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This study investigated whether the estimation error of volume-weighted mean body temperature ([DELTA][[bar.T].sub.b]) using changes in core and skin temperature can be accounted for using personal and environmental parameters. Whole body calorimetry was used to directly measure [DELTA][[bar.T].sub.b] in an Experimental group (EG) of 36 participants (24 males, 12 females) and a Validation group (VG) of 20 (9 males, 11 females) throughout 90 min of cycle ergometry at 40[degrees]C, 30% relative humidity (RH) (n = 9 EG, 5 VG); 30[degrees]C, 30% RH (n = 9 EG, 5 VG); 30[degrees]C, 60% RH (n = 9 EG, 5 VG); and 24[degrees]C, 30% RH (n = 9 EG, 5 VG). The core of the two-compartment thermometry model was represented by rectal temperature and the shell by a 12-point mean skin temperature ([DELTA][[bar.T].sub.sk]). The estimation error ([X.sub.o]) between [DELTA][[bar.T].sub.b] from calorimetry and [DELTA][[bar.T].sub.b] from thermometry using core/shell weightings of 0.66/0.34, 0.79/0.21, and 0.90/0.10 was calculated after 30, 60, and 90 min of exercise, respectively. The association between Xo and the individual variation in metabolic heat production (M - W), body surface area (BSA), body fat percentage (%fat), and body surface area-to-mass ratio (BSA/BM) as well as differences in environmental conditions (Oxford index) in the EG data were assessed using stepwise linear regression. At all time points and with all core/shell weightings tested, M - W, BSA, and Oxford index independently correlated significantly with the residual variance in [X.sub.o], but %fat and BSA/BM did not. The subsequent regression models were used to predict the thermometric estimation error ([X.sub.o-pred]) for each individual in the VG. The value estimated for [X.sub.o-pred] was then added to the [DELTA][[bar.T].sub.b] estimated using the two-compartment thermometry models yielding an adjusted estimation ([DELTA][[bar.T].sub.b_adj]) for the individuals in the VG. When comparing [DELTA][[bar.T].sub.b_adj] to the [DELTA][[bar.T].sub.b] derived from calorimetry in the VG, the best performing model used a core/shell weighting of 0.66/0.34 describing 74%, 84%, and 82% of the variation observed in [DELTA][[bar.T].sub.b] from calorimetry after 30, 60, and 90 min, respectively. body heat storage; calorimetry; core temperature; heat stress; skin temperature doi: 10.1152/ajpregu.00546.2009.

Behavioral and physiological rhythms can be entrained by daily restricted feeding (RF), indicating the existence of a food-entrainable oscillator (FEO). One manifestation of the presence of FEO is anticipatory activity to regularly scheduled feeding. In the present study, we tested if intact ghrelin signaling is required for FEO function by studying food anticipatory activity (FAA) in preproghrelin knockout (KO) and wild-type (WT) mice. Sleep-wake activity, locomotor activity, body temperature, food intake, and body weight were measured for 12 days in mice on a RF paradigm with food available only for 4 h daily during the light phase. On RF days 1-3, increases in arousal occurred. This response was significantly attenuated in preproghrelin KO mice. There were progressive changes in sleep architecture and body temperature during the subsequent nine RF days. Sleep increased at night and decreased during the light periods while the total daily amount of sleep remained at baseline levels in both KO and WT mice. Body temperature fell during the dark but was elevated during and after feeding in the light. In the premeal hours, anticipatory increases in body temperature, locomotor activity, and wakefulness were present from RF day 6 in both groups. Results indicate that the preproghrelin gene is not required for the manifestation of FAA but suggest a role for ghrelinergic mechanisms in food deprivation-induced arousal in mice. food-entrainable oscillator; food anticipatory activity; electro-encephalographic slow-wave activity; food deprivation; hypothermia doi: 10.1152/ajpregu.00557.2009

J Strength Cond Res 24(1): 68-73, 2010--The cold environments in which ice hockey players participate are counterintuitive to the predisposing factors of heat-and hypohydration-related illnesses. This population has received little consideration in hypohydration-related illness risk assessments. Protective equipment, multiple clothing layers, and performance intensity may predispose these athletes to significant decreases in hydration and increases in core temperature. The purpose of this study was to measure hydration status and gastrointestinal temperature ([T.sub.GI]) in male ice hockey players during practice sessions that focused on preseason skill development and cardiovascular conditioning. The study used a repeated measures design. Data were collected in a collegiate ice hockey rink (ambient temperature = 6.03 [+ or -] 1.65[degrees]C; relative humidity = 40.4 [+ or -] 11.89%). Seventeen ice hockey players (age = 20.6 [+ or -] 1.1, height = 180 [+ or -] 5 cm, mass = 85.04 [+ or -] 7.9 kg) volunteered for this study. Urine-specific gravity (USG) and body weight were measured before and after two 110-minute practice sessions. Urine reagent strips measured USG. Calibrated CorTemp (HQ, Inc., Palmetto, FL, USA) radio-frequency telemetered thermometers collected [T.sub.GI] before, during, and after two 110-minute practice sessions. Individual participant sweat rates were calculated. Data from both sessions were pooled. [T.sub.GI] (p < 0.0001), and USG (p < 0.0001) increased over the 110-minute session. Post-exercise body weight (83.9 [+ or -] 7.6 kg) was statistically lower (p < 0.001) than the pre-exercise weight (85.0 [+ or -] 7.9 kg). Sweat rates were calculated to be 0.83 [+ or -] 0.50 L x [h.sup.-1]. These male ice hockey players become hypohydrated during participation potentially predisposing them to dehydration-related illnesses. This change in hydration status resulted in a gastrointestinal temperature increase and significant weight loss during activity. Prevention and rehydration strategies such as those developed by the American College of Sports Medicine and National Athletic Trainers' Association should be implemented to reduce the possibility of heat-related illness for this population. KEY WORDS hydration status, sweat rate, prevention, urine-specific gravity

Cyclooxygenase-1 or -2--which one mediates lipopolysaccharide-induced hypothermia? Am J Physiol Regul Integr Comp Physio1297: R485--R494, 2009. First published June 10, 2009; doi: 10.1152/ajpregu.91026.2008.--Systemic inflammation is associated with either fever or hypothermia. Fever, a response to mild systemic inflammation, is mediated by cyclooxygenase (COX)-2 and not by COX-1. However, it is still disputed whether COX-2, COX-l, neither, or both mediate(s) responses to severe systemic inflammation, and, in particular, the hypothermic response. We compared the effects of SC-236 (COX-2 inhibitor) and SC-560 (COX-1 inhibitor) on the deep body temperature ([T.sub.b]) of rats injected with a lower (10 [micro]g/kg iv) or higher (1,000 [micro]g/kg iv) dose of LPS at different ambient temperatures ([T.sub.a]s). At a neutral [T.sub.a] (30[degrees]C), the rats responded to LPS with a polyphasic fever (lower dose) or a brief hypothermia followed by fever (higher dose). SC-236 (2.5 mg/kg iv) blocked the fever induced by either LPS dose, whereas SC-560 (5 mg/kg iv) altered neither the febrile response to the lower LPS dose nor the fever component of the response to the higher dose. However, SC-560 blocked the initial hypothermia caused by the higher LPS dose. At a subneutral [T.sub.a] (22[degrees]C), the rats responded to LPS with early (70-90 min, nadir) dose-dependent hypothermia. The hypothermic response to either dose was enhanced by SC-236 but blocked by SC-560. The hypothermic response to the higher LPS dose was associated with a fall in arterial blood pressure. This hypotensive response was attenuated by either SC-236 or SC-560. At the onset of LPS-induced hypothermia and hypotension, the functional activity of the COX-1 pathway (COX-1-mediated [PGE.sub.2] synthesis ex vivo) increased in the spleen but not liver, lung, kidney, or brain. The expression of splenic COX-1 was unaffected by LPS. We conclude that COX-1, but not COX-2, mediates LPS hypothermia, and that both COX isoforms are required for LPS hypotension. body temperature; thermoregulation; fever; inflammation

We have demonstrated that after intraperitoneal lipopolysaccharide (LPS) injection, old rats mount fevers similar to those of young rats at an ambient temperature (Ta) of 31[degrees]C, but not at 21[degrees]C. The same is true for intraperitoneal or intravenous IL-113 administration. The underlying mechanism responsible for blunted fever in old rats may be a deficiency in communication between the periphery and the brain. Possibly, peripheral cytokine actions are altered in old rats, such that the signal that reaches the brain is diminished. Here, we hypothesized that at standard laboratory temperatures, not enough 1L-1[beta] is reaching the brain for fever to occur and that a warmer Ta would increase the influx of IL-1[beta] into the brain, enabling old rats to generate fever. Young (3-5 mo) and old (23-29 mo) Long-Evans rats were maintained for 3 days at either Ta 21 or 31[degrees]C prior to intravenous injection with radiolabeled IL-1[beta] to measure passage across the blood-brain barrier. Young rats showed similar influx of IL-1[beta] into the brain at the two Tas, but old rats showed significant influx only at the warmer Ta. These data suggest that the lack of fever at a cool Ta may be due to a reduced influx of IL-1[beta] into the brain. aging; blood-brain-barrier; cytokine; ambient temperature

Recognition of temperature is a critical element of sensory perception and allows mammals to evaluate both their external environment and internal status. The respiratory epithelium is constantly exposed to the external environment, and prolonged inhalation of cold air is detrimental to human airways. However, the mechanisms responsible for adverse effects elicited by cold air on the human airways are poorly understood. Transient receptor potential melastatin family member 8 (TRPM8) is a well-established cold- and menthol-sensing cation channel. We recently discovered a functional cold- and menthol-sensing variant of the TRPM8 ion channel in human lung epithelial cells. The present study explores the hypothesis that this TRPM8 variant mediates airway cell inflammatory responses elicited by cold air/temperatures. Here, we show that activation of the TRPM8 variant in human lung epithelial cells leads to increased expression of several cytokine and chemokine genes, including IL-1[alpha], -1[beta], -4, -6, -8, and -13, granulocyte-macrophage colony-stimulating factor (GM-CSF), and TNF-[alpha]. Our results provide new insights into mechanisms that potentially control airway inflammation due to inhalation of cold air and suggest a possible role for the TRPM8 variant in the pathophysiology of asthma. transient receptor potential melastatin family member 8; menthol

The genes encoding prokineticin 2 polypeptide (Prok2) and its cognate receptor (Prokr2/ Gpcr7311) are widely expressed in both the suprachiasmatic nucleus and its hypothalamic targets, and this signaling pathway has been implicated in the circadian regulation of behavior and physiology. We have previously observed that the targeted null mutation of Prokr2 disrupts circadian coordination of cycles of locomotor activity and thermoregulation. We have now observed spontaneous but sporadic bouts of torpor in the majority of these transgenic mice lacking Prokr2 signaling. During these torpor bouts, which lasted for up to 8 h, body temperature and locomotor activity decreased markedly. Oxygen consumption and carbon dioxide production also decreased, and there was a decrease in respiratory quotient. These spontaneous torpor bouts generally began toward the end of the dark phase or in the early light phase when the mice were maintained on a 12:12-h light-dark cycle and persisted when mice were exposed to continuous darkness. Periods of food deprivation (16-24 h) induced a substantial decrease in body temperature in all mice, but the duration and depth of hypothermia was significantly greater in mice lacking Prokr2 signaling compared with heterozygous and wild-type littermates. Likewise, when tested in metabolic cages, food deprivation produced greater decreases in oxygen consumption and carbon dioxide production in the transgenic mice than controls. We conclude that Prokr2 signaling plays a role in hypothalamic regulation of energy balance, and loss of this pathway results in physiological and behavioral responses normally only detected when mice are in negative energy balance. metabolic rate; thermoregulation; CLAMS; radiotelemetry

Skin blood flow increases in response to local heat due to sensorineural and nitric oxide (NO)mediated dilation. It has been previously demonstrated that arteriolar dilation is inhibited with NO synthase (NOS) blockade. Flow, nonetheless, increases with local heat. This implies that the previously unexamined nonarteriolar responses play a significant role in modulating flow. We thus hypothesized that local heating induces capillary recruitment. We heated a portion (3 [cm.sup.2]) of the Pallid bat wing from 25[degrees]C to 37[degrees]C for 20 min, and measured changes in terminal feed arteriole (~25 [micro]m) diameter and blood velocity to calculate blood flow (n = 8). Arteriolar dilation was reduced with NOS and sensorineural blockade using a 1% (wt/vol) [N.sup.G]-nitro-L-arginine methyl ester (L-NAME) and 2% (wt/vol) lidocaine solution (n = 8). We also measured changes in the number of perfused capillaries, and the time precapillary sphincters were open with (n = 8) and without (n = 8) NOS plus sensorineural blockade. With heat, the total number of perfused capillaries increased 92.7 [+ or -] 17.9% (P = 0.011), and a similar increase occurred despite NOS plus sensorineural blockade 114.4 [+ or -] 30.0% (P = 0.014). Blockade eliminated arteriolar dilation (-4.5 [+ or -] 2.1%). With heat, the percent time precapillary sphincters remained open increased 32.3 [+ or -] 6.0% (P = 0.0006), and this increase occurred despite NOS plus sensorineural blockade (34.1 [+ or -] 5.8%, P = 0.0004). With heat, arteriolar blood flow increased (187.2 [+ or -] 28.5%, P = 0.00003), which was significantly attenuated with NOS plus sensorineural blockade (88.6 [+ or -] 37.2%, P = 0.04). Thus, capillary recruitment is a fundamental microvascular response to local heat, independent of arteriolar dilation and the well-documented sensorineural and NOS mechanisms mediating the response to local heat. microcirculation; precapillary sphincter; skin blood flow doi:10.1152/ajpregu.00873.2006

The way in which sustained attention and spatial attention are affected by mild body cooling was documented in a study undertaken to increase the understanding of thermal stress and cognition. It was observed that while spatial orienting was not affected by cooling, attentional processing was impaired by the distracting effects of cold.

Core body temperature (Tb) is influenced by many physiological factors, including behavioral state, locomotor activity, and biological rhythms. To determine the relative roles of these factors, we examined Tb in orexin knockout (KO) mice, which have a narcolepsy-like phenotype with severe sleep-wake fragmentation. Because orexin is released during wakefulness and is thought to promote heat production, we hypothesized that orexin KO mice would have lower Tb while awake. Surprisingly, Tb was the same in orexin KO mice and wild-type (WT) littermates during sustained wakefulness. Orexin KO mice had normal diurnal variations in Tb, but the ultradian rhythms of Tb, locomotor activity, and wakefulness were markedly reduced. During the first 15 min of spontaneous sleep, the Tb of WT mice decreased by 1.0[degrees]C, but Tb in orexin KO mice decreased only 0.4[degrees]C. Even during intense recovery sleep after 8 h of sleep deprivation, the Tb of orexin KO mice remained 0.7[degrees]C higher than in WT mice. This blunted fall in Tb during sleep may be due to inadequate activation of heat loss mechanisms or sustained activity in heat-generating systems. These observations reveal an unexpected role for orexin in thermoregulation. In addition, because heat loss is an essential aspect of sleep, the blunted fall in Tb of orexin KO mice may provide an explanation for the fragmented sleep of narcolepsy. hypocretin; narcolepsy; behavioral state; ultradian rhythm; thermogenesis doi:10.1152/ajpregu.00887.2005.

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 [+ or -] 0.03[degrees]C (mean [+ or -] SE) around a mean of 35.13 [+ or -] 0.11[degrees]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 min (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 ([delta] = 0.20 [+ or -] 0.02[degrees]C) and distal skin temperature ([delta] = 0.74 [+ or -] 0.05[degrees]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. sleep electroencephalogram; body and skin temperatures; thermoregulation; sleep-onset latency; circadian rhythms

Blood flow is redistributed from the viscera to the periphery during periods of heat stress to maximize heat loss. The heat-induced redistribution of blood flow is strongly influenced by nonthermal inputs such as hydration status. At present, little is known about where thermal and nonthermal information is integrated to generate an appropriate effector response. Recently, the periventricular tissue that surrounds the anteroventral third ventricle (AV3V) has been implicated in the integration of thermal and osmotic information. The purpose of the present study was to determine the effects of electrolytic lesions of the AV3V on the cardiovascular response to a passive heat stress in unanesthetized, free-moving male Sprague-Dawley rats. Core temperature was elevated at a constant rate of ~0.03[degrees]C/min in sham- and AV3V-lesion rats using an infrared heat lamp. Changes in mesenteric and hindquarter vascular resistance were determined using Doppler flow probes, and heat-induced salivation was estimated using the spit-print technique. The rise in mean arterial pressure (MAP), heart rate (HR), and mesenteric resistance in response to elevations in core temperature were all attenuated in AV3V-lesion rats; however, hindquarter resistance was unaffected. Heat-induced salivation was also diminished. In addition, AV3V-lesion rats were more affected by the novelty of the experimental environment, resulting in a higher basal core temperature, HR, and MAP. These results indicate that AV3V lesions disrupt the cardiovascular and salivatory response to a passive heat stress in rats and produce an exaggerated stress-induced fever triggered by a novel environment. thermoregulation; mesenteric resistance; Doppler flowmetry; salivation; novel environment

We investigated influences of the thermal environment on patterns of body temperature ([T.sub.b]), activity, and use of burrows during the active season in a population of free-living arctic ground squirrels (Spermophilus parryii). Arctic ground squirrels normally exhibited a daily 5[degree]C range in [T.sub.b], and had higher [T.sub.b] when above ground than when in burrows (P < 0.0001). This difference decreased as standard operative temperature ([T.sub.es] an index of environmental heat load) increased. Ground squirrels entered burrows more frequently on warmer compared to average or cooler days and when [T.sub.b] exceeded 39[degrees]C. On cool days with heavy precipitation, ground squirrels remained almost exclusively below ground, and peaks in [T.sub.b] were associated with brief aboveground forays. Time on the surface was maximal (about 80% between 0500 and 2200 h) at [T.sub.es] = 17-33[degrees]C and decreased proportionately with decreasing [T.sub.es] from 17[degrees]C to -2[degrees]C. Forty-six percent of variation in timing of presence above ground could be explained by a series of thermal and nonthermal variables related to environmental heat transfer. This suggests that diurnal activity patterns in this arctic environment with 24-h daylight result from a strategy that minimizes thermoregulatory costs. Key words: arctic ground squirrel, behavioral thermoregulation, body temperature, hyperthermia, multiple regression, Spermophilus parryii, standard operative temperature

In view of the potential involvement of peripherally synthesized, circulating amphipathic mediators [such as platelet-activating factor (PAF) and prostaglandin [E.sub.2]] in the systemic inflammatory response to lipopolysaccharide (LPS), we hypothesized that transport of amphipaths by albumin is essential for conveying peripheral inflammatory signals to the brain. Our first specific aim was to test this hypothesis by studying LPS-induced fever and hypothermia in Nagase analbuminemic rats (NAR). NAR from two different colonies and normalbuminemic Sprague-Dawley rats were preimplanted with jugular catheters, and their febrile responses to a mild dose of LPS (10 [micro]g/kg iv) at thermoneutrality and hypothermic responses to a high dose of LPS (500 [micro]g/kg iv) in the cold were studied. NAR of both colonies developed normal febrile and hypothermic responses, thus suggesting that transport of amphipathic mediators by albumin is not indispensable for LPS signaling. Although alternative carrier proteins [such as [[alpha].sub.1]-acid glycoprotein (AGP)] are known to assume transport functions of albumin in NAR, it is unknown whether inflammatory mediators are capable of inducing their actions when bound to alternative carriers. To test whether PAF, the most potent amphipathic pyrogen, causes fever when administered in an AGP-bound form was our second aim. Sprague-Dawley rats were preimplanted with jugular catheters, and their thermal responses to infusion of a 1:1 [PAF-AGP] complex (40 nmol/kg iv), AGP (40 nmol/kg iv), or various doses of free (aggregated) PAF were studied. The complex, but neither free PAF nor AGP, caused a high (~1.5[degrees]C) fever with a short ( systemic inflammation; fever; hypothermia; body temperature; platelet-activating factor; Nagase analbuminemic rats

The majority of information concerning the cardio-metabolic performance of varanids during exercise is limited to a few species at their preferred body temperature ([T.sub.b]) even though, being ectotherms, varanids naturally experience rather large changes in [T.sub.b]. Although it is well established that absolute aerobic scope declines with decreasing [T.sub.b], it is not known whether changes in cardiac output ([[??].sub.b]) and/or tissue oxygen extraction, ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.]), are in proportion to the rate of oxygen consumption ([[??]o.sub.2]). To test this, we studied six Rosenberg's goannas (Varanus rosenbergi) while at rest and while maximally exercising on a treadmill both at 25 and 36[degrees]C. During maximum exercise both at 25 and 36[degrees]C, mass-specific rate of oxygen consumption ([[??]o.sub.2kg]) increased with an absolute scope of 8.5 ml [min.sup.-1] [kg.sup.-1] and 15.7 ml [min.sup.-1] [kg.sup.-1], respectively. Interestingly, the factorial aerobic scope was temperature-independent and remained at 7.0 which, at each [T.sub.b], was primarily the result of an increase in [[??]b.sub.kg], governed by approximate twofold increases both in heart rate ([f.sub.H]) and cardiac stroke volume ([V.sub.Skg]). Both at 25[degrees]C and 36[degrees]C, the increase in [[??].sub.bkg] alone was not sufficient to provide all of the additional oxygen required to attain maximal [[??]o.sub.2kg], as indicated by a decrease in the blood convection requirement [[??].sub.bkg]/[[??]o.sub.2kg]; hence, there was a compensatory twofold increase in ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.]). Although associated with an increase in hemoglobin-oxygen affinity, a decrease in [T.sub.b] did not impair unloading of oxygen at the tissues and act to reduce ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.]); both [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.], and [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.] were maintained across [T.sub.b]. The change in [[??]o.sub.2kg] with [T.sub.b], therefore, is solely reliant on the thermal dependence of [[??].sub.bkg]. Maintaining a high factorial aerobic scope across a range of [T.sub.b] confers an advantage in that cooler animals can achieve higher absolute aerobic scopes and presumably improved aerobic performance than would otherwise be achievable. metabolic rate; Fick equation; exercise; cardiac output; oxygen consumption; heart rate; stroke volume; reptile; goanna; oxygen extraction.

Previous work indicates that sympathetic nerves participate in the vascular responses to direct cooling of the skin in humans. We evaluated this hypothesis further in a four-part series by measuring changes in cutaneous vascular conductance (CVC) from forearm skin locally cooled from 34 to 29[degrees]C for 30 min. In part 1. bretylium tosylate reversed the initial vasoconstriction (-14 [+ or -] 6.6% control CVC, first 5 rain) to one of vasodilation (+ 19.7 [+ or -] 7.7%) but did not affect the response at 30 rain (-30.6 [+ or -] 9% control, -38.9 [+ or -] 6.9% bretylium: both P < 0.05, P > 0.05 between treatments). In part 2, yohimbine and propranolol (YP) also reversed the initial vasoconstriction (14.3 [+ or -] 4.2% control) to vasodilation (+ 26.3 [+ or -] 12.1% YP), without a significant effect on the 30-rain response (-26.7 [+ or -] 6.1% YP, -43.2 [+ or -] 6.5% control: both P < 0.05, P > 0.05 between sites). In part 3, the NPY Y1 receptor antagonist BIBP 3226 had no significant effect on either phase of vasoconstriction (P > 0.05 between sites both times). In part 4, sensory nerve blockade by anesthetic cream (Em1a) also reversed the initial vasoconstriction (-20.1 [+ or -] 6.4% control) to one of vasodilation (+213.4 [+ or -] 87.0% Em1a), whereas the final levels did not differ significantly (37.7 [+ or -] 10.1% control, -37.2 [+ or -] 8.7% Em1a: both P < 0.05, P > 0.05 between treatments). These results indicate that local cooling causes cold-sensitive afferents to activate sympathetic nerves to release norepinephrine, leading to a local cutaneous vasoconstriction that masks a nonneurogenic vasodilation. Later, a vasoconstriction develops with or without functional sensory or sympathetic nerves. human: peripheral circulation: local control of blood flow: skin circulation: microdialysis; iontophoresis: neuropeptide Y; norepinephrine: axon reflex

The circadian rhythm of the body core temperature ([T.sub.c]) and the effects of changes in ambient temperatures on the homeostasis of [T.sub.c] in Otsuka Long Evans Tokushima Fatty (OLETF) rats, which are naturally occurring cholecystokinin (CCK)-A receptor (CCK-AR) gene knockout (-/-) rats, were examined. In addition, the peripheral responses to warming or cooling of the preoptic and anterior hypothalamic region (PO/AH) were determined. The circadian rhythm of [T.sub.c] in OLETF rats was similar to that in Long-Evans Tokushima (LETO) rats; this rhythm was characterized by a higher [T.sub.c] during the dark period and a lower [T.sub.c] during the light period. When the ambient temperature was changed within the limits of 0[degrees]C to 30[degrees]C, the changes in [T.sub.c] of LETO rats were associated with the changes in ambient temperature, whereas those in OLETF rats were dissociated from the temperature changes. The OLETF rats showed a large hysteresis. The peripheral responses to warming or cooling of PO/AH, including shivering of the neck muscle and changes in skin temperature of the tail and footpad, were similar in OLETF and LETO rats. To confirm the role of CCK-AR in the regulation of body temperature, the values of [T.sub.c] in the CCK-AR(-/-) mice were compared with those in CCK-B receptor (CCK-BR) (-/-), CCK-AR(-/-)BR (-/-), and wild-type mice. In the mice, the circadian rhythms of [T.sub.c] were the same, regardless of the genotype. Mice without CCK-AR showed larger hysteresis than mice with CCK-AR. From these results, we conclude that the lack of CCK-AR causes homeostasis of [T.sub.c] in rats and mice to deteriorate. knockout mice

To investigate the mechanism involved in the reduction of body core temperature ([T.sub.core]) during fasting in rats, which is selective in the light phase, we measured [T.sub.core], surface temperature, and oxygen consumption rate in fed control animals and in fasted animals on day 3 of fasting and day 4 of recovery at an ambient temperature ([T.sub.a]) of 23[degrees]C by biotelemetry, infrared thermography, and indirect calorimetry, respectively. On the fasting day, 1) [T.sub.core] in the light phase decreased (P < 0.05) from the control; however, [T.sub.core] in the dark phase was unchanged, 2) tail temperature fell from the control (P < 0.05, from 30.7 [+ or -] 0.1 to 23.9 [+ or -] 0.1[degrees]C in the dark phase and from 29.4 [+ or -] 0.1 to 25.2 [+ or -] 0.2[degrees]C in the light phase), 3) oxygen consumption rate decreased from the control (P < 0.05, from 24.37 [+ or -] 1.06 to 16.24 [+ or -] 0.69 ml*[min.sup.-1]* kg body [wt.sup.-0.75] in the dark phase and from 18.91 [+ or -] 0.64 to 14.00 [+ or -] 0.41 ml*[min.sup.-1]*kg body [wt.sup.-0.75] in the light phase). All these values returned to the control levels on the recovery day. The results suggest that, in the fasting condition, [T. sub.core] in the dark phase was maintained by suppression of the heat loss mechanism, despite the reduction of metabolic heat production. In contrast, the response was weakened in the light phase, decreasing [T.sub.core] greatly. Moreover, the change in the regulation of tail blood flow was a likely mechanism to suppress heat loss. core temperature; oxygen consumption; heat loss mechanism

The relationship between mammalian basal metabolic rate (BMR, ml of [O.sub.2] per h) and body mass (M, g) has been the subject of regular investigation for over a century. Typically, the relationship is expressed as an allometric equation of the form BMR = a[M.sup.b]. The scaling exponent (b) is a point of contention throughout this body of literature, within which arguments for and against geometric (b = 2/3) and quarter-power (b = 3/4) scaling are made and rebutted. Recently, interest in the topic has been revived by published explanations for quarter-power scaling based on fractal nutrient supply networks and four-dimensional biology. Here, a new analysis of the allometry of mammalian BMR that accounts for variation associated with body temperature, digestive state, and phylogeny finds no support for a metabolic scaling exponent of 3/4. Data encompassing five orders of magnitude variation in M and featuring 619 species from 19 mammalian orders show that BMR [varies] [M.sup.2/3].

Three experiments were conducted to evaluate the effect of different management strategies on body temperature of feedlot steers finished in the summer months. In Exp. 1, 24 crossbred steers were chosen to assess the effect of altered feed intake and feeding time on tympanic temperature (TT) response. Managed feeding (MF) treatments were applied for 22 d only and provided 1) ad libitum access to feed at 0800 (ADLIB), 2) feed at 1600 with amount adjusted so that no feed was available at 0800 (BKMGT), 3) feed at 1600 at 85% of predicted ad libitum levels (LIMFD). During heat stress conditions on d 20 to 22 of MF, LIMFD and BKMGT had lower (P < 0.05) TT than ADLIB from 2100 through 2400. A carryover effect of limit-feeding was evident during a severe heat episode (d 36 to 38) with LIMFD steers having lower (P < 0.05) TT than ADLIB. In Exp. 2, TT were obtained from 24 crossbred steers assigned to three treatments, consisting of no water application (CON), water applied to feedlot mound surfaces from 1000 to 1200 (AM) or 1400 to 1600 (PM). From 2200 to 0900 and 1200 to 1400, steers assigned to morning sprinkling treatment had lower (P < 0.05) TT than steers assigned to afternoon sprinkling treatment. In Exp. 3, 24 steers were utilized in a 2 x 2 factorial arrangement of treatments with factors of feeding time [0800 (AMF) and 1400 (PMF)] and sprinkling (WET and DRY). Tympanic temperatures were monitored under hot environmental conditions on d 30 to 32 and 61 to 62. A feeding time x sprinkling interaction (P < 0.001) was evident on d 30 to 32, although AMF/DRY steers had the highest (P < 0.05) TT. On d 61 to 62, TT of PMF steers was higher (P < 0.05) than AMF between 1500 to 1800. Use of sprinklers can effectively reduce TT of feedlot cattle, whereas shifting to an afternoon vs morning feeding time was most beneficial when bunks were empty several hours prior to feeding. Key Words: Body Temperature, Cattle, Feedlots, Heat Stress, Management

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.sub.db]), 2) to specify alterations in activity, HR, and [T.sub.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.sub.db] was assessed using radiotelemeters implanted in AKR/J (n = 17) inbred mice at ~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 ([+ or -] SE) life span of surgically treated animals did not differ from untreated controls (319 [+ or -] 12 vs. 319 [+ or -] 14 days). Cardiac and thermal stability were characterized by a circadian periodicity, which oscillated around stable daily averages of 640 [+ or -] 14 beats/min in HR and 36.6 [+ or -] 0.1[degrees]C in [T.sub.db]. Stable HR and [T.sub.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.sub.db] of ~29 and ~13% lower (i.e., 456 [+ or -] 22 beats/min and 31.7 [+ or -] 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. survivorship curves; circadian regulation of body temperature; circadian regulation of heart rate; homeostasis; homeostatic instability

The exposure of a subject in the far field of radiofrequency sources operating in the 10-900-MHz range has been studied. The electromagnetic field inside an anatomical heterogeneous model of the human body has been computed by using the finite-difference time-domain method; the corresponding temperature increase has been evaluated through an explicit finite-difference formulation of the bio-heat equation. The thermal model used, which takes into account the thermoregulatory system of the human body, has been validated through a comparison with experimental data. The results show that the peak specific absorption rate (SAR) as averaged over 10 g has about a 25-fold increase in the trunk and a 50-fold increase in the limbs with respect to the whole body averaged SAR ([SAR.sub.WB]). The peak SAR as averaged over 1 g, instead, has a 30- to 60-fold increase in the trunk, and up to 135-fold increase in the ankles, with respect to [SAR.sub.WB]. With reference to temperature increases, at the body resonance frequency of 40 MHz, for the ICNIRP incident power density maximum permissible value, a temperature increase of about 0.7[degrees]C is obtained in the ankles muscle. The presence of the thermoregulatory system strongly limits temperature elevations, particularly in the body core. Index Terms--Dosimetry, electromagnetic heating, finite difference methods, safety standards, temperatures.

Our previous studies showed that the eyes of Japanese quail contain a biological clock that drives a daily rhythm of melatonin synthesis. Furthermore, we hypothesized that these ocular clocks are pacemakers because eye removal abolishes freerunning rhythms in constant darkness (DD). If the eyes are indeed acting as pacemakers, we predicted that the two ocular pacemakers in an individual bird must remain in phase in DD and, furthermore, the two ocular pacemakers would rapidly regain coupling after being forced out of phase. These predictions were confirmed by demonstrating that 1) the ocular melatonin rhythms of the two eyes maintained phase for at least 57 days in DD and 2) after ocular pacemakers were forced out of phase by alternately patching the eyes in constant light, two components of body temperature were observed that fused into a consolidated rhythm after 5-6 days in DD, showing pacemaker recoupling. The ability to maintain phase in DD and rapidly recouple after out-of-phase entrainment demonstrates that the eyes are strongly coupled pacemakers that work in synchrony to drive circadian rhythmicity in Japanese quail. melatonin; body temperature; eye; circadian; Coturnix

Oxygen consumption, heat production, and muscular efficiency for walking are parameters important to know for ergonomics models and equipment design. Most of these assume that the oxygen consumption and heat production of downhill walking are the same as for uphill walking. Eight subjects wearing insulating clothing walked on a treadmill at three uphill and three downhill grades, and at level grade at a rate of 1.1 m/s. Oxygen consumption V[O.sub.2] was calculated from steady state measurements of respiratory minute volume and oxygen percentage. Heat production (q) was calculated from the rate of heat storage in the body and clothing. Least-squares best fit equations for oxygen consumption and heat production found were to be V[O.sub.2] = 0.813 + 0.0361G + 0.000810[G.sup.2] - 0.0000302[G.sup.3] and q = 6.55 + 0.185G + 0.0114[G.sup.2] - 0.000190[G.sup.3] where G is percent grade. Approximations show that V[O.sub.2] (downhill) = 0.5 V[O.sub.2] (uphill), q (downhill) = 0.67 q (uphill), and muscular efficiency [eta] (downhill)= -2[eta] (uphill). Keywords: Walking; Energetics; Negative work

Research has been conducted on the ectothermic organisms. The hypothesis that the body temperature differences resulting from the phenotypic properties including color pattern can translate into selection against thermally inferior phenotypes has been tested and the details are presented.

Baroreflex modulation of sympathetic nerve activity to muscle in heat-stressed humans. Am J Physiol Regulatory Integrative Comp Physiol 282: R252-R258, 2002; 10.1152/ajpregu. 00337.2001.--To identify whether whole body heating alters arterial baroreflex control of muscle sympathetic nerve activity (MSNA), MSNA and beat-by-beat arterial blood pressure were recorded in seven healthy subjects during acute hypotensive and hypertensive stimuli in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature (P < 0.01), MSNA (P < 0.01), heart rate (P < 0.01), and skin blood flow (P < 0.001), whereas mean arterial blood pressure did not change significantly (P > 0.05). During both normothermic and heat stress conditions, MSNA increased and then decreased significantly when blood pressure was lowered and then raised via intravenous bolus infusions of sodium nitroprusside and phenylephrine HCl, respectively. The slope of the relationship between MSNA and diastolic blood pressure during heat stress (-128.3 [+ or -] 13.9 U * [beats.sup.-1] * mm[Hg.sup.-1]) was similar (P = 0.31) with normothermia (-140.6 [+ or -] 21.1 U * [beats.sup.-1] * mm[Hg.sup.-1]). Moreover, no significant change in the slope of the relationship between heart rate and systolic blood pressure was observed. These data suggest that arterial baroreflex modulation of MSNA and heart rate are not altered by whole body heating, with the exception of an upward shift of these baroreflex curves to accommodate changes in these variables that occur with whole body heating. baroreflex sensitivity; muscle sympathetic nerve activity; heart rate; heat stress

Perret, M., and F. Aujard. Daily hypothermia and torpor in a tropical primate: synchronization by 24-h light-dark cycle. Am J Physiol Regulatory Integrative Comp Physiol 281: R1925-R1933, 2001.--To study the temporal organization of daily hypothermia and torpor in a nocturnal Malagasy primate, the gray mouse lemur, body temperature ([T.sub.b]) and locomotor activity were recorded using telemetry on 39 males held in 24-h light-dark cycles of different photoperiods. Under free-running condition, the circadian [T.sub.b] and locomotor activity rhythms had a period shorter than 24 h. Circadian daily hypothermia started by a rapid drop in [T.sub.b] (0.24 [degrees] C/10 min) at the end of subjective night (13 h 25 [+ or -] 20 min) and was characterized by minimal [T.sub.b] values 3 h 20 [+ or -] 5 min later. Spontaneous arousal from daily hypothermia occurred at a fixed time (6 h 05 [+ or -] 15 min, n = 7) after the beginning of subjective day. In animals exposed to 24-h light-dark cycles with night duration varying from 10 to 14 h, locomotor activity was strictly restricted to dark time, but the temporal organization of daily hypothermia was not modified, although changes in amplitude of [T.sub.b] rhythm were observed. Daily hypothermia was directly induced by light and lasted 5 h 10 [+ or -] 10 min, with minimal [T.sub.b] values 3 h 30 [+ or -] 30 min (n = 28) after lights on, on condition that nighttime did not exceed the duration of subjective night. However, in animals exposed to 24-h light-dark cycles with night duration varying from 10 to 5 h, the limit of induction of daily hypothermia by light was ~9 h after the beginning of night. Finally, under short days (14:10-h light-dark cycle), long bouts (6 h 50 [+ or -] 40 min) of actual torpor (minimum [T.sub.b] 27.6 [+ or -] 0.9 [degrees] C) were observed and would involve mechanisms depending on physiological changes induced by short day exposure. circadian rhythm; body temperature; locomotor activity; light response; mouse lemur Received 8 February 2001; accepted in final form 21 August 2001

Byline: Hae-Kyung Ko (1), Andreas Flemmer (2), Caroline Haberl (2), Georg Simbruner (2) Keywords: Newborn Brain Nasopharyngeal temperature Rectal temperature Noninvasive measurement Animal Abstract: Objectives: (a) To investigate in a newborn animal model whether nasopharyngeal temperature is more closely related to epidural brain temperature than rectal temperature and (b) to investigate in human neonates whether measurement of nasopharyngeal temperature is dependent on the measurement site and other conditions. Design and setting: (a) Animal experiment in newborn piglets, at an institute for surgical research. (b) Prospective study in human neonates, at a neonatal intensive care unit of a tertiary care university hospital. Animals and patients: (a) Nineteen tracheostomized ventilated newborn piglets. (b) Twenty-two spontaneously breathing human newborns nursed either in an incubator or a cot. Measurements and results: (a) In the piglets nasopharyngeal temperature (T.sub.nasoph) measured at the nose-ear distance, defined as distance from the inner brim of the nostril to the tragus and inner rim of the meatus accusticus, most closely reflected epidural temperature (T.sub.epidur) at the epidural surface (r .sup.2=0.89), followed by skin temperature at the temple, rectal temperature (T.sub.rectum) at 2 cm depth, and esophageal temperature (T.sub.esoph) in the middle esophagus. T.sub.nasoph did not significantly differ before and after tracheostomy. (b) In the newborns T.sub.nasoph was significantly lower than T.sub.rectum. Measurements of T.sub.nasoph at nose-ear distance within a feeding tube had a high precision and were unaffected by breathing or head turning. A nasopharyngeal probe was imaged by magnetic resonance imaging in four newborns of various body weight its tip when inserted to a depth equal to nose-ear distance was anatomically closest to the brain base but separated from it by tissue layer 2.2 cm thick. Conclusions: T.sub.nasoph measured at a position anatomically closest to the brain reflects epidural brain temperature more closely than T.sub.rectum. When measured at nose-ear distance it is unaffected by breathing or head turning. Measuring T.sub.nasoph within a feeding tube and standardizing the measuring position is crucial for its use as brain temperature analogue. Author Affiliation: (1) Department of Neonatology, Charite Campus Virchow-Klinikum, Humboldt University Berlin, Augustenburger Platz 1, 13353 Berlin, Germany (2) Department of Neonatology, Dr. von Hauner'sches Kinderspital, Ludwig Maximilian University Munich, Lindwurmstrasse 4, 80337 Munich, Germany Article History: Received Date: 05/04/2000 Accepted Date: 18/09/2000 Article note: Final revision received: 13 September 2000 Electronic Publication

Leptin regulates energy balance through its actions in the brain on appetite and energy expenditure and also shares properties with cytokines such as IL-1. We report here that leptin, injected into rats intracerebroventricularly or peripherally, induces significant dose-dependent increases in core body temperature as well as suppression of appetite. Leptin failed to affect food intake or body temperature in obese (fa/fa) Zucker rats, which posses a defective leptin receptor. Furthermore, injection of leptin increased levels of the proinflammatory cytokine IL-1[Beta] in the hypothalamus of normal Sprague-Dawley rats. Central injection of IL-1 receptor antagonist (IL-1ra) inhibited the suppression of food intake caused by central or peripheral injection of leptin (60 and 84%, respectively) and abolished the leptin-induced increase in body temperature in both cases. Mice lacking (gene knockout} the main IL-1 receptor (80 kDa, R1) responsible for IL-1 actions showed no reduction in food intake in response to leptin. These data indicate that leptin actions in the brain depend on IL-1, and we show further that the effect of leptin on fever, but not food intake, is abolished by a cyclooxygenase inhibitor. Thus, we propose that in addition to its role in body weight regulation, leptin may mediate neuroimmune responses via actions in the brain dependent on release of IL-1 and prostaglandins.

The influence of core temperature on cytokine expression using an anesthetized mouse model was studied. Raising core temperature from basal to febrile levels increased peak plasma tumor necrosis factor-alpha and Interleukin-6 levels by 4.1- and 2.7-fold and changed the kinetics of IL-1beta expression in response to lipopolysaccharide challenge. TNF-alpha levels were predominantly increased in liver while IL-1beta levels were higher in lung. IL-6 levels were widely increased in multiple organs in the warmer mice.

Transitions between light and dark affect the circadian rhythms in hamsters. This was gleaned from an experiment in which circadian rhythms of activity and body temperature were analyzed in male Syrian hamsters under square-wave and simulated natural light-dark cycles. Results show that the hamsters exhibited different circadian entrainment behavior under square-wave and simulated natural light-dark cycles, indicating that gradual and abrupt transitions between light and dark may generate different temporal cues.

The link between initiation of torpor and reduction of blood glucose concentrations is investigated in Siberian hamsters. Results showed that changes in blood glucose concentrations may be a consequence rather than a cause of the torpid state and leads to the question whether induction of torpor by 2-deoxy-D-glucose is due to its general glucoprivic actions. Analysis indicates that the critical signal for torpor onset may be one of several adipocyte feedback mechanisms.

Body temperature and ventilatory and metabolic parameters in lean and obese Zucker rats were measured. Results showed that matching body temperature in lean and obese rats increased the differences in respiratory and metabolic parameters between the two groups. Hence, differences in respiration between lean and obese Zucker rats are not caused by differences in body temperature.

Voltage clamp and macropatch techniques were employed in the investigation of the ionic and gating currents of Shaker potassium channels heterologously expressed in Xenopus laevis oocytes. The experiments were conducted at different temperatures to determine the temperature dependence of these currents. Results reveal that the channel conformation approaching the transition to the open state have high temperature dependence.

The role of the beta adrenergic system on the modulation of plasma triglyceride levels after cold exposure was investigated using beta adrenergic receptor blocking studies with propranolol. Results reveal that triglyceride secretion increased after cold exposure and this was blunted by propranolol. Further, despite the increase in triglyceride secretion, its serum level dropped indicating that it is hydrolyzed intravascularly.