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The purpose of this study was to compare smokers and non-smokers' sudomotor and cutaneous vascular responses to whole-body passive heat stress. 9 regularly smoking (SMK; 29±9 y; 10±6 cigarettes/day) and 13 non-smoking (N-SMK; 27±8 y) males were passively heated until core temperature (TC) increased 1.5°C from baseline. Forearm local sweat rate via ventilated-capsule (LSR), sweat gland activation (SGA), sweat gland output (SGO), and cutaneous vasomotor activity via Laser Doppler flowmetry (CVC) were measured as mean body temperature increased (ΔTb) during passive heating using a water-perfused suit. Compared to N-SMK, SMK had a smaller ΔTb at the onset of sweating (0.52±0.19 versus 0.35±0.14°C, respectively; p=0.03) and cutaneous vasodilation (0.61±0.21 versus 0.31±0.12°C, respectively; p<0.01). Increases in LSR and CVC per °C ΔTb (i.e., sensitivity) were similar in N-SMK and SMK (LSR: 0.63±0.21 versus 0.60±0.40 versus Δmg/²/min/°C ΔTb, respectively, p=0.81; CVC: 82.5±46.2 versus 58.9±23.3 Δ%max/°C ΔTb, respectively; p=0.19). However, plateau in LSR during whole-body heating was higher in N-SMK versus SMK (1.00±0.13 versus 0.79±0.26 mg·cm²·min; p=0.03), which was likely a result of higher SGO (8.94±3.99 versus 5.94±3.49 μg·gland-1·min-1, respectively; p=0.08) and not number of SGA (104±7 versus 121±9 glands/cm², respectively; p=0.58). During whole-body passive heat stress, smokers had an earlier onset for forearm sweating and cutaneous vasodilation, but a lower local sweat rate that was likely due to lower sweat output per gland. These data provide insight to local (i.e. forearm) thermoregulatory responses of young smokers during uncompensatory whole-body passive heat stress. [ABSTRACT FROM AUTHOR]

Human and animal studies on sleep-disordered breathing and respiratory regulation show that the effects of sex hormones are heterogeneous. Because neonatal stress results in sex-specific disruption of the respiratory control in adult rats, we postulate that it might affect respiratory control modulation induced by ovarian steroids in female rats. The hypoxic ventilatory response (HVR) of adult female rats exposed to neonatal maternal separation (NMS) is 30% smaller than controls (24), but consequences of NMS on respiratory control in aging female rats are unknown. To address this issue, whole body plethysmography was used to evaluate the impact of NMS on the HVR (12% O2, 20 min) of middle-aged (MA; 57 wk old) female rats. Pups subjected to NMS were placed in an incubator 3 h/day for 10 consecutive days (P3 to P12). Controls were undisturbed. To determine whether the effects were related to sexual hormone decline or aging per se, experiments were repeated on bilaterally ovariectomized (OVX) young (12 wk old) adult female rats. OVX and MA both reduced the HVR significantly in control rats but had little effect on the HVR of NMS females. OVX (but not aging) reduced the anapyrexic response in both control and NMS animals. These results show that hormonal decline decreases the HVR of control animals, while leaving that of NMS female animals unaffected. This suggests that neonatal stress alters the interaction between sex hormone regulation and the development of body temperature, hormonal, and ventilatory responses to hypoxia. [ABSTRACT FROM AUTHOR]

Maintenance of body water homeostasis is critical for preventing hyperthermia, because evaporative cooling is the most efficient means of dissipating excess body heat. Water homeostasis is achieved by regulation of water intake and water loss by the kidneys. The former is achieved by sensations of thirst that motivate water acquisition, whereas the latter is regulated by the antidiuretic action of vasopressin. Vasopressin secretion and thirst are stimulated by increases in the osmolality of the extracellular fluid as well as decreases in blood pressure and/or blood volume, signals that are precipitated by water depletion associated with the excess evaporative water loss required to prevent hyperthermia. In addition, they are stimulated by increases in body temperature. The sites and molecular mechanisms involved in integrating thermal and osmotic regulation of thirst and vasopressin secretion are reviewed here with a focus on the role of the thermal and mechanosensitive transient receptor potential-vanilloid (TRPV) family of ion channels. [ABSTRACT FROM AUTHOR]

Increasing body core temperature reflexly decreases renal blood flow (RBF), and the hypothalamic paraventricular nucleus (PVN) plays an essential role in this response. ANG II in the brain is involved in the cardiovascular responses to hyperthermia, and ANG II receptors are highly concentrated in the PVN. The present study investigated whether ANG II in the PVN contributes to the cardiovascular responses elicited by hyperthermia. Rats anesthetized with urethane (1-1.4 g/kg iv) were microinjected bilaterally into the PVN (100 nl/side) with saline (n = 5) or losartan (1 nmol/100 nl) (n = 7), an AT1 receptor antagonist. Body core temperature was then elevated from 37°C to 41°C and blood pressure (BP), heart rate (HR), RBF, and renal vascular conductance (RVC) were monitored. In separate groups losartan (n = 4) or saline (n = 4) was microinjected into the PVN, but body core temperature was not elevated. Increasing body core temperature in control rats elicited significant decreases in RBF (-48 ± 5% from a resting level of 14.3 ± 1.4 ml/min) and MVC (-40 ± 4% from a resting level of 0.128 ± 0.013 ml/min·mmHg), and these effects were entirely prevented by pretreatment with losartan. In rats in which body core temperature was not altered, losartan microinjected into the PVN had no significant effects on these variables. The results suggest that endogenous ANG II acts on AT1 receptors in the PVN to mediate the reduction in RBF induced by hyperthermia. [ABSTRACT FROM AUTHOR]

Neonatal rodents deficient in medullary serotonin neurons have respiratory instability and enhanced spontaneous bradycardias. This study asks if, in Pet-1-/- mice over development: 1) the respiratory instability leads to hypoxia; 2) greater bradycardia is related to the degree of hypoxia or concomitant hypopnea; and 3) hyperthermia exacerbates bradycardias. Pet-1+/+, Pet-1+/-, and Pet-1-/- mice [postnatal days (P) 4-5, P11-12, P14-15] were held at normal body temperature (Tb) and were then made 2°C hypo- and hyperthermic. Using a pneumotach-mask system with ECG, we measured heart rate, metabolic rate (Vo2), and ventilation. We also calculated indexes for apnea-induced hypoxia (total hypoxia: apnea incidence × O2 consumed during apnea = μ1·g-1·min-1) and bradycardia (total bradycardia: bradycardia incidence × magnitude = beats missed/min). Resting heart rate was significantly lower in all Pet-1-/- animals, irrespective of Tb. At P4-5, Pet-1-/- animals had approximately four- to eightfold greater total bradycardia (P < 0.001), owing to an approximately two- to threefold increase in bradycardia magnitude and a near doubling in bradycardia incidence. Pet-1-/- animals had a significantly reduced Vo2 at all Tb; thus there was no genotype effect on total hypoxia. At P11-12, total bradycardia was nearly threefold greater in hyperthermic Pet-1-/- animals compared with controls (P < 0.01). In both genotypes, bradycardia magnitude was positively related to the degree of hypopnea (P = 0.02), but there was no genotype effect on degree of hypopnea or total hypoxia. At P14-15, genotype had no effect on total bradycardia, but Pet-1-/- animals had up to seven times more total hypoxia (P < 0.001), owing to longer and more frequent apneas and a normalized Vo2. We infer from these data that 1) Pet-1-/- neonates are probably not hypoxic from respiratory dysfunction until P14-15; 2) neither apnea-related hypoxia nor greater hypopnea contribute to the en- hanced bradycardias of Pet-1-/- neonates from approximately P4 to approximately P12; and 3) an enhancement of a temperature-sensitive reflex may contribute to the greater bradycardia in hyperthermic Pet-1-/- animals at approximately P12. [ABSTRACT FROM AUTHOR]

In mammals, procedures such as handling, restraint, or exposure to open spaces induces an increase in body temperature (Tb). The increase in temperature shares some characteristics with pyrogen-induced fever and so is often called "stress fever." Birds also respond to acute handling with a stress fever, which may confound thermoregulatory studies that involve animal restraint. We have measured the Tb responses of Pekin ducks on days when they were restrained and compared them to days when the birds remained unrestrained. Restraint induced a 0.5°C increase in Tb that was sustained for the entire 8 h of restraint. To determine whether the restraint-induced increase in Tb is mediated by prostaglandins (PGs) we compared the Tb responses during restraint after intraperitoneal injection with saline to the responses during restraint after injection with diclofenac sodium (15 mg/kg). There was no difference in response, suggesting that restraint affects Tb by a PG-independent mechanism. We also compared the Tb response to intramuscular injection of lipopolysaccharide (LPS; 100 μg/kg), a bacterial pyrogen, when the ducks were restrained or unrestrained. Despite Tb being higher at the time of LPS injection when the ducks were restrained, the maximum temperature reached after LPS injection was higher, and the period that Tb remained elevated was longer when the ducks were unrestrained. We conclude that restraint should be considered as a potential confounder in thermoregulatory studies in birds and presumably other species too. [ABSTRACT FROM AUTHOR]

This study examined whether the exercise-increased extracellular heat shock protein 72 (eHsp72) levels in rats was associated with body temperature elevation during exercise. In all, 26 female Sprague-Dawley rats (3 mo old) were assigned randomly to control (CON; n = 8), exercise under warm temperature (WEx; n = 9), or exercise under cold temperature (CEx; n = 9). The WEx and CEx were trained at 25°C or 4°C, respectively, for nine days using a treadmill. Before and immediately after the final exercise bout, the colonic temperatures were measured as an index of body temperature. The animals were subsequently anesthetized, and blood samples were collected and centrifuged. Plasma samples were obtained to assess their eHsp72 levels. Only the colonic temperature in WEx was increased significantly (P < 0.05) by exercise. The eHsp72 level in WEx was significantly higher (P < 0.05) than that of either the CON or CEx. However, no significant difference was found between CON and CEx. Regression analyses revealed that the eHsp72 level increased as a function of the body temperature. In another experiment, the eHsp72 level of animals with body temperature that was passively elevated through similar kinetics to those of the exercise was studied. Results of this experiment showed that mere body temperature elevation was insufficient to induce eHsp72 responses. Collectively, our results suggest that body temperature elevation during exercise is important for induction of exercise-increased eHsp72. In addition, the possible role of body temperature elevation is displayed when the exercise stressor is combined with it. [ABSTRACT FROM AUTHOR]

Although light is considered the primary entrainer of circadian rhythms in humans, nonphotic stimuli, including exercise and melatonin also phase shift the biological clock. Furthermore, in birds and nonhuman mammals, auditory stimuli are effective zeitgebers. This study investigated whether a nonphotic auditory stimulus phase shifts human circadian rhythms. Ten subjects (5 men and 5 women, ages 18–72, mean age ± SD, 44.7 ± 21.4 yr) completed two 4-day laboratory sessions in constant dim light (<20 lux). They received two consecutive presentations of either a 2-h auditory or control stimulus from 0100 to 0300 on the second and third nights (presentation order of the stimulus and control was counterbalanced). Core body temperature (CBT) was collected and stored in 2-rain bins throughout the study and salivary melatonin was obtained every 30 min from 1900 to 2330 on the baseline and poststimulus/postcontrol nights. Circadian phase of dim light melatonin onset (DLMO) and of CBT minimum, before and after auditory or control presentation was assessed. The auditory stimulus produced significantly larger phase delays of the circadian melatonin (mean ± SD, -0.89 ± 0.40 h vs. -0.27 ± 0.16 h) and CBT (-1.16 ± 0.69 h vs. -0.44 ± 0.27 h) rhythms than the control. Phase changes for the two circadian rhythms also positively correlated, indicating direct effects on the biological clock. In addition, the auditory stimulus significantly decreased fatigue compared with the control. This study is the first demonstration of an auditory stimulus phase-shifting circadian rhythms in humans, with shifts similar in size and direction to those of other nonphotic stimuli presented during the early subjective night. This novel stimulus may be a useful countermeasure to facilitate circadian adaptation after transmeridian travel or shift work. [ABSTRACT FROM AUTHOR]

Sleep occurs in close relation to changes in body temperature. Both the monophasic sleep period in humans and the polyphasic sleep periods in rodents tend to be initiated when core body temperature is declining. This decline is mainly due to an increase in skin blood flow and consequently skin warming and heat loss. We have proposed that these intrinsically occurring changes in core and skin temperatures could modulate neuronal activity in sleep-regulating brain areas (Van Someren EJW, Chronobiol Int 17:313-54, 2000). We here provide results compatible with this hypothesis. We obtained 144 sleep-onset latencies while directly manipulating core and skin temperatures within the comfortable range in eight healthy subjects under controlled conditions. The induction of a proximal skin temperature difference of only 0.78 ± 0.03°C (mean ± SE) around a mean of 35.13 ± 0.11°C changed sleep-onset latency by 26%, i.e., by 3.09 minutes [95% confidence interval (CI), 1.91 to 4.28] around a mean of 11.85 mm (CI, 9.74 to 14.41), with faster sleep onsets when the proximal skin was warmed. The reduction in sleep-onset latency occurred despite a small but significant decrease in subjective comfort during proximal skin warming. The induction of changes in core temperature (δ = 0.20 ± 0.02°C) and distal skin temperature (δ = 0.74 ± 0.05°C) were ineffective. Previous studies have demonstrated correlations between skin temperature and sleep-onset latency. Also, sleep disruption by ambient temperatures that activate thermoregulatory defense mechanisms has been shown. The present study is the first to experimentally demonstrate a causal contribution to sleep-onset latency of skin temperature manipulations within the normal nocturnal fluctuation range. Circadian and sleep-appetitive behavior-induced variations in skin temperature might act as an input signal to sleep-regulating systems. [ABSTRACT FROM AUTHOR]

Studies using core temperature (Tc) have contributed greatly to theoretical explanations of drug tolerance and its relation- ship to key features of addiction, including dependence, withdrawal, and relapse. Many theoretical accounts of tolerance propose that a given drug-induced psychobiological disturbance elicits opponent responses that contribute to tolerance development. This proposal and its theoretical extensions (e.g., conditioning as a mechanism of chronic tolerance) have been inferred from dependent variables, such as Tc, which represent the summation of multiple underlying determinants. Direct measurements of determinants could increase the understanding of opponent processes in tolerance, dependence, and withdrawal. The proximal determinants of Tc are metabolic heat production (HP) and heat loss (HL). We developed a novel system for simultaneously quantifying HP (indirect calorimetry), HL (direct gradient layer calorimetry), and Tc (telemetry) during steady-state administrations of nitrous oxide (N2O), an inhalant with abuse potential that has been previously used to study acute and chronic tolerance development to its hypothermia-inducing property. Rats were administered 60% N2O (n = 18) or placebo gas (n = 16) for 5 h after a 2-h placebo baseline exposure. On average, N2O rapidly but transiently lowered HP and increased HL, each by ∼16% (P < 0,001). On average, rats reestablished and maintained thermal equilibrium (HP = HL) at a hypothermic Tc (-1.6°C). However, some rats entered positive heat balance (HP > HL) after becoming hypothermic such that acute tolerance developed, i.e., Tc rose despite continued drug administration. This work is the first to directly quantify the thermal determinants of Tc during administration of a drug of abuse and establishes a new paradigm for studying opponent processes involved in acute and chronic hypothermic tolerance development. [ABSTRACT FROM AUTHOR]

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

Romanovsky, Andrej A. Do fever and anapyrexia exist? Analysis of set point-based definitions. Am J Physiol Regul Integr Comp Physiol 287: R992-R995, 2004. First published June 24, 2004; 10.1152/ ajpregu.00068.2004.—Fever and anapyrexia are the most studied thermoregulatory responses. They are defined as a body temperature (Tb) increase and decrease, respectively, occurring because of a shift in the set point (SP) and characterized by active defense of the new Tb. Although models of Tb control with a single SP (whether obvious or hidden) have been criticized, the SP-based definitions have remained unchallenged. In this article, the SP-based definitions of fever and anapyrexia were subjected to two tests. In test 1, they were compared with experimental data on changes in thresholds for activation of different thermoeffectors. Changes in thresholds were found compatible with an SP increase in some (but not all) cases of fever. In all cases of what is called anapyrexia, its mechanism (dissociation of thresholds of different effectors) was found incompatible with a decrease in a single SP. In test 2, experimental data on the dependence of Tb on ambient temperature (Ta) were analyzed. It was found that the febrile level of Tb is defended in some (but not all) cases. However, strong dependence on Ta was found in all cases of anapyrexia, which agrees with threshold dissociation but not with a decrease of the SP. It is concluded that fever (as defined) has only limited experimental support, whereas anapyrexia (as defined) does not exist. Two solutions are offered. A palliative is to accept that SP-based terms (anapyrexia, cryexia, regulated hypothermia, and such) are inadequate and should be abandoned. A radical solution is to transform all definitions based on comparing Tb with the SP into definitions based on balancing active and passive processes of Tb control. [ABSTRACT FROM AUTHOR]

Mphahlele, Noko R., Andrea Fuller, Joachim Roth, and Peter R. Kamerman. Body temperature, behavior, and plasma cortisol changes induced by chronic infusion of Staphylococcus aureus in goats. Am J Physiol Regul Integr Comp Physio1 287: R863-R869, 2004. First published June 24, 2004; 10.1152/ajpregu.00064.2004.—Most ex- perimentally induced fevers are acute, usually lasting ∼6–12 h, and thus do not mimic chronic natural fevers, which can extend over several days or more. To produce a model of chronic natural fever, we infused eight goats (Capra hircus) intravenously with 2 ml of 2 × 1011 cell walls of Staphylococcus aureus (S. aureus) for 6 days using osmotic infusion pumps (10 μ1/h) while measuring changes in body temperature, behavior, and plasma cortisol concentration. Seven control animals were infused with sterile saline. Abdominal temperature- sensitive data loggers and osmotic infusion pumps were implanted under halothane anesthesia. To compare our new model with existing models of experimental fever, we also administered 2-ml bolus intravenous injections of 2 × 1011 S. aureus cell walls, 0.1 μg/kg lipopolysaccharide (Escherichia coli, serotype 011l:B4), and sterile saline in random order to six other goats. Bolus injection of lipopoly- saccharide and S. aureus induced typical acute phase responses, characterized by fevers lasting ∼6 h, sickness behavior, and increased plasma cortisol concentration. Infusion of S. aureus evoked prolonged fevers, which lasted for ∼3 days, starting on day 4 of infusion (ANOVA, P < 0.05), and did not disrupt the normal circadian rhythm of body temperature. However, pyrogen infusion did not cause plasma cortisol concentration to rise (ANOVA, P > 0.05) or the expression of sickness behavior. In conclusion, infusion of S. aureus produced a fever response resembling that of sustained natural fevers but did not elicit the cortisol and behavioral responses that often are described clinically and during short-term experimental fevers. [ABSTRACT FROM AUTHOR]

Presents a study that characterized the relationship between ingestive behavior and body temperature during natural ovarian cycle in normotensive and hypertensive rats. Analysis of body temperature during ovarian cycle; Evaluation of food and water intake; Examination of ingestive behavior during ovarian cycle.

Studies the effects of repeated ethanol intake over a 24-hour period which is a pattern of consumption closer to the clinical condition of chronic alcoholism. Comparison of body temperature during alcohol session at night and at daytime; Percent reduction in the amplitude of the circadian temperature rhythm between the control and alcohol session; Number of volunteers who experienced a hyperthermic effect at night.

Focuses on a study which examined the body temperature and metabolic rate of hybernating Alpine marmots (Marmota marmota). Methodology of the study; Results and discussion; Conclusion.

Presents a study on the age-dependent role of adenosine in mediating the regulated decrease in core temperature that occurs in newborn and older guinea pigs during exposure to acute hypoxemia. Effect of the intraperitoneal administration of aminophylline on oxygen consumption; Methodology of the study; Results and discussion; Summary.

Presents information on a study which determined how the core temperature level and sweating response to heat load differs in humans acclimated to heat given daily at a fixed time. Methods of the study; Data analysis and statistics; Discussion of results.

Explores the hypothesis which states that a reduction in resting rectal temperature (Tre) is associated with the attenuation in in the rise of core temperature during heat exposure following acclimation to humid heat. Methodology used in the study; Factors which influenced the changes in core temperature of the subjects; Effects of humid heat acclimation in temperature change.

Clarifies the role of the serotonergic system in mediating interleukin-1 (IL-1) effects on sleep and temperature regulation. Induction of a biphasic increase in slow-wave sleep and an early increase in serotenergic metabolism by IL-1; Role of time course of the serotonergic activation in mediating Il-1 effects on sleep.

Studies the body temperature (Tb) and locomotor activity of Siberian hamsters. Extension of the light phase; Expression of free-running Tb rhythms; Changes in tau and phase of activity rhythms; Entrainment process in Siberian hamsters; Housing conditions.

Editorial. Comments on the historical significance of three papers on the hypothalamic control of body temperature previously published in several issues of the "American Journal of Physiology". "Thermoregulatory responses to hypothalamic cooling in unanesthetized dogs," by H.T. Hammel et al; "Temperature regulation by hypothalamic proportional control with an adjustable set point," by D.C. Jackson et al; "Some characteristics of temperature regulation in the unanesthetized dog," by B. Hellstrom et al.