The effects of evening bright-light on human body temperature and sleep architecture

A number of influential theories of sleep function argue for a close relationship between body temperature and sleep architecture. The energy conservation theory and thermoregulatory theories of sleep, including the central nervous system restoration and protection theories, each predict increased Slow Wave Sleep (SWS) following elevations in body temperature at sleep onset and during sleep. It has recently become apparent that appropriately timed evening bright-light (BL) (>2500 lux) may suppress melatonin, elevate core temperature, and produce delays of the human Core Temperature Rhythm (CTR). While these effects are being investigated for their potential within industry and to treat various affective and sleep related disorders, the effects of evening BL on sleep are unclear as the literature is small and differing results are reported. The effects of BL on temperature suggest that enhanced SWS might follow evening BL, as increased SWS has been empirically associated with elevations in temperature at sleep onset and, to a lesser extent, with a phase-delay of the CTR. However, the suppression of melatonin associated with evening BL suggests sleep might be disrupted, as melatonin has been proposed to be a hypnotic agent. In the present thesis three experiments are reported which were designed to investigate the effects of evening BL on rectal temperature and sleep. In the first experiment 11 male subjects were twice exposed to BL or Dim-Light (DL) (normal room illumination) for 2hrs prior to habitual bedtime for two consecutive nights in a crossover design. Rectal temperature was significantly elevated during the first and second hours following BL, and significantly more Stage 3 sleep and SWS occurred with a trend for increased SWS in the fourth sleep cycle. The second experiment was designed to assess the immediate effects of evening BL on core temperature and sleep, independent from potential CTR phase-shifting effects produced after multiple exposures to evening BL on consecutive evenings. 11 male subjects were run in two conditions. In the BL condition Ss were exposed to BL for three consecutive evenings and to DL on the fourth. In the dim-light condition Ss were exposed to DL on all four evenings. It was anticipated that three consecutive exposures to evening BL would phasedelay the CTR such that the effects of a temperature rhythm delay on sleep could be assessed independent of BL itself on night 4. On night 1 no significant elevation in rectal temperature was found but SWS was increased in the fourth sleep cycle. On night 3 rectal temperature was significantly elevated during the first two hours following BL, and SWS and Slow Wave Activity (SWA) (.25-3 Hz EEG activity) were significantly increased across the night, most noticeably in the third sleep cycle. No differences in the position of the CTR were evident on night 4, but temperature in the BL condition was significantly lower than in the DL condition during the first and fifth hours following light exposure. In addition, sleep onset latency (SOL) and amounts of Wake were increased in the BL condition on this night. The results indicated that BL administered until habitual bedtime over three consecutive nights may produce immediate effects on core temperature without necessarily delaying the CTR. The SWS enhancing effects of evening BL were found when, and only when, core temperature was significantly elevated around the time of sleep onset. This experiment also suggested that these effects are found more robustly following more than one exposure to BL. The third experiment was designed to test this hypothesis. A betweensubjects design was utilised in which three groups of 12 male subjects were run in three conditions. In the Dim-Dim (DD) condition subjects were exposed to DL for two consecutive nights. In the Dim-Bright (DB) condition subjects were exposed to DL on night 1 and BL on night 2 over consecutive nights. In the Bright-Bright (BB) condition subjects were exposed to BL on both nights. Rectal temperature during the first hour following light treatment was significantly elevated in the BB condition and non-significantly elevated in the , DB condition compared to the DD condition. SWA and Total EEG Power (TP) (0.25 Hz to 50 Hz EEG activity) were enhanced in both the DB and BB conditions. In addition, significantly more SWS was found to occur in the fourth sleep cycle in the DB and BB conditions compared with the DD condition. Thus, evening BL elevated rectal temperature and enhanced SWS upon a single exposure, but these effects were enhanced by exposure to the light on the previous night. Taken together these experiments indicate that evening bright light elevates rectal temperature and SWS/SWA increases during subsequent sleep, particularly late in the night. These results are consistent with other experimental paradigms in which temperature is raised (e.g. exercise and passive heating) and SWS is observed to increase. Interpreted this way the results add to the body of evidence that suggests SWS and thermoregulation are intimately linked. Another possible interpretation is that a rebound in melatonin following early suppression by bright-light produced increased SWS later the same night. It is also possible that both thermal and melatonin rebound effects occurred following evening bright-light; the thermal effects maintained SWS levels under conditions of melatonin suppression early in the sleep period while melatonin rebound later in the sleep period resulted in the most prominent increases in SWS. Further research might examine this possibility by monitoring plasma melatonin levels, temperature and SWS continuously following evening bright-light. The major finding of this thesis is that bright-light administered until habitual bedtime produces immediate elevations in temperature and increased SWS/SWA, especially late in the night.