Saul S. Gilbert

Thermoregulation as a sleep signalling system

Temperature and sleep are interrelated processes. Under normal environmental conditions, the rhythms of core body temperature Tc and sleep propensity vary inversely across the day and night in healthy young adults. Although this relationship has drawn considerable interest, particularly in recent years, it is still not known whether this relationship is causative or merely coincidental. As somnogenic brain areas contain thermosensitive cells, it is possible that the sleep/wake cycle may be directly affected by thermoregulatory changes themselves. That is, that changes in temperature may trigger, either directly or indirectly, somnogenic brain areas to initiate sleep. There is now an emerging body of evidence from both physiological and neuroanatomical studies to indicate that this may indeed be the case. This paper will examine the literature relating to this relationship and propose a model where thermoregulatory changes provide an additional signal to the brain regions that regulate sleep and wakefulness. The model attempts to explain how temperature changes before and after sleep onset act in a positive feedback loop to maintain a consolidated sleep bout.

Daytime melatonin and temazepam in young adult humans: equivalent effects on sleep latency and body temperatures

1 As changes in core body temperature are generally associated with concomitant changes in sleep propensity, it is possible that the effects of hypnotic/soporific agents may be related to changes in thermoregulation. Therefore, to increase our knowledge of the mechanisms by which these agents exert their soporific effects, we compared the thermoregulatory and soporific effects of temazepam (20 mg per os (p.o.)) with those of melatonin (5 mg p.o.) when administered at 14.00 h to 20 young healthy adults (13 male, 7 female; age, 23·5 ± 0·4 years). 2 From 08.00 to 20.30 h, subjects lay in bed, and foot and rectal (Tc) temperatures were recorded. Sleep onset latency (SOL) was measured using 20 min multiple sleep latency tests, performed hourly from 11.00 to 20.00 h, during which time heart rate was recorded. 3 Compared with placebo, both melatonin and temazepam significantly reduced Tc (‐0·17 ± 0·02 and ‐0·15 ± 0·03 °C, respectively) and SOL (by 4·8 ± 1·49 and 6·5 ± 1·62 min, respectively). Although both treatments significantly increased heat loss, only melatonin demonstrated cardiac effects. Importantly, there was a temporal relationship between minimum SOL and the maximum rate of decline in Tc for both melatonin (r= 0·48) and temazepam (r= 0·44). 4 A possible role of thermoregulation in sleep initiation is suggested by the similar temporal relationship between Tc and SOL for two different classes of soporific agents.

The Relationship Between the Dim Light Melatonin Onset and Sleep on a Regular Schedule in Young Healthy Adults

The endogenous melatonin onset in dim light (DLMO) is a marker of circadian phase that can be used to appropriately time the administration of bright light or exogenous melatonin in order to elicit a desired phase shift. Determining an individuals circadian phase can be costly and time-consuming. We examined the relationship between the DLMO and sleep times in 16 young healthy individuals who slept at their habitual times for a week. The DLMO occurred about 2 hours before bedtime and 14 hours after wake. Wake time and midpoint of sleep were significantly associated with the DLMO (r = 0.77, r = 0.68 respectively), but bedtime was not (r = 0.36). The possibility of predicting young healthy normally entrained peoples DLMOs from their sleep times is discussed.

A sedentary day: effects on subsequent sleep and body temperatures in trained athletes

Exercise effects on sleep in fit healthy people have been difficult to determine because their sleep is close to optimal, leaving little room for improvement. Another method for assessing exercise effects on sleep is to significantly reduce the degree of activity in highly active people. Fifteen trained athletes who exercised daily at a moderate to high intensity were employed. By requesting that subjects remain sedentary in the laboratory for an entire day, the effect of reduced exercise on subsequent sleep parameters was assessed. Sleep and temperature were recorded after a sedentary day and after a normal day of moderate to high activity (control condition) in a counterbalanced design. In the sedentary condition, slow-wave sleep (SWS) decreased by a mean of 15.5+/-7.0 min and slow-wave activity (SWA) differed significantly (P<.05) between conditions in the first hour of sleep only. Rapid eye movement (REM) sleep increased by a mean of 17.9+/-5.7 min in the sedentary condition, while sleep onset latency (SOL) to Stages 1 and 2 increased by 10.2 and 10.7 min, respectively, and REM sleep latency decreased by 24.0+/-6.8 min (all P<.05). Between conditions, there was no overall effect on total sleep time (TST), sleep efficiency, wake after sleep onset or core or foot temperatures (P>.05). With reduced exercise load, SWS pressure may have been reduced, resulting in lower levels of SWS and increased REM sleep. Thus, the data indicate that reducing exercise has significant effects on sleep that may have implications for athletes tapering for competition.

Peripheral heat loss: a predictor of the hypothermic response to melatonin administration in young and older women.

Core hypothermia following daytime melatonin administration typically displays significant interindividual variability. As this hypothermia has been associated with significant increases in skin temperature, the mechanism by which melatonin decreases core temperature may involve increasing peripheral heat loss. If so, the interindividual variability in this effect may reflect concomitant interindividual variability in heat loss capacity at the distal periphery. For six younger (mean +/- SEM: 23.4 +/- 0.3 years) and 10 older women (mean +/- SEM: 65.6 +/- 0.7 years), the maximum decrease in core body temperature following a 5-mg (p.o.) dose of melatonin was correlated with the capacity to lose heat. This was determined by the maximum increase in contralateral hand temperature following a mild positive thermal challenge (PTC). The regression analysis yielded a significant (p < 0.01) correlation of 0.80, suggesting that the individual magnitude of hypothermia following melatonin administration may reflect the capacity of an individual to dissipate heat at the distal periphery.

Comparison of digital infrared thermal imaging (DITI) with contact thermometry: pilot data from a sleep research laboratory

Body temperature regulation is associated with changes in sleep propensity; therefore, sleep research often necessitates concomitant assessment of core and skin surface temperatures. Attachment to thermistors may limit the range of movement and comfort, introducing a potential confound that may prolong sleep initiation or increase wakefulness after sleep onset. It has been suggested that contact thermometry may artificially increase temperatures due to insulation. We report here on a method of remote sensing skin temperatures using a digital infrared thermal imaging (DITI) system, which can reduce these potential confounds. Using data from four healthy young adult volunteers (age = 26.8 +/- 2.2 years; mean +/- SEM), we compared measures of skin temperature using a DITI system with contact thermometry methods already in use in our sleep laboratory. A total of 416 skin temperature measurements (T(sk)) were collected from various sites, resulting in an overall correlation coefficient of R = 0.99 (p < 0.0001) between both methods. Regression analyses for individuals resulted in correlation coefficients between 0.80 and 0.97. These pilot results suggest that DITI can assess skin surface temperatures as accurately as contact thermometry, provided the interest is in relative and not absolute temperature changes. This and some other important limitations are discussed in more detail hereafter.