Thermophysiology and sleep : a comparison between women with and without vascular dysregulation and difficulties initiating sleep

Temperature and sleep are closely interrelated. The fall of core body temperature (CBT) at the end of the waking period is caused by heat loss via distal vasodilatation, (warm hands and feet). This process induces sleepiness. The opposite takes place at the end of the sleep episode when heat production is dominant over heat loss: distal vasoconstriction and consequently a CBT increase occur leading to an increase in the propensity to wake up. Certain individuals, mostly women, experience unusual cold thermal discomfort from cold extremities throughout their daily life. They are diagnosed as suffering from a primary vascular dysregulation (VD). VD is associated with difficulties initiating sleep (DIS), hence manifest prolonged sleep onset latency (SOL). This is possibly related to vasoconstricted distal skin regions before habitual bedtimes. The general aim of this thesis was to obtain deeper insights into the relationship between thermoregulation and sleep. Individuals with VD and DIS provide a “model of nature” to study this relationship. A higher vasoconstriction level at habitual bedtimes, i.e. a lower distal-proximal temperature gradient (DPG), can be caused by: (1) a circadian phase delay of the thermoregulatory system; (2) a larger circadian amplitude of DPG; or (3) a generally lower 24-h mean level of DPG. Therefore a first study was designed aiming at a chronobiological characterization of women with VD and DIS (WVD) by means of a constant routine protocol comprising an episode of 40-h total sleep deprivation (SD) after and before an 8-h sleep episode. Compared with a similar young group of women who do not have VD and DIS (CON), WVD showed no differences in habitual bed times, but a 1-h circadian phase delay of the circadian patterns of CBT, DPG, melatonin and sleepiness (Chapter 2). Sleep deprivation had no effect on the thermoregulatory system in either WVD or CON. The difference in internal phase of entrainment (ψint) could be a cause of DIS, i.e. could impact sleep onset. Centered on the analysis of sleep stage and electroencephalogram (EEG) power spectral analysis, Chapterfocussed on whether the sleep architecture of WVD and CON varies and whether the challenge of SD impacts sleep of WVD and CON differently. WVD exhibited a diminished first Non-Rapid-Eye-Movement sleep (NREMS) episode, and hence reduced duration of the first NREM-REM sleep cycle. They also manifested a different evolution of delta power density (EEG power density in the 0.5 - 2.0 Hz range) across successive NREM-REM sleep cycles, i.e. the
decrease in delta-power was less pronounced from the first to the second cycle. EEG
power density in the delta and alpha frequency range (0.5 - 2.0 Hz and 7.25 - 9.75
Hz, respectively) tended to be lower in WVD compared to CON. A change in internal
phase of entrainment (i.e. phase delayed thermoregulatory heat loss with respect to
the sleep-wake cycle) may influence not only SOL but also ultradian sleep patterns.
The second study aimed at disclosing effects of a temperature stimulus on sleep,
simulating in WVD and CON reinforced heat retention and heat loss by means of
cool (28°C) and warm (39°C) 35-min head-out water i mmersions, respectively,
together with a neutral (35°C) bathing condition (C hapter 4). These conditions
resemble the thermoregulatory effects of the falling and rising limbs of the CBT in the
evening and morning, respectively. A subsequent 2-h afternoon nap revealed in CON
that bathing at those temperatures in the afternoon decreases and increases
convective body heat loss via the distal skin regions, prolonging and shortening SOL
in a subsequent sleep episode, respectively, without affecting REM sleep (REMS) ,
SWS, slow-wave activity (SWA; EEG power density in the 0.5 - 4.5 Hz range), and
REMS onset latency (REML). In contrast, the heat retention condition after cool
bathing generated a shorter REML and a faster REMS accumulation in WVD
compared to CON. Additionally, WVD had a longer lasting distal vasoconstriction,
hence lower DPG values during the sleep episode after cool bathing and
consequently a less pronounced CBT drop (afterdrop) than CON. WVD showed in
general a lower EEG power density in frequency bins of the theta and alpha
frequency ranges (4.5 - 9.75 Hz) irrespective of topography, i.e. frontal or occipital
region, or bathing condition, indicating a trait-dependent feature. However, reduced
SWA was found after cool bathing in the frontal region, a difference to CON that was
no longer detectable in the occipital region and after warm bathing, indicating SWA
as a state (temperature)-dependent characteristic in WVD. Reinforced heat retention
in WVD accentuates alterations of sleep parameters already existing under normal
night sleep conditions, and this indicates that at least some sleep parameters in WVD
may be influenced by the different thermophysiological conditions in these individuals
compared to CON.
Summarized together, the observed variations of thermoregulatory and circadian
processes in WVD compared to CON are not fully reflected in the sleep EEG. The
changes in these parameters are not directly related to changes in sleep stages and
EEG power density.