded periodic bolus injections of phenylephrine or sodium nitroprusside were given to assess baroreceptor sensitivity (beats.min-1.mmHg-1) up to 60 mmHg (1 mmHg = 133.3 Pa) above and below resting ABP. The following day the experiment was repeated with the ANP-vehicle regimen reversed. Finally, the rats were anesthetized and the rate of left ventricular pressure increase (dP/dt) was measured. Data evaluation included calculation of least squares linear regression slopes of peak delta HR vs. peak delta ABP, applying corrections for experimental errors in both the dependent and independent variables. Adriamycin rats (A) did not differ significantly from control rats (C) with respect to either initial ABP (A = 105 +/- 5; C = 100 +/- 3; mean mmHg +/- SEM) or initial HR (335 +/- 9 vs. 312 +/- 13 beats.min-1). However, their indices of cardiac performance were significantly depressed.(ABSTRACT TRUNCATED AT 250 WORDS)