Linearity and temperature control of the Fleisch pneumotachograph

We have investigated the optimal thermal conditions of a Fleisch no. 4 pneumotachograph (PT) necessary for recording maximal forced expiratory maneuvers (MFEM). Our PT assembly was tested with a computer-driven pump and found to be linear up to 14 l/s. Thermocouples (TC) were placed in a peripheral, mid, and a central capillary of the PT. Stable temperature control and consistent PT calibration were best obtained by proportional thermostatic control via the peripheral TC. When the PT was heated to 35 degrees C or above, expirations from either the pump (air at 33 degrees C saturated) or a subject cooled the PT, thus affecting its response. With the PT heated to 30 degrees C, repeated blows caused little change in PT temperature, with no evidence of condensation, thus indicating optimal thermal conditions for recording MFEM.     

Brain and abdominal temperatures at fatigue in rats exercising in the heat

We measured brain and abdominal temperatures ineight male Sprague-Dawley rats (350-450 g) exercising voluntarilyto a point of fatigue in two hot environments. Rats exercised, at thesame time of the day, in three different trials, in random order: rest 23°C, exercise 33°C; rest 23°C, exercise 38°C; and rest38°C, exercise 38°C. Running time to fatigue was 29.4 ± 5.9 (SD), 22.1 ± 3.7, and 14.3 ± 2.9 min for the three trials,respectively. Abdominal temperatures, measured withintraperitoneal radiotelemeters, at fatigue in the three trials (39.9 ± 0.3, 39.9 ± 0.3, and 39.8 ± 0.3°C, respectively) werenot significantly different from each other. Corresponding braintemperatures, measured with thermocouples in the hypothalamic region(40.2 ± 0.4, 40.2 ± 0.4, and 40.1 ± 0.4°C), also didnot differ. Our results are consistent with the concept that there is acritical level of body temperature beyond which animals will notcontinue to exercise voluntarily in the heat. Also, in our study, braintemperature was higher than abdominal temperature throughout exercise;that is, selective brain cooling did not occur when body temperaturewas below the level limiting exercise.

     

Effect of heat stress on glucose kinetics during exercise

Hargreaves, Mark, Damien Angus, Kirsten Howlett, Nelly MarmyConus, and Mark Febbraio. Effect of heat stress on glucose kinetics during exercise. J. Appl.Physiol. 81(4): 1594-1597, 1996.To identify themechanism underlying the exaggerated hyperglycemia during exercise inthe heat, six trained men were studied during 40 min of cyclingexercise at a workload requiring 65% peak pulmonary oxygen uptake(O_{2 peak}) on twooccasions at least 1 wk apart. On one occasion, the ambient temperaturewas 20°C [control (Con)], whereas on the other, it was40°C [high temperature (HT)]. Rates ofglucose appearance and disappearance were measured by using a primedcontinuous infusion of[6,6-²H]glucose. Nodifferences in oxygen uptake during exercise were observed betweentrials. After 40 min of exercise, heart rate, rectal temperature,respiratory exchange ratio, and plasma lactate were all higher in HTcompared with Con (P < 0.05). Plasmaglucose levels were similar at rest (Con, 4.54 ± 0.19 mmol/l; HT,4.81 ± 0.19 mmol/l) but increased to a greater extent duringexercise in HT (6.96 ± 0.16) compared with Con (5.45 ± 0.18;P < 0.05). This was the result of ahigher glucose rate of appearance in HT during the last 30 min ofexercise. In contrast, the glucose rate of disappearance and metabolicclearance rate were not different at any time point during exercise.Plasma catecholamines were higher after 10 and 40 min of exercise in HTcompared with Con (P < 0.05),whereas plasma glucagon, cortisol, and growth hormone were higher in HTafter 40 min. These results indicate that the hyperglycemia observedduring exercise in the heat is caused by an increase in liver glucoseoutput without any change in whole body glucoseutilization.

     

Heat stroke: opioid-mediated mechanisms

Romanovsky, Andrej A., and Clark M. Blatteis. Heatstroke: opioid-mediated mechanisms. J. Appl.Physiol. 81(6): 2565-2570, 1996.In our previousstudy in guinea pigs, intensive and prolonged intraperitoneal heating(IPH) caused heat stroke characterized by high mortality andaccompanied by two paradoxical phenomena: ear skin vasoconstriction ata high body temperature (T_b)(hyperthermia-induced vasoconstriction) and a post-IPHT_b fall at an ambient temperature (T_a) below thermoneutrality(hyperthermia-induced hypothermia). In this study, we tested thehypothesis that the mechanisms of the two phenomena involve endogenousopioid agonists. Experiments were conducted in 24 unanesthetized,lightly restrained guinea pigs, each chronically implanted with anintraperitoneal thermode and intrahypothalamic thermocouple. Thethermoregulatory effects of a wide-spectrum opioid-receptor antagonist,naltrexone (NTX; 50 or 0 µmol/kg sc), were studied in IPH-inducedheat stroke and under normal conditions. IPH was accomplished byperfusing (50 ml/min; 80 min) water (45°C) through the thermode.T_a was maintained at ~24°C.Skin vasodilation occurred at the onset of IPH but later changed tovasoconstriction despite high T_band continuing IPH. IPH-induced hyperthermia (1.8 ± 0.1°C) was followed by a post-IPH T_b fall (5.1 ± 0.7°C; calculated for the survivors only). The 48-h mortality ratewas 50%. NTX prevented the hyperthermia-induced vasoconstriction andattenuated the hyperthermia-induced hypothermia (1.8 ± 0.4°C). None of the NTX-treated animals died. The effects of NTX onT_b regulation under normalconditions were minor. These results indicate that the phenomena ofboth hyperthermia-induced vasoconstriction and hyperthermia-inducedhypothermia are opioid dependent. The latter is speculated to reflectopioid-mediated inhibition of metabolism; the former is thought toresult from opioid-induced hemodynamic alterations. Because bothphenomena did not occur in the NTX-treated survivors, the skinvasoconstriction at high T_b andthe posthyperthermia T_b fall maybe viewed as markers of the severity of heat stroke. It is suggestedthat opioid antagonists may have therapeutic potential in heat-induceddisorders.

     

Inhibition of shivering increases core temperature afterdrop and attenuates rewarming in hypothermic humans

Giesbrecht, Gordon G., M. S. L. Goheen, C. E. Johnston, G. P. Kenny, Gerald K. Bristow, and John S. Hayward. Inhibition ofshivering increases core temperature afterdrop and attenuates rewarmingin hypothermic humans. J. Appl.Physiol. 83(5): 1630-1634, 1997.During severehypothermia, shivering is absent. To simulate severe hypothermia,shivering in eight mildly hypothermic subjects was inhibited withmeperidine (1.5 mg/kg). Subjects were cooled twice (meperidine andcontrol trials) in 8°C water to a core temperature of 35.9 ± 0.5 (SD) °C, dried, and then placed in sleeping bags. Meperidinecaused a 3.2-fold increase in core temperature afterdrop (1.1 ± 0.6 vs. 0.4 ± 0.2°C), a 4.3-fold increase in afterdrop duration(89.4 ± 31.4 vs. 20.9 ± 5.7 min), and a 37% decrease inrewarming rate (1.2 ± 0.5 vs. 1.9 ± 0.9°C/h).Meperidine inhibited overt shivering. Oxygen consumption, minuteventilation, and heart rate decreased after meperidine injection butsubsequently returned toward preinjection values after 45 minpostimmersion. This was likely due to the increased thermoregulatorydrive with the greater afterdrop and the short half-life ofmeperidine. These results demonstrate the effectiveness of shiveringheat production in attenuating the postcooling afterdrop of coretemperature and potentiating core rewarming. The meperidine protocolmay be valuable for comparing the efficacy of various hypothermiarewarming methods in the absence of shivering.

     

Hypoxia, temperature, and pH/CO2 effects on respiratory discharge from a turtle brain stem preparation

Johnson, Stephen M., Rebecca A. Johnson, and Gordon S. Mitchell. Hypoxia, temperature, andpH/CO₂ effects on respiratory discharge from a turtle brain stem preparation. J. Appl. Physiol. 84(2): 649-660, 1998.An in vitrobrain stem preparation from adult turtles (Chrysemyspicta) was used to examine the effects of anoxia andincreased temperature and pH/CO₂on respiration-related motor output. At pH ~7.45, hypoglossal (XII)nerve roots produced patterns of rhythmic bursts (peaks) of discharge(0.74 ± 0.07 peaks/min, 10.0 ± 0.6 s duration) that werequantitatively similar to literature reports of respiratory activity inconscious, vagotomized turtles. Respiratory discharge was stable for 6 h at 22°C; at 32°C, peak amplitude and frequency progressivelyand reversibly decreased with time. Two hours of hypoxia had no effecton respiratory discharge. Acutely increasing bath temperature from 22 to 32°C decreased episode and peak duration and increased peakfrequency. Changes in pH/CO₂increased peak frequency from zero at pH 8.00-8.10 to maxima of0.81 ± 0.01 and 1.44 ± 0.02 peaks/min at 22°C (pH 7.32) and32°C (pH 7.46), respectively;pH/CO₂ sensitivity was similar atboth temperatures. We conclude that1) insensitivity to hypoxiaindicates that rhythmic discharge does not reflect gasping behavior,2) increased temperature altersrespiratory discharge, and 3)central pH/CO₂ sensitivity isunaffected by temperature in this preparation (i.e.,Q₁₀ ~1.0).

     

Heat acclimation does not modify autonomic responses to core cooling and the skin thermal comfort zone

Exercise heat acclimation (HA) is known to magnify the sweating response by virtue of a lower threshold as well as increased gain and maximal capacity of sweating. However, HA has been shown to potentiate the shivering response in a cold-air environment. We investigated whether HA would alter heat loss and heat production responses during water immersion. Twelve healthy male participants underwent a 10-day HA protocol comprising daily 90-min controlled-hyperthermia (target rectal temperature, T_re 38.5 °C) exercise sessions. Preceding and following HA, the participants performed a maximal exercise test in thermoneutral conditions (ambient temperature 23 °C, relative humidity 50%) and were, following exercise, immersed in 28 °C water for 60 min. Thermal comfort zone (TCZ) was also assessed with participants regulating the temperature of a water-perfused suit during heating and cooling. Baseline pre-immersion T_re was similar pre- and post-HA (pre: 38.33 ± 0.33 °C vs post: 38.12 ± 0.36 °C, p = 0.092). The T_re cooling rate was identical pre-to post-HA (−0.03 ± 0.01 °C·min⁻¹, p = 0.31), as was the vasomotor response reflected in the forearm-fingertip temperature difference. Shivering thresholds (p = 0.43) and gains (p = 0.61) were not affected by HA. TCZ was established at similar temperatures, with the magnitude in regulated water temperature being 7.6 (16.3) °C pre-HA and 5.1 (24.7) °C post-HA (p = 0.65). The present findings suggest that heat production and heat loss responses during whole body cooling as well as the skin thermal comfort zone remained unaltered by a controlled-hyperthermia HA protocol.     

Dietary Magnesium Sulfate Supplementation Protects Heat Stress-Induced Oxidative Damage by Restoring the Activities of Anti-oxidative Enzymes in Broilers

The purpose of this study was to investigate the effect of dietary magnesium sulfate supplementation on heat stress-induced oxidative damage in broilers. One hundred twenty 14-day-old broilers were randomly assigned into four treatment groups with three replicates of ten birds each. The broilers were reared under normal ambient temperature (24 ± 1°C) fed with a basal (control) diet or reared under high ambient temperature (35 ± 1°C between 1000 and 1800 h, 8 h each day) fed with a basal diet supplemented with magnesium sulfate (0, 2.5 or 5.0 mg/kg of diet) from 14 to 42 days of age. Growth performance and oxidative damage were evaluated in each treatment group. Our results demonstrated that dietary magnesium sulfate supplementation significantly prevented heat stress-induced oxidative damage and improved growth performance in broilers compared with that of control. Mechanistically, this beneficial effect was mediated, at least partly, by restoring the activity of anti-oxidative enzymes. This finding suggests that magnesium sulfate supplementation might be a potential strategy to attenuate heat stress-induced detrimental effects in broilers raised in summer season or tropical areas.     

Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise

González-Alonso, José, RicardoMora-Rodríguez, Paul R. Below, and Edward F. Coyle.Dehydration markedly impairs cardiovascular function inhyperthermic endurance athletes during exercise. J. Appl. Physiol. 82(4): 1229-1236, 1997.Weidentified the cardiovascular stress encountered by superimposingdehydration on hyperthermia during exercise in the heat and themechanisms contributing to the dehydration-mediated stroke volume (SV)reduction. Fifteen endurance-trained cyclists [maximalO₂ consumption(O_{2 max}) = 4.5 l/min] exercised in the heat for 100-120 min and either became dehydrated by 4% body weight or remained euhydrated by drinkingfluids. Measurements were made after they continued exercise at 71%O_{2 max} for 30 minwhile 1) euhydrated with anesophageal temperature (T_es) of38.1-38.3°C (control); 2)euhydrated and hyperthermic (39.3°C);3) dehydrated and hyperthermic withskin temperature (T_sk) of34°C; 4) dehydrated withT_es of 38.1°C and T_sk of 21°C; and5) condition4 followed by restored blood volume. Compared withcontrol, hyperthermia (1°C T_esincrease) and dehydration (4% body weight loss) each separatelylowered SV 7-8% (11 ± 3 ml/beat;P < 0.05) and increased heart ratesufficiently to prevent significant declines in cardiac output.However, when dehydration was superimposed on hyperthermia, thereductions in SV were significantly (P < 0.05) greater (26 ± 3 ml/beat), and cardiac output declined 13% (2.8 ± 0.3 l/min). Furthermore, mean arterialpressure declined 5 ± 2%, and systemic vascular resistanceincreased 10 ± 3% (both P < 0.05). When hyperthermia wasprevented, all of the decline in SV with dehydration was due to reducedblood volume (~200 ml). These results demonstrate that thesuperimposition of dehydration on hyperthermia during exercise in theheat causes an inability to maintain cardiac output and blood pressurethat makes the dehydrated athlete less able to cope with hyperthermia.

     

Studies of the effect of environmental factors on the rotifer predator–prey system in freshwater

The aim of this work is to evaluate the effect of environmental factors: temperature and photoperiod on the zooplankton predator–prey system. Rotifers, an important and cosmopolitan group of zooplankton in freshwater, were used in our study. We investigated the effect of temperature (20, 23, and 30°C) and of photoperiod (L:D = 12:0 and 0:12) on the predatory rotifer Asplanchna brightwelli consuming rotifer Brachionus calyciflorus as prey. Under A. brightwelli predation, populations of B. calyciflorus prey were consumed more slowly at 20 ± 1 and 30 ± 1°C as compared to 23 ± 1°C. Prey consumption by A. brightwelli increased from 0.63 ± 0.09 ind. predator⁻¹ at 20°C to a peak of 1.22 ± 0.12 ind. predator⁻¹ at 23°C, then decreased significantly to 0.93 ± 0.14 ind. predator⁻¹ at 30 ± 1°C. In addition, predation responded to temperature changing sensitively and rapidly. Statistical analysis showed that the prey consumption were significant different under altered temperature periods during 12 h. Photoperiod also significantly influenced the rate of A. brighwelli predation. B. calyciflorus suffered less predation in darkness than in light. The rate of prey consumption in light (1.06 ind. predator⁻¹) was twice the average of that in darkness (0.51 ind. predator⁻¹). Furthermore, predation rate varied under changing photoperiod but predators moved back into the light did not resume their original consumption rate. Our results demonstrate that whether the predation in rotifer successfully or not is strongly influenced by temperature and photoperiod.     

Comparison of thermoregulatory responses to heat between Malaysian and Japanese males during leg immersion

The objective of this study was to investigate thermoregulatory responses to heat in tropical (Malaysian) and temperate (Japanese) natives, during 60 min of passive heating. Ten Japanese (mean ages: 20.8 ± 0.9 years) and ten Malaysian males (mean ages: 22.3 ± 1.6 years) with matched morphological characteristics and physical fitness participated in this study. Passive heating was induced through leg immersion in hot water (42°C) for 60 min under conditions of 28°C air temperature and 50% RH. Local sweat rate on the forehead and thigh were significantly lower in Malaysians during leg immersion, but no significant differences in total sweat rate were observed between Malaysians (86.3 ± 11.8 g m⁻² h⁻¹) and Japanese (83.2 ± 6.4  g m⁻² h⁻¹) after leg immersion. In addition, Malaysians displayed a smaller rise in rectal temperature (0.3 ± 0.1°C) than Japanese (0.7 ± 0.1°C) during leg immersion, with a greater increase in hand skin temperature. Skin blood flow was significantly lower on the forehead and forearm in Malaysians during leg immersion. No significant different in mean skin temperature during leg immersion was observed between the two groups. These findings indicated that regional differences in body sweating distribution might exist between Malaysians and Japanese during heat exposure, with more uniform distribution of local sweat rate over the whole body among tropical Malaysians. Altogether, Malaysians appear to display enhanced efficiency of thermal sweating and thermoregulatory responses in dissipating heat loss during heat loading. Thermoregulatory differences between tropical and temperate natives in this study can be interpreted as a result of heat adaptations to physiological function.     

Augmentation of exercise-induced muscle sympathetic nerve activity during muscle heating

Ray, Chester A., and Kathryn H. Gracey. Augmentation ofexercise-induced muscle sympathetic nerve activity during muscle heating. J. Appl. Physiol. 82(6):1719-1725, 1997.The muscle metabo- and mechanoreflexes have beenshown to increase muscle sympathetic nerve activity (MSNA) duringexercise. Group III and IV muscle afferents, which are believed tomediate this response, have been shown to be thermosensitive inanimals. The purpose of the present study was to evaluate the effect ofmuscle temperature on MSNA responses during exercise. Eleven subjectsperformed ischemic isometric handgrip at 30% of maximal voluntarycontraction to fatigue, followed by 2 min of postexercise muscleischemia (PEMI), with and without local heating of the forearm. Localheating of the forearm increased forearm muscle temperature from 34.4 ± 0.2 to 38.9 ± 0.3°C(P = 0.001). Diastolic andmean arterial pressures were augmented during exercise in the heat.MSNA responses were greater during ischemic handgrip with local heatingcompared with control (no heating) after the first 30 s. MSNA responsesat fatigue were greater during local heating. MSNA increased by 16 ± 2 and 20 ± 2 bursts per 30 s for control and heating,respectively (P = 0.03). Whenexpressed as a percent change in total activity (total burstamplitude), MSNA increased 531 ± 159 and 941 ± 237% forcontrol and heating, respectively (P = 0.001). However, MSNA was not different during PEMI between trials.This finding suggests that the augmentation of MSNA during exercisewith heat was due to the stimulation of mechanically sensitive muscleafferents. These results suggest that heat sensitizes skeletal muscleafferents during muscle contraction in humans and may play a role inthe regulation of MSNA during exercise.

     

Predicting military working dog core temperature during exertional heat strain: Validation of a Canine Thermal Model

Military working dogs (MWDs) operate under a wide range of conditions, including hot environments. Predicting how long a MWD can safely work without overheating is important for both health and performance. A Canine Thermal Model (CTM) was developed to predict core temperature (Tc) of MWDs. The CTM calculates heat storage from the balance of heat production from metabolism and heat exchange with the environment. Inputs to the CTM are: meteorological conditions (ambient temperature, relative humidity, solar radiation and wind speed), physical characteristics of the dog (mass, length), and metabolic activity (MET level, estimated from accelerometer data). The CTM was validated against Tc measured in 23 MWDs during training sessions (11.6 ± 5.0 min (mean ± standard deviation), range 4–26 min) in October (24 °C, 52% RH), March (14 °C, 74% RH), or August (28 °C, 64% RH), and 24 kennel MWDs during a standard exercise walk (11.4 ± 3.3 min, range 5.6–18 min) in July (26 °C, 77% RH). The CTM was considered acceptable if predicted Tc was within ±0.5 °C of measured Tc at the end of exercise. Compared to Tc at the end of training sessions (39.8 ± 0.6 °C, range 38.4–41.1 °C) and exercise walks (40.0 ± 0.7 °C, range 38.9–41.4 °C), the CTM-predicted Tc was within ±0.5 °C for 71 of 84 cases (85%) and 19 of 24 cases (79%), respectively. The mean difference between CTM-predicted and measured final Tc during training was -0.04 ± 0.43 °C, with 80 of 84 cases (95%) within the range of ±2 SD (Bland Altman comparison). During exercise walks the mean difference was -0.15 °C ± 0.57, with 23 of 24 cases (96%) within ±2 SD. These results support the use of the CTM to predict Tc of MWDs for the types of physical activities described above.     

Modification of active cutaneous vasodilation by oral contraceptive hormones

Charkoudian, Nisha, and John M. Johnson. Modificationof active cutaneous vasodilation by oral contraceptive hormones. J. Appl. Physiol. 83(6):2012-2018, 1997.It is not clear whether the alteredthermoregulatory reflex control of the cutaneous circulation seen amongphases of the menstrual cycle also occurs with the synthetic estrogenand progesterone in oral contraceptive pills and whether any suchmodifications include altered control of the cutaneous activevasodilator system. To address these questions, we conducted controlledwhole body heating experiments in seven women at the end of the thirdweek of hormone pills (HH) and at the end of the week of placebo/nopills (LH). A water-perfused suit was used to control body temperature.Laser Doppler flowmetry was used to monitor cutaneous blood flow at acontrol site and at a site at which noradrenergic vasoconstrictorcontrol had been eliminated by iontophoresis of bretylium (BT),isolating the active cutaneous vasodilator system. The oral temperature(T_or) thresholds for cutaneousvasodilation were higher in HH at both control [37.09 ± 0.12 vs. 36.83 ± 0.07°C (LH), P < 0.01] and BT-treated [37.19 ± 0.05 vs. 36.88 ± 0.12°C (LH), P < 0.01]sites. The T_or threshold forsweating was similarly shifted (HH: 37.15 ± 0.11°C vs. LH: 36.94 ± 0.11°C, P < 0.01). Arightward shift in the relationship of heart rate toT_or was seen in HH. Thesensitivities (slopes of the responses vs.T_or) did not differstatistically between phases. The similar threshold shifts at controland BT-treated sites suggest that the hormones shift the function ofthe active vasodilator system to higher internal temperatures. Thesimilarity of the shifts among thermoregulatory effectors suggests acentrally mediated action of these hormones.

     

Thermal and metabolic responses to cold-water immersion at knee, hip, and shoulder levels

Lee, Dae T., Michael M. Toner, William D. McArdle, IoannisS. Vrabas, and Kent B. Pandolf. Thermal and metabolic responses tocold-water immersion at knee, hip, and shoulder levels.J. Appl. Physiol. 82(5):1523-1530, 1997.To examine the effect of cold-water immersion atdifferent depths on thermal and metabolic responses, eight men (25 yrold, 16% body fat) attempted 12 tests: immersed to the knee (K), hip(H), and shoulder (Sh) in 15 and 25°C water during both rest (R) orleg cycling [35% peak oxygen uptake; (E)] for up to 135 min. At 15°C, rectal (T_re)and esophageal temperatures(T_es) between R and E were notdifferent in Sh and H groups (P > 0.05), whereas both in K group were higher during E than R(P < 0.05). At 25°C,T_re was higher(P < 0.05) during E than R at alldepths, whereas T_es during E washigher than during R in H and K groups.T_re remained at control levels inK-E at 15°C, K-E at 25°C, and in H-E groups at 25°C,whereas T_es remained unchanged inK-E at 15°C, in K-R at 15°C, and in all 25°C conditions (P > 0.05). During R and E, themagnitude of T_re change wasgreater (P < 0.05) than themagnitude of T_es change in Sh andH groups, whereas it was not different in the K group(P > 0.05). Total heat flow wasprogressive with water depth. During R at 15 and 25°C, heatproduction was not increased in K and H groups from control level(P > 0.05) but it did increase in Shgroup (P < 0.05). The increase inheat production during E compared with R was smaller(P < 0.05) in Sh (121 ± 7 W/m² at 15°C and 97 ± 6 W/m² at 25°C) than in H (156 ± 6 and 126 ± 5 W/m²,respectively) and K groups (155 ± 4 and 165 ± 6 W/m², respectively). These datasuggest that T_re andT_es respond differently duringpartial cold-water immersion. In addition, water levels above knee in15°C and above hip in 25°C cause depression of internal temperatures mainly due to insufficient heat production offsetting heatloss even during light exercise.

     

Posthemorrhagic antipyresis: what stage of fever genesis is affected?

Romanovsky, Andrej A., and Yelena K. Karman.Posthemorrhagic antipyresis: what stage of fever genesis isaffected? J. Appl. Physiol. 83(2):359-365, 1997.It has been shown that hemorrhage leads to adecreased thermal responsiveness to lipopolysaccharide (LPS). The aimof this study was to clarify what stage of fever genesis[production of endogenous pyrogens such as interleukin-1 (IL-1),increase of the prostaglandin E₂(PGE₂) concentration in braintissue, activation of cold-defense effectors] is deficient inposthemorrhagic antipyresis. In adult rabbits, we evaluated the effectof acute hemorrhage (15 ml/kg) on the rectal temperature (T_re) responses to LPS fromSalmonella typhi (200 ng/kg iv),ethanol-purified preparation of homologous IL-1 (1 ml from 3.5 × 10⁷ cells, 1.5 ml/kg iv), andPGE₂ (1 µg,intracisternal injection). The effect of hemorrhage onT_re was also studied in afebrilerabbits, both at thermoneutrality (23°C) and during ramp cooling(to 7°C). The hemorrhage strongly attenuated the biphasicLPS-induced fever (a T_re rise of0.4 ± 0.1 instead of 1.2 ± 0.2°C at the time of the secondpeak), the monophasic T_re responseto IL-1 (by ~0.5°C for over 1-5 h postinjection), and thePGE₂-induced hyperthermia (0.4 ± 0.1 vs. 0.9 ± 0.1°C, maxima). In afebrileanimals, the hemorrhage neither affectedT_re at thermoneutrality norchanged the T_re response to coldexposure. The data suggest that neither insufficiency of cold-defenseeffectors nor lack of endogenous mediators of fever (IL-1,PGE₂) can be the only or eventhe major cause of posthemorrhagic antipyresis. Wespeculate that fever genesis is altered at a stage occurring after theintrabrain PGE₂ level is increasedbut before thermoeffectors are activated.

     

Reflex tracheal smooth muscle contraction and bronchial vasodilation evoked by airway cooling in dogs

Pisarri, Thomas E., and Gordon G. Giesbrecht. Reflextracheal smooth muscle contraction and bronchial vasodilation evoked byairway cooling in dogs. J. Appl.Physiol. 82(5): 1566-1572, 1997.Coolingintrathoracic airways by filling the pulmonary circulation with coldblood alters pulmonary mechanoreceptor discharge. To determine whetherthis initiates reflex changes that could contribute to airwayobstruction, we measured changes in tracheal smooth muscle tension andbronchial arterial flow evoked by cooling. In ninechloralose-anesthetized open-chest dogs, the right pulmonary artery wascannulated and perfused; the left lung, ventilated separately, providedgas exchange. With the right lung phasically ventilated, filling theright pulmonary circulation with 5°C blood increased smooth muscletension in an innervated upper tracheal segment by 23 ± 6 (SE) gfrom a baseline of 75 g. Contraction began within 10 s of injection andwas maximal at ~30s. The response was abolished by cervical vagotomy.Bronchial arterial flow increased from 8 ± 1 to 13 ± 2 ml/min, withlittle effect on arterial blood pressure. The time course wassimilar to that of the tracheal response. This response was greatlyattenuated after cervical vagotomy. Blood at 20°C also increasedtracheal smooth muscle tension and bronchial flow, whereas 37°Cblood had little effect. The results suggest that alteration ofairway mechanoreceptor discharge by cooling can initiate reflexes thatcontribute to airway obstruction.

     

Hypohydration and thermoregulation in cold air

O'Brien, Catherine, Andrew J. Young, and Michael N. Sawka.Hypohydration and thermoregulation in cold air.J. Appl. Physiol. 84(1): 185-189, 1998.This study examined the effects of hypohydration onthermoregulation during cold exposure. In addition, the independentinfluences of hypohydration-associated hypertonicity and hypovolemiawere investigated. Nine male volunteers were monitored for 30 min at25°C, then for 120 min at 7°C, under three counterbalancedconditions: euhydration (Eu), hypertonic hypohydration (HH), andisotonic hypohydration (IH). Hypohydration was achieved 12 h beforecold exposure by inducing sweating (HH) or by ingestion of furosemide(IH). Body weight decrease (4.1 ± 0.2%) caused by hypohydrationwas similar for HH and IH, but differences(P < 0.05) were found between HH andIH in plasma osmolality (292 ± 1 vs. 284 ± 1 mosmol/kgH₂O) andplasma volume reduction (8 ± 2 vs. 18 ± 3%).Heat debt (349 ± 14 among) did not differ(P > 0.05) among trials. Mean skintemperature decreased throughout cold exposure during Eu but plateauedafter 90 min during HH and IH. Forearm-fingertemperature gradient tended (P = 0.06)to be greater during Eu (10.0 ± 0.7°C) than during HH or IH(8.9 ± 0.7°C). This suggests weaker vasoconstrictor tone duringhypohydration than during Eu. Final mean skin temperature was higherfor HH than for Eu or IH (23.5 ± 0.3, 22.6 ± 0.4, and 22.9 ± 0.3°C, respectively), and insulation was lower on HH than onIH (0.13 ± 0.01 vs. 0.15 ± 0.01°C · W¹ · m²,respectively), but not with Eu (0.14 ± 0.01°C · W¹ · m²).This provides some evidence that hypertonicity impairs the vasoconstrictor response to cold. Although mild hypohydration did notaffect body heat balance during 2-h whole body exposure to moderatecold, hypohydration-associated hypertonicity may have subtle effects onvasoconstriction that could become important during a more severe coldexposure.

     

Thermal and circulatory responses during exercise: effects of hypohydration, dehydration, and water intake

Armstrong, Lawrence E., Carl M. Maresh, Catherine V. Gabaree, Jay R. Hoffman, Stavros A. Kavouras, Robert W. Kenefick, JohnW. Castellani, and Lynn E. Ahlquist. Thermal and circulatory responses during exercise: effects of hypohydration, dehydration, andwater intake. J. Appl. Physiol. 82(6):2028-2035, 1997.This investigation examined the distinct andinteractive effects of initial hydration state, exercise-induceddehydration, and water rehydration in a hot environment. On fouroccasions, 10 men performed a 90-min heat stress test (treadmillwalking at 5.6 km/h, 5% grade, 33°C, 56% relative humidity).These heat stress tests differed in pretest hydration [2euhydrated (EU) and 2 hypohydrated (HY) trials] and water intakeduring exercise [2 water ad libitum (W) and 2 no water (NW)trials]. HY + NW indicated greater physiological strain than allother trials (P < 0.05-0.001)in heart rate, plasma osmolality(P_osm), sweat sensitivity(g / °C · min), and rectal temperature.Unexpectedly, final HY + W and EU + W responses for rectal temperature,heart rate, and P_osm were similar,despite the initial 3.9 ± 0.2% hypohydration in HY + W. Weconcluded that differences in pretestP_osm (295 ± 7 and 287 ± 5 mosmol/kg for HY + W and EU + W, respectively) resulted in greaterwater consumption (1.65 and 0.31 liter for HY + W and EU + W,respectively), no voluntary dehydration (0.9% body mass increase), andattenuated thermal and circulatory strain during HY + W.

     

Do fluctuating temperature environments elevate coral thermal tolerance?

In reef corals, much research has focused on the capacity of corals to acclimatize and/or adapt to different thermal environments, but the majority of work has focused on distinctions in mean temperature. Across small spatial scales, distinctions in daily temperature variation are common, but the role of such environmental variation in setting coral thermal tolerances has received little attention. Here, we take advantage of back-reef pools in American Samoa that differ in thermal variation to investigate the effects of thermally fluctuating environments on coral thermal tolerance. We experimentally heat-stressed Acropora hyacinthus from a thermally moderate lagoon pool (temp range 26.5–33.3°C) and from a more thermally variable pool that naturally experiences 2–3 h high temperature events during summer low tides (temp range 25.0–35°C). We compared mortality and photosystem II photochemical efficiency of colony fragments exposed to ambient temperatures (median: 28.0°C) or elevated temperatures (median: 31.5°C). In the heated treatment, moderate pool corals showed nearly 50% mortality whether they hosted heat-sensitive (49.2 ± 6.5% SE; C2) or heat-resistant (47.0 ± 11.2% SE; D) symbionts. However, variable pool corals, all of which hosted heat-resistant symbionts, survived well, showing low mortalities (16.6 ± 8.8% SE) statistically indistinguishable from controls held at ambient temperatures (5.1–8.3 ± 3.3–8.3% SE). Similarly, moderate pool corals hosting heat-sensitive algae showed rapid rates of decline in algal photosystem II photochemical efficiency in the elevated temperature treatment (slope = −0.04 day⁻¹ ± 0.007 SE); moderate pool corals hosting heat-resistant algae showed intermediate levels of decline (slope = −0.039 day⁻¹ ± 0.007 SE); and variable pool corals hosting heat-resistant algae showed the least decline (slope = −0.028 day⁻¹ ± 0.004 SE). High gene flow among pools suggests that these differences probably reflect coral acclimatization not local genetic adaptation. Our results suggest that previous exposure to an environmentally variable microhabitat adds substantially to coral–algal thermal tolerance, beyond that provided by heat-resistant symbionts alone.