Circadian Rhythm Of Body Temperature Research Articles

Metabolic heat production, heat loss and the circadian rhythm of body temperature in the rat.

Metabolic heat production (calculated from oxygen consumption), dry heat loss (measured in a calorimeter) and body temperature (measured by telemetry) were recorded simultaneously at 6 min intervals over five consecutive days in rats maintained in constant darkness. Robust circadian rhythmicity (confirmed by chi square periodogram analysis) was observed in all three variables. The rhythm of heat production was phase-advanced by about half an hour in relation to the body temperature rhythm, whereas the rhythm of heat loss was phase-delayed by about half an hour. The balance of heat production and heat loss exhibited a daily oscillation 180 deg out of phase with the oscillation in body temperature. Computations indicated that the amount of heat associated with the generation of the body temperature rhythm (1.6 kJ) corresponds to less than 1 % of the total daily energy budget (172 kJ) in this species. Because of the small magnitude of the fraction of heat balance associated with the body temperature rhythm, it is likely that the daily oscillation in heat balance has a very slow effect on body temperature, thus accounting for the 180 deg phase difference between the rhythms of heat balance and body temperature.

Compromised neuroimmune status in rats with experimental colitis

In colitis, chronic and recurrent inflammation is associated with a breakdown in host defence mechanisms that leads to local and systemic infection. Whether this is due to a compromised neuroimmune response has not been studied. Our aim was to determine if colitis altered the host neuroimmune response as reflected in either body temperature rhythm or the febrile responses to lipopolysaccharide (LPS). Body temperature was monitored by telemetry from conscious, unrestrained male rats treated with trinitrobenzene sulphonic acid or saline. Twenty-six days after initial induction, colitis was reactivated. Animals were given LPS (50 μg kg−1Escherichia coli LPS) during colitis and after reactivation. At the peak of colitis, treated rats showed a disruption of circadian body temperature rhythm, manifested as day-time fever followed by night-time hypothermia. In response to LPS, controls displayed a characteristic fever, whereas treated animals had a significantly reduced fever and low plasma levels of interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α). During reactivation of colitis, treated animals did not mount a fever or exhibit increased plasma levels of IL-6 and TNF-α after LPS. We conclude that experimental colitis is associated with a compromised neuroimmune status.

Effet de l’entraînement physique et sportif sur le rythme circadien de la température et le rythme veille–sommeil chez la personne âgée

Aim. – Access the relations between physical fitness and body temperature rhythm and sleep-activity rhythm with ageing. Materials and methods. – Twenty-one subjects, men and women, athletics or sedentary, aged 64.7 ± 5.2 years, were distributed in 3 groups. The first group (E, n = 8), sedentary subjects, had to train during 4 months with a physical aerobic training program. The second group (CE, n = 6), athletics subjects, had to train as usual. The last group (AE, n = 7), athletics subjects, stopped their physical program training during the winter period as they usually do every year. At the beginning (t 0) and at the end (t 4) of the experimental protocol, the 3 groups performed a maximal graded cycling test ( V ̇ O 2 max ) to determine their physical fitness. Subsequently, during 3 days, parameters of body temperature rhythm and sleep/activity rhythm were recorded. Results and conclusion. – that subjects of the group (E) improve their physical fitness ( V ̇ O 2 max increase). In parallel the amplitude of circadian body temperature rhythm were enhanced without alteration of the sleep/activity rhythm between the pre-test and the post-test. These results showed that the improvement on circadian body temperature rhythms depends on the modification of endogenous body clock that controlled the synchronisation of the endogenous rhythms mechanisms and on the physical program training effects. In addition, results of the other groups show the necessity of conserving a minimal physical training level to keep the characteristics, structure and a regularity in the fluctuation of the biologic rhythm of body temperature.

Development of fetal and neonatal sleep and circadian rhythms

The origin of sleep and circadian rhythms development is found during the fetal period. Both quiet (NREM) and active (REM) sleep are distinguishable during the last 10 weeks of gestation. Comparable to fetuses, low risk preterm infants recorded at 30-40 weeks postconceptional age, had a similar development of sleep i.e. an increase in quiet sleep and a decrease in indeterminate sleep. A further development in sleep organization characterized by increased slow wave and spindle activity during quiet sleep and coupling with circadian rhythm takes place during the first 6 months of life in both term and preterm infants.Circadian rhythm of fetal heart rate synchronized with maternal rest-activity, heart rate, cortisol, melatonin, and body temperature rhythms is present during the last 10 weeks of gestation. Although maternally influenced, circadian rhythm antenatally becomes ultradian at birth. Both preterm and term infants show a significant increase in circadian body temperature rhythm amplitude during the first 3 months of life.

Compromised neuroimmune status in rats with experimental colitis.

In colitis, chronic and recurrent inflammation is associated with a breakdown in host defence mechanisms that leads to local and systemic infection. Whether this is due to a compromised neuroimmune response has not been studied. Our aim was to determine if colitis altered the host neuroimmune response as reflected in either body temperature rhythm or the febrile responses to lipopolysaccharide (LPS). Body temperature was monitored by telemetry from conscious, unrestrained male rats treated with trinitrobenzene sulphonic acid or saline. Twenty-six days after initial induction, colitis was reactivated. Animals were given LPS (50 microg kg-1 Escherichia coli LPS) during colitis and after reactivation. At the peak of colitis, treated rats showed a disruption of circadian body temperature rhythm, manifested as day-time fever followed by night-time hypothermia. In response to LPS, controls displayed a characteristic fever, whereas treated animals had a significantly reduced fever and low plasma levels of interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha). During reactivation of colitis, treated animals did not mount a fever or exhibit increased plasma levels of IL-6 and TNF-alpha after LPS. We conclude that experimental colitis is associated with a compromised neuroimmune status.

Circadian rhythms of body temperature and liver function in fed and food-deprived goats

Daily rhythms of body core temperature and liver function were recorded in goats maintained under various schedules of lighting and feeding. Concentration of urea in the blood was used as an index of digestion-driven hepatic activity, whereas concentration of cholesterol served as an index of autonomous hepatic activity. Body temperature exhibited robust circadian rhythmicity in the presence and absence of a light–dark cycle and/or a feeding regime. The rhythm was more responsive to shifts in feeding time than to shifts in the light–dark cycle. Urea concentration in the blood exhibited daily rhythmicity only in the presence of a daily feeding regime and, therefore, was driven by ingestive and digestive processes. The rhythm of cholesterol concentration persisted in the presence or absence of a light–dark cycle and/or a feeding regime, except when the feeding time was shifted under constant light. However, the cholesterol rhythm did not respond either to shifts in the light–dark cycle or, more importantly, to shifts in feeding time. Thus, based on this index of hepatic function, the liver cannot be identified as the site of the putative food-entrainable pacemaker.

The Development of New Purification Methods to Assess the Circadian Rhythm of Body Temperature in Mongolian Gerbils

Six Mongolian gerbils were studied for 8–10d while housed in separate cages in a 12:12h light–dark (L–D) cycle (lights on at 07:00h). Recordings of body temperature, heart rate, and spontaneous activity were made throughout. The temperature and heart rate rhythms were “purified” to take into account the effects of activity, and then the rhythm of temperature was further purified to take into account other masking influences (“non-activity masking effects” or NAME,). The methods employed in the purification processes involved linear regression analysis or analysis of covariance, the latter using functions of activity and NAME as covariates. From these methods, it was possible to obtain not only an estimate of the endogenous component of the temperature rhythm but also a measure of circadian changes in the sensitivity of temperature to masking effects.Even though all purification methods removed many of the effects of spontaneous activity from the temperature record, there remained temperature fluctuations at the L–D and D–L transitions that appeared to be independent of activity. The NAME was of only very marginal value in the purification process. Comparison of the purification methods indicated that the linear methods were inferior (both from a biological viewpoint and when the results were compared mathematically) to those that allowed the rate of rise of temperature due to increasing amounts of activity to become progressively less. The sensitivity of temperature and heart rate to the masking effects of activity showed a circadian rhythm, with sensitivities in the resting phase being greater than those in the active phase. These findings are compatible with the view that thermoregulatory reflexes are induced by spontaneous activity of sufficient amount, and that there is a circadian rhythm in the body temperature at which these reflexes are initiated and in their effectiveness.

Thermal chronobiology of domestic animals.

This article reviews the literature on the circadian and estrous rhythms of body temperature in farm animals. Although most research in this area has lacked the methodological sophistication of research conducted on laboratory animals, the experimental results are consistent with the general principles of thermal chronobiology derived from laboratory studies and, at the same time, provide specific information about the peculiarities of livestock species. Detailed knowledge of the normal parameters of the body temperature rhythms is important for the advancement of diagnostic procedures in veterinary medicine and for the optimization of farm yield in the dairy and meat industry.

A longer biological night in long sleepers than in short sleepers.

Habitual sleep duration varies greatly among individuals. The physiological basis of this variation is unknown. We sought to determine whether individual differences in sleep duration are associated with systematic differences in the duration of the biological night that is programmed by the circadian pacemaker and reflected in the nocturnal interval of circadian rhythms in neuroendocrine function, body temperature, and arousal. Ten young, healthy long sleepers (sleep duration >9 h) and 14 short sleepers (<6 h) were studied under constant environmental conditions and in the absence of sleep. The nocturnal intervals of high plasma melatonin levels, increasing cortisol levels, low body temperature, and increasing sleepiness were longer in long sleepers than in short sleepers. The maxima in cortisol and sleepiness exhibited a close relationship to habitual wake-up time, which occurred approximately 2.5 h later in long sleepers than in short sleepers. It is concluded that the circadian pacemaker programs a longer biological night in long sleepers than in short sleepers. We propose that individual differences in the circadian pacemaker's program may contribute to the variability of sleep duration in the general population. The persistence or inertia of an individual's circadian program, as was evident in constant conditions, may underlie the commonly experienced difficulty of changing habitual sleep duration willfully.

Circadian adaptation to night-shift work by judicious light and darkness exposure.

In this combined field and laboratory investigation, the authors tested the efficacy of an intervention designed to promote circadian adaptation to night-shift work. Fifteen nurses working permanent night schedules (> or = 8 shifts/ 15 days) were recruited from area hospitals. Following avacation period of > or = 10 days on a regular daytime schedule, workers were admitted to the laboratory for the assessment of circadian phase via a 36-h constant routine. They returned to work approximately 12 night shifts on their regular schedules under one of two conditions. Treatment group workers (n = 10, mean age +/- SD = 41.7 +/- 8.8 years) received an intervention including 6 h of intermittent bright-light exposure in the workplace (approximately 3,243 lux) and shielding from bright morning outdoor light with tinted goggles (15% visual light transmission). Control group workers (n = 9, mean age +/- SD = 42.0 +/- 7.2 years) were observed in their habitual work environments. On work days, participants maintained regular sleep/wake schedules including a single 8-h sleep/darkness episode beginning 2 h after the end of the night shift. A second 36-h constant routine was performed following the series of night shifts. In the presence of the intervention, circadian rhythms of core body temperature and salivary melatonin cycles were delayed by an average (+/- SEM) of -9.32 +/- 1.06 h and -11.31 +/- 1.13 h, respectively. These were significantly greater than the phase delays of -4.09 +/- 1.94 h and -5.08 +/- 2.32 h displayed by the control group (p = 0.03 and p = 0.02, respectively). The phase angle between circadian markers and the shifted schedule was reestablished to its baseline position only in the treatment group of workers. These results support the efficacy of a practical intervention for promoting circadian adaptation to night-shift work under field conditions. They also underline the importance of controlling the overall pattern of exposure to light and darkness in circadian adaptation to shifted sleep/wake schedules.

Normal Thyroid Thermogenesis but Reduced Viability and Adiposity in Mice Lacking the Mitochondrial Glycerol Phosphate Dehydrogenase

The mitochondrial glycerol phosphate dehydrogenase (mGPD) is important for metabolism of glycerol phosphate for gluconeogenesis or energy production and has been implicated in thermogenesis induced by cold and thyroid hormone treatment. mGPD in combination with the cytosolic glycerol phosphate dehydrogenase (cGPD) is proposed to form the glycerol phosphate shuttle, catalyzing the interconversion of dihydroxyacetone phosphate and glycerol phosphate with net oxidation of cytosolic NADH. We made a targeted deletion in Gdm1 and produced mice lacking mGPD. On a C57BL/6J background these mice showed a 50% reduction in viability compared with wild-type littermates. Uncoupling protein-1 mRNA levels in brown adipose tissue did not differ between mGPD knockout and control pups, suggesting normal thermogenesis. Pups lacking mGPD had decreased liver ATP and slightly increased liver glycerol phosphate. In contrast, liver and muscle metabolites were normal in adult animals. Adult mGPD knockout animals had a normal cold tolerance, normal circadian rhythm in body temperature, and demonstrated a normal temperature increase in response to thyroid hormone. However, they were found to have a lower body mass index, a 40% reduction in the weight of white adipose tissue, and a slightly lower fasting blood glucose than controls. The phenotype may be secondary to consequences of the obligatory production of cytosolic NADH from glycerol metabolism in the mGPD knockout animal. We conclude that, although mGPD is not essential for thyroid thermogenesis, variations in its function affect viability and adiposity in mice.

Phase-dependent effect of room light exposure in a 5-h advance of the sleep-wake cycle: implications for jet lag.

The acute disruption in sleep quality, vigilance levels, and cognitive and athletic performance observed after transmeridian flights is presumed to be the result of a transient misalignment between the endogenous circadian pacemaker and the shifted sleep schedule. Several laboratory and field experiments have demonstrated that exposure to bright artificial light can accelerate circadian entrainment to a shifted sleep-wake schedule. In the present study, the authors investigated whether the schedule of exposure to indoor room light, to which urban dwellers are typically exposed, can substantially affect circadian adaptation to a simulated eastward voyage. We enrolled 15 healthy young men in a laboratory simulation of a Montreal-to-London voyage. Subjects were exposed to 6 h of room light (mean +/- SD: 379+/-10) prior to bedtime (n = 7) or when on a progressively advancing schedule (n = 8) early in the day. The remaining 10 hours of wakefulness were spent in dim light (4+/-1 lux). Circadian assessments, performed via the constant routine procedure, evaluated the phase of the endogenous circadian rhythms of core body temperature and plasma melatonin before and after 1 week on the shifted schedule. At the end of the study, only subjects exposed to room light on the advancing schedule expressed oscillations of the endogenous circadian pacemaker in phase with the new sleep-wake cycle. In this group, a mean advance shift of the nadir of core body temperature of +5:22+/-0:15 h was observed, with parallel shifts in plasma melatonin concentration and subjective alertness. The circadian rhythms of subjects exposed to room light later in the day remained much more adjusted to the departure than to the destination time zone. These results demonstrate that the schedule of exposure to room light can substantially affect circadian adaptation to a shifted sleep-wake schedule.

Different Behavior of the Circadian Rhythms of Activity and Body Temperature During Resynchronization Following an Advance of the LD Cycle

Spontaneous activity and the body temperature of laboratory mice were recorded telemetrically using implantable transmitters. Following ten control days (L : D = 12 : 12; light from 07:00 to 19:00), the LD cycle was phase-advanced by shortening the light time by 8 h. Recordings were continued for a further 3 weeks. The raw temperature data were unmasked or ‘purified’ — that is, the temperature changes due to locomotor activity were removed, so revealing the endogenous component of the rhythm — using a regression method previously developed by us. The circadian rhythms of activity and measured body temperature resynchronized on average after 8 days. During resynchronization, both rhythms tended to show two components, one adjusting by a phase advance and the other by a phase delay. However, after purification of the body temperature rhythm, only the advancing component remained. These results indicate that the delaying component of the measured temperature rhythm was caused by masking due to activity, and that the endogenous component of this rhythm did not divide into two components during the resynchronization process. Also, the endogenous component of the circadian rhythm of body temperature and one component of the activity rhythm seemed to be controlled by the same oscillator. It remains uncertain how the other component of the activity rhythm is regulated.

The Circadian Activity and Body Temperature Rhythms of Mice During Their Last Days of Life

Motor activity and body temperature rhythms have been investigated telemetrically in old mice until their death. The present paper is based mainly on the data of two animals which could be monitored over a sufficient length of time (more than three weeks), though the other three animals showed similar results. The daily body temperature rhythm of old mice was more stable as compared to the activity rhythm and was detectable until the last day of life. Its magnitude, defined as the difference between maximum and minimum, was similar to that obtained in middle-aged mice. By contrast, the activity rhythm disappeared or started to become erratic earlier. Unlike the position in younger animals, the body temperature rhythm was phase delayed with respect to the activity rhythm. In one mouse, the increased instability of the phase position two weeks before its death led to a free run with a period length of about 23.7 h. Both activity and temperature rhythms were fragmented in old mice. In the case of the body temperature this was obviously caused by masking. After purifying the raw temperatures, the fragmentation disappeared. On the other hand, the free-run condition was not caused by masking. The sensitivity of body temperature to motor activity was different from younger mice, and this probably reflects changes/deteriorations in the physiology of thermoregulation during the last days of life. In one mouse, during the last 4 days of life, a sharp, torpor-like decrease of body temperature corresponding with the time of the daily minimum was observed. This phenomenon was not found in other mice, though all of them died during the falling period of the temperature rhythm. The results confirm our hypothesis that the endogenous clock may work even during the very last days of life. The ability to synchronize with the periodic environment deteriorates earlier. Also they suggest that these phenomena are not only typical for the activity rhythm but apply also to the body temperature rhythm.

The Circadian Rhythm of Body Temperature of the Horse

Rectal temperature of 10 female adult horses was recorded every 2 h for 10 consecutive days under a natural winter photoperiod (9 h of light and 15 h of darkness per day). A robust daily rhythm of body temperature was observed in all animals. The rhythm had a mean level of 38.3°C and a range of excursion of 1.0°C. Temperature started its daily ascent at dawn each day and reached a maximum 14 hours later. Body temperature of 5 of the horses was studied for 10 more days under constant illumination. The rhythm persisted under this condition, although with a slightly longer period of 24.2 h, which confirms the endogenous nature of the rhythm. Despite the fact that the body size of the horse is several orders of magnitude greater than that of rodents, the various parameters of the body temperature rhythm of the horse are similar to those of several species of rodents previously studied.

TEMPERATURE EFFECT ON ENTRAINMENT, PHASE SHIFTING, AND AMPLITUDE OF CIRCADIAN CLOCKS AND ITS MOLECULAR BASES

Effects of temperature and temperature changes on circadian clocks in cyanobacteria, unicellular algae, and plants, as well as fungi, arthropods, and vertebrates are reviewed. Periodic temperature with periods around 24 h even in the low range of 1–2°C (strong Zeitgeber effect) can entrain all ectothermic (poikilothermic) organisms. This is also reflected by the phase shifts—recorded by phase response curves (PRCs)—that are elicited by step- or pulsewise changes in the temperature. The amount of phase shift (weak or strong type of PRC) depends on the amplitude of the temperature change and on its duration when applied as a pulse. Form and position of the PRC to temperature pulses are similar to those of the PRC to light pulses. A combined high/low temperature and light/dark cycle leads to a stabile phase and maximal amplitude of the circadian rhythm—when applied in phase (i.e., warm/light and cold/dark). When the two Zeitgeber cycles are phase-shifted against each other the phase of the circadian rhythm is determined by either Zeitgeber or by both, depending on the relative strength (amplitude) of both Zeitgeber signals and the sensitivity of the species/individual toward them. A phase jump of the circadian rhythm has been observed in several organisms at a certain phase relationship of the two Zeitgeber cycles.Ectothermic organisms show inter- and intraspecies plus seasonal variations in the temperature limits for the expression of the clock, either of the basic molecular mechanism, and/or the dependent variables. A step-down from higher temperatures or a step-up from lower temperatures to moderate temperatures often results in initiation of oscillations from phase positions that are about 180° different. This may be explained by holding the clock at different phase positions (maximum or minimum of a clock component) or by significantly different levels of clock components at the higher or lower temperatures. Different permissive temperatures result in different circadian amplitudes, that usually show a species-specific optimum.In endothermic (homeothermic) organisms periodic temperature changes of about 24 h often cause entrainment, although with considerable individual differences, only if they are of rather high amplitudes (weak Zeitgeber effects). The same applies to the phase-shifting effects of temperature pulses. Isolated bird pineals and rat suprachiasmatic nuclei tissues on the other hand, respond to medium high temperature pulses and reveal PRCs similar to that of light signals. Therefore, one may speculate that the self-selected circadian rhythm of body temperature in reptiles or the endogenously controlled body temperature in homeotherms (some of which show temperature differences of more than 2°C) may, in itself, serve as an internal entraining system. The so-called heterothermic mammals (undergoing low body temperature states in a daily or seasonal pattern) may be more sensitive to temperature changes.Effects of temperature elevation on the molecular clock mechanisms have been shown in Neurospora (induction of the frequency (FRQ) protein) and in Drosophila (degradation of the period (PER) and timeless (TIM) protein) and can explain observed phase shifts of rhythms in conidiation and locomotor activity, respectively.Temperature changes probably act directly on all processes of the clock mechanism some being more sensitive than the others. Temperature changes affect membrane properties, ion homeostasis, calcium influx, and other signal cascades (cAMP, cGMP, and the protein kinases A and C) (indirect effects) and may thus influence, in particular, protein phosphorylation processes of the clock mechanism. The temperature effects resemble to some degree those induced by light or by light-transducing neurons and their transmitters. In ectothermic vertebrates temperature changes significantly affect the melatonin rhythm, which in turn exerts entraining (phase shifting) functions.

Pharmacological effects of vinorelbine on body temperature and locomotor activity circadian rhythms in mice

The effects of vinorelbine (VRL) on the circadian rhythms in body temperature and locomotor activity were investigated in unrestrained B6D2F1 mice implanted with radio-telemetry transmitters. A single intravenous VRL dose (24 or 12 mg/kg) was given at 7 h after light onset (HALO), a time of high VRL toxicity, and resulted in transient suppression of temperature and activity circadian rhythms in mice kept in light–dark (LD) 12h:12h. Such suppression was dose-dependent. It occurred within 1–5 d after VRL dosing. Recovery of both rhythms was partially complete within 5 d following the high dose and within 2 or 3 d after the low dose and was not influenced by suppression of photoperiodic synchronization by housing in continuous darkness. Moreover, VRL induced a dose-dependent relative decrease in amplitude and phase shift of the temperature circadian rhythm. The mesor and amplitude of the activity rhythm were markedly reduced following the VRL administration. The relevance of VRL dosing time was studied in mice housed in LD 12h:12h. Vinorelbine was injected weekly (20 mg/kg/injection) for 3 wk at 6 or 18 HALO. Vinorelbine treatment ablated the rest–activity and temperature rhythms 3–6 d after each dose, with fewer alterations after VRL dosing at 18 HALO compared to 6 HALO, especially for the body temperature rhythm. There was at least partial recovery 1 wk after dosing, suggesting the weekly schedule of drug treatment is acceptable for therapeutic purposes. Our findings demonstrate that VRL can transiently, yet profoundly, alter circadian clock function. Vinorelbine-induced circadian dysfunction may contribute to the toxicokinetics of this and possibly other anticancer drugs.

Intermittent Exposure to Social Defeat and Open-field Test in Rats: Acute and Long-term Effects on ECG, Body Temperature and Physical Activity

This study investigated the effects of exposure to an intermittent homotypic stressor on: (i) habituation of acute autonomic responsivity (i.e. cardiac sympathovagal balance and susceptibility to arrhythmias), and (ii) circadian rhythmicity of heart rate, body temperature, and physical activity. After implantation of a transmitter for the radiotelemetric recording of electrocardiogram (ECG), body temperature and physical activity, adult male rats ( Rattus norvegicus, Wild Type Groningen strain) were repeatedly exposed (10 consecutive times, on alternate days) to either a social stressor (defeat by a con-specific, n =15 ) or an open-field, control challenge (transfer to a new cage; n =8 ). ECGs, body temperature and physical activity were continuously recorded in baseline, test and recovery periods (each lasting 15 u min), at the 1st and 10th episodes of both defeat and open-field challenge. The circadian rhythms of heart rate, body temperature and physical activity were monitored before (5 days), during (16 days) and after (21 days) the intermittent stress protocol. This study indicates that there is no clear habituation of either acute cardiac autonomic responsivity (as estimated by means of time-domain indexes of heart rate variability) or arrhythmia occurrence to a brief, intermittent, homotypic challenge, regardless of the nature of the stressor (social or non-social). On the other hand, rats exposed to social challenge also failed to show adaptation of acute temperature and activity stress responsiveness, whereas rats facing open-field challenge developed habituation of activity and sensitization of temperature responses. Repeated social challenge produced remarkable reductions of the heart rate circadian rhythm amplitude (this effect being significantly greater than that produced by intermittent open-field), but only minor changes in the daily rhythms of body temperature and physical activity.

The Suprachiasmatic Nucleus Is Essential for Circadian Body Temperature Rhythms in Hibernating Ground Squirrels

Body temperature (T(b)) was recorded at 10 min intervals over 2.5 years in female golden-mantled ground squirrels that sustained complete ablation of the suprachiasmatic nucleus (SCNx). Animals housed at an ambient temperature (T(a)) of 6.5 degrees C were housed in a 12 hr light/dark cycle for 19 months followed by 11 months in constant light. The circadian rhythm of T(b) was permanently eliminated in euthermic and torpid SCNx squirrels, but not in those with partial destruction of the SCN or in neurologically intact control animals. Among control animals, some low-amplitude T(b) rhythms during torpor were driven by small (<0.1 degrees C) diurnal changes in T(a). During torpor bouts in which T(b) rhythms were unaffected by T(a), T(b) rhythm period ranged from 23.7 to 28.5 hr. Both SCNx and control squirrels were more likely to enter torpor at night and to arouse during the day in the presence of the light/dark cycle, whereas entry into and arousal from torpor occurred at random clock times in both SCNx and control animals housed in constant light. Absence of circadian rhythms 2.5 years after SCN ablation indicates that extra-SCN pacemakers are unable to mediate circadian organization in euthermic or torpid ground squirrels. The presence of diurnal rhythms of entry into and arousal from torpor in SCNx animals held under a light/dark cycle, and their absence in constant light, suggest that light can reach the retina of hibernating ground squirrels maintained in the laboratory and affect hibernation via an SCN-independent mechanism.

Effects of intermittent cold exposure varying in intensity on core body temperature and resting heat production of beef cattle

Crossbred beef heifers (n = 18) fed at 1.3× maintenance were exposed to summer daytime temperatures (20 ± 0.2°C) for 8 h (08:00 until 16:00) and to control (22°C), moderate (–6°C) or cold (–15°C) environments for 16 h daily (16:00 until 08:00) for a minimum 21-d adaptation period to investigate the effects of in tensity of intermittent cold exposure on vaginal temperature and resting heat production. Resting heat production was measured at the end of the adaptation period. Vaginal temperature was continuously monitored throughout the experiment using radiotelemetry. Vaginal temperature increased immediately after the onset of cold exposure in both moderate and cold treatments, peaked after 3 h, and returned to pre-exposure levels by the time the 16-h treatment ended. In contrast, vaginal temperatures of control heifers peaked only after feeding at 08:30. Treatment did not affect daily maximum (P= 0.60), mean (P = 0.72) or minimum (P = 0.34) vaginal temperatures, but heifers in both cold-exposed treatments spent more time (P = 0.03) with vaginal temperatures exceeding the daily mean vaginal temperature than control heifers. Compared to control heifers, the variability of vaginal temperature increased 1.8- and 2.2-fold in the moderate and cold treatments, respectively (P = 0.04), and did not change with time (P = 0.98 ). Resting heat production did not increase following 21 d of exposure to moderate and cold conditions. Results of this study indicate that intermittent cold exposure influenced circadian body temperature rhythms without increasing resting heat production. Key words: Beef cattle, thermoregulation, vaginal temperature, heat production.