Do chronic primary insomniacs have impaired heat loss when attempting sleep?

2006 ◽  
Vol 290 (4) ◽  
pp. R1115-R1121 ◽  
Author(s):  
Michael Gradisar ◽  
Leon Lack ◽  
Helen Wright ◽  
Jodie Harris ◽  
Amber Brooks

For good sleepers, distal skin temperatures (e.g., hands and feet) have been shown to increase when sleep is attempted. This process is said to reflect the body’s action to lose heat from the core via the periphery. However, little is known regarding whether the same process occurs for insomniacs. It would be expected that insomniacs would have restricted heat loss due to anxiety when attempting sleep. The present study compared the finger skin temperature changes when sleep was attempted for 11 chronic primary insomniacs [mean age = 40.0 years (SD 13.3)] and 8 good sleepers [mean age = 38.6 years (SD 13.2)] in a 26-h constant routine protocol with the inclusion of multiple-sleep latency tests. Contrary to predictions, insomniacs demonstrated increases in finger skin temperature when attempting sleep that were significantly greater than those in good sleepers ( P = 0.001), even though there was no significant differences in baseline finger temperature ( P = 0.25). These significant increases occurred despite insomniacs reporting significantly greater sleep anticipatory anxiety ( P < 0.0008). Interestingly, the core body temperature mesor of insomniacs (37.0 ± 0.2°C) was significantly higher than good sleepers (36.8 ± 0.2°C; P = 0.03). Whether insomniacs could have impaired heat loss that is masked by elevated heat production is discussed.

1995 ◽  
Vol 78 (1) ◽  
pp. 314-317 ◽  
Author(s):  
A. Cagnacci ◽  
R. Soldani ◽  
S. S. Yen

In young humans, the nocturnal rise of the hypothermic hormone melatonin generates 40–50% of the circadian core body temperature (Tc) decline. The nocturnal Tc decline is reduced with aging in men. In this study we investigated whether a similar attenuation occurs in women and whether it is associated with a reduced serum concentration and/or action of melatonin. The circadian rhythms of melatonin and Tc (measured in the vagina) and the responses of both Tc (measured into the auricolar canal) and finger skin temperature to melatonin administration (100 mg at 0800) were investigated in two experiments involving young (22–32 yr) and aged (54–62 yr) women. In aged women, the nocturnal onset of the melatonin rise was phase advanced and Tc decline and Tc rhythm amplitude were reduced (P < 0.0005). The serum melatonin concentrations in aged women were similar to those of young women, but the melatonin capability to reduce Tc and increase skin temperature was markedly impaired. Our data show that, in women, an aging-associated reduction of temperature responses to melatonin is probably involved in inducing an attenuation of the nocturnal Tc decline and circadian Tc rhythm amplitude.


1989 ◽  
Vol 69 (3-2) ◽  
pp. 1339-1345
Author(s):  
Alex M. Babcock ◽  
Chris Barton

Bombesin-like peptides are widely distributed in the mammalian central nervous system and appear to participate in the regulation of a variety of autonomic functions. Bombesin has been shown to alter feeding behavior, locomotor activity, and thermoregulation. Microinfusion of bombesin into the preoptic area of the hypothalamus produces a reduction in core body temperature, but only if the rat has been cold-exposed, food-deprived, or pretreated with insulin. The mechanism for bombesin-induced hypothermia under the latter two conditions is unknown. The present study evaluated the possible contribution of peripheral heat loss mechanisms in bombesin-induced hypothermia. Rats were administered insulin (10U/kg, Regular Iletin I i.m.) or saline followed by an intrahypothalamic injection of bombesin (.05 μg/ .25 μl) or peptide vehicle. Rectal and tail-skin temperatures were measured continuously for 120 min. Changes in temperature were evaluated at 30, 60, 90, and 120 min., using analysis of variance. As previously demonstrated, bombesin produced hypothermia in rats pretreated with insulin. This reduction in core temperature was not associated with any significant alteration in tail-skin temperature. Results suggest that bombesin-induced hypothermia in rats pretreated with insulin may not be mediated by an increase in peripheral heat loss.


1989 ◽  
Vol 69 (3_suppl) ◽  
pp. 1339-1345 ◽  
Author(s):  
Alex M. Babcock ◽  
Chris Barton

Bombesin-like peptides are widely distributed in the mammalian central nervous system and appear to participate in the regulation of a variety of autonomic functions. Bombesin has been shown to alter feeding behavior, locomotor activity, and thermoregulation. Microinfusion of bombesin into the preoptic area of the hypothalamus produces a reduction in core body temperature, but only if the rat has been cold-exposed, food-deprived, or pretreated with insulin. The mechanism for bombesin-induced hypothermia under the latter two conditions is unknown. The present study evaluated the possible contribution of peripheral heat loss mechanisms in bombesin-induced hypothermia. Rats were administered insulin (10U/kg, Regular Iletin I i.m.) or saline followed by an intrahypothalamic injection of bombesin (.05 μg/.25 μl) or peptide vehicle. Rectal and tail-skin temperatures were measured continuously for 120 min. Changes in temperature were evaluated at 30, 60, 90, and 120 min., using analysis of variance. As previously demonstrated, bombesin produced hypothermia in rats pretreated with insulin. This reduction in core temperature was not associated with any significant alteration in tail-skin temperature. Results suggest that bombesin-induced hypothermia in rats pretreated with insulin may not be mediated by an increase in peripheral heat loss.


2016 ◽  
Vol 96 (5) ◽  
pp. 650-658 ◽  
Author(s):  
Coen C.W.G. Bongers ◽  
Thijs M.H. Eijsvogels ◽  
Ilse J.W. van Nes ◽  
Maria T.E. Hopman ◽  
Dick H.J. Thijssen

Background People with spinal cord injury (SCI) have an altered afferent input to the thermoregulatory center, resulting in a reduced efferent response (vasomotor control and sweating capacity) below the level of the lesion. Consequently, core body temperature rises more rapidly during exercise in individuals with SCI compared with people who are able-bodied. Cooling strategies may reduce the thermophysiological strain in SCI. Objective The aim of this study was to examine the effects of a cooling vest on the core body temperature response of people with a thoracic SCI during submaximal exercise. Methods Ten men (mean age=44 years, SD=11) with a thoracic lesion (T4–T5 or below) participated in this randomized crossover study. Participants performed two 45-minute exercise bouts at 50% maximal workload (ambient temperature 25°C), with participants randomized to a group wearing a cooling vest or a group wearing no vest (separate days). Core body temperature and skin temperature were continuously measured, and thermal sensation was assessed every 3 minutes. Results Exercise resulted in an increased core body temperature, skin temperature, and thermal sensation, whereas cooling did not affect core body temperature. The cooling vest effectively decreased skin temperature, increased the core-to-trunk skin temperature gradient, and tended to lower thermal sensation compared with the control condition. Limitations The lack of differences in core body temperature among conditions may be a result of the relative moderate ambient temperature in which the exercise was performed. Conclusions Despite effectively lowering skin temperature and increasing the core-to-trunk skin temperature gradient, there was no impact of the cooling vest on the exercise-induced increase in core body temperature in men with low thoracic SCI.


2012 ◽  
Vol 26 (2) ◽  
Author(s):  
Joanna Pawlak ◽  
Paweł Zalewski ◽  
Jacek J. Klawe ◽  
Monika Zawadka ◽  
Anna Bitner ◽  
...  

2008 ◽  
Vol 109 (2) ◽  
pp. 318-338 ◽  
Author(s):  
Daniel I. Sessler ◽  
David S. Warner ◽  
Mark A. Warner

Most clinically available thermometers accurately report the temperature of whatever tissue is being measured. The difficulty is that no reliably core-temperature-measuring sites are completely noninvasive and easy to use-especially in patients not undergoing general anesthesia. Nonetheless, temperature can be reliably measured in most patients. Body temperature should be measured in patients undergoing general anesthesia exceeding 30 min in duration and in patients undergoing major operations during neuraxial anesthesia. Core body temperature is normally tightly regulated. All general anesthetics produce a profound dose-dependent reduction in the core temperature, triggering cold defenses, including arteriovenous shunt vasoconstriction and shivering. Anesthetic-induced impairment of normal thermoregulatory control, with the resulting core-to-peripheral redistribution of body heat, is the primary cause of hypothermia in most patients. Neuraxial anesthesia also impairs thermoregulatory control, although to a lesser extent than does general anesthesia. Prolonged epidural analgesia is associated with hyperthermia whose cause remains unknown.


1984 ◽  
Vol 57 (6) ◽  
pp. 1738-1741 ◽  
Author(s):  
T. G. Waldrop ◽  
D. E. Millhorn ◽  
F. L. Eldridge ◽  
L. E. Klingler

Respiratory responses to increased skin temperatures were recorded in anesthetized cerebrate and in unanesthetized decerebrate cats. All were vagotomized, glomectomized, and paralyzed. Core body temperature and end-tidal Pco2 were kept constant with servoncontrollers. Stimulation of cutaneous nociceptors by heating the skin to 46 degrees C caused respiration to increase in both cerebrate and decerebrate cats. An even larger facilitation of respiration occurred when the skin temperature was elevated to 51 degrees C. However, respiration did not increase in either group of cats when the skin was heated to 41 degrees C to activate cutaneous warm receptors. The phenomenon of sensitization of nociceptors was observed. Spinal transection prevented all the respiratory responses to cutaneous heating. We conclude that noxious, but not nonnoxious, increases in skin temperature cause increases in respiratory output.


2019 ◽  
Vol 163 ◽  
pp. 104849 ◽  
Author(s):  
Wataru Iwasaki ◽  
Shuichi Ishida ◽  
Daisuke Kondo ◽  
Yuichi Ito ◽  
Jun Tateno ◽  
...  

2017 ◽  
Vol 12 (5) ◽  
pp. 662-667 ◽  
Author(s):  
Matthijs T.W. Veltmeijer ◽  
Dineke Veeneman ◽  
Coen C.C.W. Bongers ◽  
Mihai G. Netea ◽  
Jos W. van der Meer ◽  
...  

Purpose:Exercise increases core body temperature (TC) due to metabolic heat production. However, the exercise-induced release of inflammatory cytokines including interleukin-6 (IL-6) may also contribute to the rise in TC by increasing the hypothalamic temperature set point. This study investigated whether the exercise-induced increase in TC is partly caused by an altered hypothalamic temperature set point.Methods:Fifteen healthy, active men age 36 ± 14 y were recruited. Subjects performed submaximal treadmill exercise in 3 randomized test conditions: (1) 400 mg ibuprofen and 1000 mg acetaminophen (IBU/APAP), (2) 1000 mg acetaminophen (APAP), and (3) a control condition (CTRL). Acetaminophen and ibuprofen were used to block the effect of IL-6 at a central and peripheral level, respectively. TC, skin temperature, and heart rate were measured continuously during the submaximal exercise tests.Results:Baseline values of TC, skin temperature, and heart rate did not differ across conditions. Serum IL-6 concentrations increased in all 3 conditions. A significantly lower peak TC was observed in IBU/APAP (38.8°C ± 0.4°C) vs CTRL (39.2°C ± 0.5°C, P = .02) but not in APAP (38.9°C ± 0.4°C) vs CTRL. Similarly, a lower ΔTC was observed in IBU/APAP (1.7°C ± 0.3°C) vs CTRL (2.0°C ± 0.5°C, P < .02) but not in APAP (1.7°C ± 0.5°C) vs CTRL. No differences were observed in skin temperature and heart-rate responses across conditions.Conclusions:The combined administration of acetaminophen and ibuprofen resulted in an attenuated increase in TC during exercise compared with a CTRL. This observation suggests that a prostaglandin-E2-induced elevated hypothalamic temperature set point may contribute to the exercise-induced rise in TC.


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