Sleep. 15(4):337-343
© 1992 American Sleep Disorders Association and Sleep Research Society
Fundamental Research
Dynamics ofEEG Slow-Wave Activity and Core Body
Temperature in Human Sleep After
Exposure to Bright Light
Christian Cajochen, *Derk-Jan Dijk and Alexander A. BorbeIy
Institute of Pharmacology, University of Zurich, Zurich. Switzerland
Summary: In seven subjects sleep was recorded after a single 3-hour (2100-0000 hours) exposure to either bright
light (BL, approx. 2,500 lux) or dim light (DL, approx. 6 lux) in a crossover design. The latency to sleep onset was
increased after BL. Whereas rectal temperature before sleep onset and during the first 4 hours of sleep was higher
after BL than after DL, the time course of electroencephalographic (EEG) slow-wave activity (SWA, EEG power
density in the range of 0.75-4.5 Hz) in nonrapid eye movement sleep (NREMS) differed only slightly between the
conditions. After BL, SWA tended to be lower than after DL in the first NREMS-REMS cycle and was higher in
the fourth cycle at the time when the rectal temperature did not differ. The differences in SWA may have been due
to a minor sleep-disturbing aftereffect of BL, which was followed by a rebound. The data are not in support of a
close relationship between SWA and core body temperature. Key Words: Core body temperature-Light-Slowwave sleep-Slow-wave activity-Spectral analysis-Sleep homeostasis.
Until the early eighties it was assumed that light
exposure does not affect the human circadian system
(1). Lewy et al. (2) were the first to demonstrate that
bright light (BL) (approx. 2,500 lux) suppresses the
plasma melatonin level in humans.
Subsequently, it was shown that the circadian
rhythms of core body temperature, cortisol, urine output and alertness exhibit phase shifts after scheduled
exposure to BL (3-5). For example, the rhythms of
both body temperature and cortisol were phase delayed
after repeated exposure to BL in the evening (4), whereas a repeated exposure to BL in the early morning
resulted in an advance in the rise of body temperature
(6). When the sleep-wake cycle was held constant, BL
exposure in the morning advanced the circadian
rhythms of melatonin and body temperature and
shortened rapid eye movement sleep (REMS) latency,
whereas BL exposure in the evening delayed these
Accepted for publication March 1992.
Address correspondence and reprint requests to A. A. BorbeIy,
Institute of Pharmacology, University of Zurich, Gloriastr. 32, 8006
Zurich, Switzerland.
*Present address: Center for Circadian and Sleep Disorders Medicine, Harvard Medical School, Brigham and Women's Hospital,
Boston, MA 02115, U.S.A.
rhythms (7). Taken together, the results indicate that
light affects the phase of a single circadian pacemaker.
Also, the findings could contribute to the understanding of light therapy for disorders in which a circadian
pathophysiology is thought to be prevalent [e.g. certain
sleep disorders (8), jet lag (9), shift work difficulties
(10) and seasonal affective disorder (SAD) (11)].
The effects of BL exposure on sleep parameters and
the sleep electroencephalogram (EEG) are not yet well
documented. In most studies with repeated BL exposure in the morning or in the evening, only selected
sleep parameters (e.g. sleep onset time, REMS latency
and total sleep time) were analyzed (12,13). Light
scheduled in the morning reduced sleep duration at the
expense of REMS, whereas the EEG power density (in
the range of 0.25-15 Hz) was not affected (6,14).
Effects of light on body temperature have been recently documented. Thus, Badia et al. (15) reported
that a single exposure to BL in the evening caused an
immediate elevation of tympanic temperature.
We confirmed that a single 3-hour exposure to BL
in the evening elevates core body temperature (16).
This manipulation had an immediate effect that persisted for the first 4 hours of the subsequent sleep episode. Whereas the elevated rectal temperature was
337
338
C. CAJOCHEN ET AL.
accompanied by an increase in sleep latency, no significant effect on the visually scored sleep stages was
found. This finding was surprising as manipulations of
body temperature both prior to sleep and during sleep
have been shown to increase slow-wave sleep (SWS)
(17-19). Also other authors have proposed a close n~­
lationship between SWS and temperature regulation
(20,21).
To examine the repercussions oflight-induced temperature changes on sleep regulation, we analyzed the
dynamics ofEEG slow-wave activity (SW A; EEG power density in the 0.75-4.5-Hz band), an indicator of
sleep homeostasis, and its relation to core body temperature.
METHODS
Subjects and design
The experiment was carried out in February and
March at the Institute of Pharmacology, University tDf
Zurich. Eight male subjects (age range 23-32 years)
were selected. All had regular sleep habits and were
free of sleep complaints. The selection of subjects was
based on a questionnaire in which the sleep habits, the
medical history and the use of caffeine, alcohol and
other drugs were assessed. Subjects with sleep complaints, a significant medical history or drug use were
excluded from the study. The data of one subject could
not be used for analysis for technical reasons. The experiment took place on three consecutive days. A first
night in the sleep laboratory served for adaptation. On
the evenings of the second and third day, subjects reported at 1930 hours to the laboratory where the EEG,
electromyogram (EMG) and electrooculogram (EOG)
electrodes were attached, and a rectal probe was provided. From 2100 to 0000 hours they were exposed to
either BL (approx. 2,500 lux measured at eye level) or
dim light (DL, approx. 6 lux) in a crossover design
(three subjects were first exposed to BL; four first to
DL). During the BL, subjects sat at a desk in front of
a light screen (65 x 120 cm) consisting of eight white
fluorescent tubes (Luxsana, true light with UV A and
B, Duro-Test). The lower edge of the light screen was
situated 80 cm above the floor. The distance between
the subjects and the light source was not more than
1.5 m. They were allowed to read, play games or listen
to music from a local radio station and were under
continuous surveillance to prevent sleep.
During the exposure period and the subsequent skep
period, rectal temperature was recorded continuously.
Every 30 minutes (between 2115 and 2345 hours) a
3-minute period was scheduled for recording the waking EEG. The subjects were requested to close their
eyes for 1 minute and then to fixate a point on the wall
for 2 minutes. After the 3-hour light exposure period
Sleep, Vol. 15, No.4, 1992
the subjects went to bed at 0000 hour in a completely
darkened and sound-attenuated room in the sleep laboratory. Polygraphic sleep recordings were obtained.
Bed rest was terminated at 0745 hours.
EEG recording and analysis
EEG, EOG and submental EMG were recorded on
paper (paper speed of 10 mm/second) with a Grass
78-D polygraph. The amplitude frequency of the highpass filters for the EEG was set to 0.1 Hz, which corresponds to a time constant of 0.6 second. EEGs were
derived from C3-A2 and C4-Al, but only one derivation (usually C3-A2) was used for the analysis. All
signals were recorded with gold disc electrodes (Grass
Instruments type E5GH), filled with electrode cream
(EC2 Grass) and fixed with collodium. The data were
stored on analog magnetic tape (Hewlett Packard
3968A). In addition, two EEGs, one EMG and one
EOG were on-line digitized (sampling rate: 128 Hz)
by a signal processor board (containing a TMS-32010 chip of Texas Instruments) of a personal computer
(PC; Olivetti-M24). Before digitizing, the EEG was
low-pass filtered at 25 Hz (24 dB/octave) and on-line
processed by a Radix 8 FFT routine, which was implemented on the signal processor board. The spectra
were computed with a rectangular window for 4-second epochs. To obtain a mean spectrum per 20 seconds, five 4-second spectra were averaged off-line.
Four-second epochs, during which the limit of the AD
converter was reached (usually due to artifacts caused
by movements), were excluded. Further data reduction
was achieved by collapsing values into 0.5-Hz (in the
range of 0.25-5.0 Hz) or I-Hz (5.25-25.0 Hz) bins.
All EEG recordings were visually scored for 20-second epochs according to the criteria of Rechtschaffen
and Kales (22). A time signal generated by the PC every
20 seconds allowed an accurate sychronization between power spectra and visual scores. The sleep scores
were also stored in the pc.
Rectal temperature recording
Rectal temperature was continuously recorded during the exposure period and bed period. The temperature values were digitized and stored every 8 seconds
by a portable temperature sampler (Minilog TA, V2).
The temperature probe (diameter 5 mm, resolution
0.02°C) was inserted approximately 10 cm into the
rectum.
Statistics
For statistical analyses (ANOV A, two-tailed t test)
the SAS statistical package (SAS software, SAS Institute Inc., Cary, NC, U.S.A) was used.
339
LIGHT EFFECTS ON SLEEP EEG AND TEMPERATURE
TABLE 1. Sleep stages per NREMS-REMS cycle for the dim light (DL) and bright light (BL) conditiona
Stage
Cycle
Condition
W
2
I
DL
BL
0.2
0.1
0.1
0.1
0.5
0.2
0.2
0.1
1.9
1.2
0.6
0.5
6.6
0.8
2.9
0.2
12.0
4.0
3.5
0.8
DL
BL
0.7
0.7
5.7
4.9
1.4
1.6
7.8
8.2
2.0
1.6
1.2
1.5
36.8
36.2
5.1
2.1
51.7
47.1
5.2
6.1
41.5
33.5
179.3
175.6
5.5
3.8
4.1
2.3
11.5
8.9
40.6
39.1
2.3
5.6
2
DL
BL
1.8
1.9
21.6
19.3
3
DL
BL
13.6
11.8
1.9
2.0
9.6
10.6
1.6
1.8
8.0
11.5
4
DL
BL
DL
BL
33.1
28.1
5.0
8.1
16.0
18.7
5.4
6.0
1.8
4.9
46.7
39.9
4.7
9.2
25.5
29.3
5.1
5.3
9.8
16.4
1.8
1.7
0.7
1.9
2.2
2.8
REMS
DL
BL
14.5
13.3
6.4
2.5
24.1
27.8
3.2
5.6
19.7
36.5
MT
DL
BL
0.8
0.7
0.2
0.2
2.3
1.2
0.4
0.3
1.8
1.9
SWS
Total sleep
episode
4
3
1.1
3.3
4.5
4.5
1.4
2.3
1.1
3.4
9.0
1.6
2.5
3.8
5.5
4.3
31.7
22.1
6.8 b
3.9 b
0.5
0.4
2.6
2.1
0.6
0.5
36.2
40.5
8.6
8.9
2.9
4.4
53.5
55.0
8.3
11.5
89.8
95.5
6.7
12.4
111.4
111.6
9.4
7.5
9.4
7.8
1.3
12.1
11.2
1.2
REMSL
DL
BL
58.6
49.4
SL
DL
BL
9.9
29.7
1.5'
12.6 c
TST
DL
BL
422.0
416.2
7.5
13.3
49.4
DL
395.7
409.1
58.6
BL
u Mean values (minutes) SEM (n = 7); W, waking; MT, movement time; SWS, stages 3 + 4; REMSL, REM sleep latency; SL, sleep
latency; TST, total sleep time; SWA, slow-wave activity (0.75-4.5 Hz) in NREMS (/LV2).
h REMS episode 4 not completed in all subjects (see Methods).
,. Significant differences between DL and BL (p < 0.05; paired t test).
SWA
RESULTS
Sleep stages
Table 1 indicates the sleep stages for the four nonrapid eye movement sleep (NREMS)-REMS cycles and
for the total sleep episode. The cycles were defined
according to the criteria of Feinberg and Floyd (23),
with two exceptions: for cycle 4, a minimum of
5-minute REMS following NREMS was required, and
for cycle 2-4 the first 20-second interval after REMS
was taken as the starting epoch of the cycle. The latency
to sleep onset (i.e. the interval from lights off to the
first occurrence of stage 2 or REMS) was significantly
longer after the exposure to BL (BL: 29.7 ± 12.6; DL:
9.9 ± 1.5 minutes ± SEM; p < 0.05 paired t test on
log-transformed values; the data were log transformed
because the original data were not normally distributed), whereas the latency to REMS (i.e. the interval
between sleep onset and the first occurrence of REM
sleep) was slightly shorter but not significantly different
from DL (BL: 49.4 ± 11.2; DL: 58.6 ± 12.1 minutes;
p > 0.05). The midpoints of corresponding NREMSREMS cycles did not differ significantly between the
conditions.
Over the entire sleep episode, none of the sleep stages
differed significantly between the conditions (p > 0.05;
paired t test). The time course of SWS and REMS was
analyzed with a two-factor ANOYA for repeated measures on both factors (cycle: 1-4; condition: DL, BL).
For this analysis SWS and REMS were expressed as a
percentage of total sleep time per NREMS-REMS cycle. The effect of cycle was significant for both SWS
(F3 ,I8 = 52.83; P < 0.001) and REMS (F2 • I8 = 5.31; P
< 0.05). However, neither for SWS (F I •6 = 0.35) nor
for REMS (F I ,6 = 5.90) was a significant effect of condition observed (SWS: p > 0.2; REMS: p = 0.051).
No significant interaction between the factors condition and cycle was present (SWS, F 3,I8 = 0.71; P > 0.5;
REMS, F2• I8 = 1.10; p > 0.1).
Time course of EEG power density
Because only four cycles were completed by all subjects, the analysis was limited to these cycles. The upper two panels of Fig. 1 illustrate the changes of EEG
power density in NREMS for the BL and DL condition.
As previously (24), the mean power density iIi NREMS
was expressed for each of the cycles 2-4 relative to
Sleep, Vol. 15, No.4, 1992
1C. CAJOCHEN ET AL.
340
-
NREMS-eplsodes
en
c: .!
G> U
C >-
...
G>
~
0
-
,...
>-
~
-
Bright Light
(Bll
O~-----'-l--~lr---~Ir----'I------
0
0
a. f!-
100
Dim Light
Dynamics of slow-wave activity and body
temperature in NREMS-REMS cycles
(DU
. .I
C
150
-
c: 125
z:.
.2l
..I
CD
c:
...0
75
c:
.!!
>- u
>c: u
.-.,
"0
...G>
~
0
a.
For a more detailed visualization of the time course
ofSWA and rectal temperature, each NREMS episode
was subdivided into 20 5-percentiles, and each REMS
episode
into 4 25-percentiles regardless of the absolute
NREMS-eplsodes
episode duration (25). Mean values for SWA and rectal
(BUDl)
temperature were computed for each of these percentiles (Fig. 2).
SWA exhibited a buildup in the first part ofNREMS
episodes and a rapid decline prior to the REMS episodes. Also, the typical declining trend of SWA over
successive NREMS episodes was present (26). Although the first three REMS episodes in the BL condition showed an earlier onset than in the DL condition, the differences were not significant. Rectal
temperature in DL was significantly lower than in BL
during the last hour of the exposure time (Table 2) and
in the first 4 hours of sleep (16). In the second part of
sleep the differences became progressively smaller.
For a statistical analysis of the change of SWA over
cycles and its buildup within NREMS episodes, mean
SWAin NREMS (SW Amean) and SWA averaged over
the first 30 minutes of an NREMS episode (NREMSSWA30 min) were computed for each cycle. A repeatedmeasure ANOV A for each SWA parameter with fac10
15
20
25' tors time and condition revealed a significant effect of
time and condition (p < 0.05, for both SWA paramFrequency (Hz)
eters). Posthoc comparisons of BL and DL showed
--
C)
c:
"0
c:
0
Co
en
......G>
0
u
0
~
0
o
5
-~
FIG. 1. Change of power density during NREMS over consecutive
NREMS-REMS cycles after exposure to BL and DL (upper two
panels). For each frequency bin, subject and condition spectral values
are expressed'relative to the value in the first NREMS-REMS cycle
(=100%). Geometric means are plotted. Lines above the abscissa
ipdicate frequencies for which a one-way ANOV A on the log-transformed spectral values reveal a significant effect of cycle (p < 0.05).
In the lower two panels spectral values of BL are expressed relative
Sleep, Vol. 15, No.4, -1992
cycle 1. In both experimental conditions power density
decreased from cycle 1 to 4, particularly in the delta
and theta frequencies. The largest reduction was present in the 1.5-2.0-Hz band.
In the third panel of Fig. 1 the BL values are expressed relative to the corresponding DL values. In
cycle 1 power density in the 0.75-1.00-Hz band was
significantly lower in BL than in DL, whereas in cycle
4 the opposite changes were seen for the 0.25-2.00-Hz
band. Significantly lower values in BL were observed
also in the 15.25-17.00-Hz band in cycle 3 and in the
16.25-18.00-Hz and 22.25-23.00-Hz bands in cycle
4. In REMS, significant reductions in BL occurred only
in the first cycle (4.75-5.00 Hz; 15.25-18.00 Hz; 24.2525.00 Hz; data not shown).
Over the entire sleep episode no significant changes
were seen in the spectra ofNREMS and REMS (bottom
panel Fig. 1).
to the average value ofDL (=100%). Lines above the abscissa indicate frequency bins in which a significant difference between corresponding cycles (1-4) was present (paired t test on log-transformed
.
data; p < 0.05).
341
LIGHT EFFECTS ON SLEEP EEG AND TEMPERATURE
TABLE 2. Rectal temperature during dim light (DL) and
bright light (BL) exposure prior to sleepa
-u
0
-
Time of day
36.25
36.67 (0.15)
36.61 (0.14)
36.54 (0.13)
36.48 (0.13)
36.44 (0.12)*
36.40 (0.13)*
36.62 (0.13)
21.00-21.30
36.51 (0.12)
21.30-22.00
36.41 (0.13)
22.00-22.30
36.32 (0.16)
22.30-23.00
36.19 (0.16)
23.00-23.30
36.04 (0.15)
23.30-24.00
a Mean values ("C) SEM per 30 minutes (n = 7). Significant differences between DL and BL indicated by *p < 0.01 (paired t test).
....Q)::J
ro
....
36.00
~
E
~
-
(ij
BL
DL
35.75
0
Q)
a:
condition (F1.6 = 0.41; p > 0.05) and no significant
interaction (F3 18 = 0.36; P > 0.05).
The mean r~ctal temperature per cycle (TEMP~ean)
was higher in the first three cycles after BL than after
DL (p < 0.01).
The change of rectal temperature in the first 30 minutes of a NREMS episode was determined by computing the difference between the mean 5-minute value
preceding the episode and the mean value of the 2530-minute interval. There were no significant differences between BL and DL.
300
:.~!
)..
iii
rfi.
->:~
:
0
«
r
Q)
>
ro
;:
100
I
:!=
0
Ci5
o
o
o
).
:
200
EEG power density in the waking EEG
•
1.5
3
Hours
4.5
6
FIG. 2. Dynamics of SWA and rectal temperature for BL (interrupted lines) and DL (continuous lines). Hatched areas indicate ± I
SE. Mean percentiles (n = 7); SWA is expressed as the percentage
of the mean NREMS value (100%). The bars above the abscissa
indicate REMS episodes (REMS episode 4 is incomplete; open bars
= BL; filled bars·= DL). The curves connect mean values for percentiles and are plotted relative to the mean onset and termination
9f each cycle (see text).
The analysis of the waking EEG was limited to artifact-free epochs (59.5% of all epochs; artifacts were
frequent due to movements and eye blinks). The EEG
power density in the 3.75-8.00-Hz range showed a
trend toward lower values in the BL condition (eyes
open) compared to DL (p < 0.1; data not shown).
However, neither for the eyes open nor for the eyes
closed condition were there any significant differences
between BL and DL.
DISCUSSION
Exposure to BL in the evening increased core body
temperature, a result that is in accordance with the
significant differences in cycle 4 of SWAmean and findings of Badia et al. (15). This prominent effect on
NREMS-SWA30 min (p < 0.05; paired t test). An anal- temperature was accompanied by only minor changes
ysis of consecutive 5-minute intervals revealed that of sleep and the EEG. In contrast to the increase in
the significant change in cycle 4 occurred in the last sleep latency after BL, the REMS latency was not aftwo 5-minute intervals of the first 30 minutes. Aver- fected. Although the REMS latencies in DL were rather
aged over the entire sleep episode, SWAin NREMS short, they are within the range of normal healthy young
did not differ significantly between conditions (DL = subjects when they are well adapted to. the laboratory
100%; BL = 103.4%; Table O.
(27). There were no significant differences in the sleep
The rise rate of SWAin the first 30 minutes in each stages, and the typical decline of SWA over successive
of the four NREMS episodes (NREMS-SWArise) was cycles was similar under both experimental conditions
estimated by calculating for each individual the me- (Fig. 1). For the entire sleep episode, SW A as well as
dian of the differences in SWA over consecutive power density in the other frequency bands showed no
5-minute intervals (24). A repeated measure ANOVA significant differences between the conditions. Nev(two factors: condition, cycle) revealed a significant ertheless, small but significant differences in the time
effect of cycle (F3•18 = 21.17; P < 0.001), no effect of course of SWA were present. In the first NREMS.,..
Sleep. Vol. 15. No.4. 1992
C. CAJOCHEN ET AL.
342
.~.
TABLE 3. Slow-wave activity (SWA) and rectal temperature parameters/or the NREMS-REMS cycles
Cycle
Parameter
SWAme"o
(%)
NREMS-SWA30minb
(%)
NREMS-SWAri~e
(%)
Tempmean d
("C)
Condition
I
2
DL
BL
189.0 (8.5)
165.1 (16.5)
147.8 (10.7)
153.8 (17.2)
34.1(1.7)
36.5 (5.7)
122.1 (12.6)
129.6 (14.9)
DL
BL
DL
BL
DL
BL
DL
BL
35.8 (0.1)**
36.1 (0.1 )**
-10.5 (7.2)
-15.4 (3.1)
3
4
70.3 (9.1)
85.2 (5.0)
52.8 (7.1)
64.2 (9.4)
44.7 (4.1)*
64.6 (9.2)*
10.9 (3.0)
11.6(1.7)
6.0 (0.9)
10.9 (2.4)
35.7 (0.1)**
36.0 (0.1)**
35.8 (0.1)**
36.1 (0.1 )**
36.0 (0.1)
36.0 (0.1)
0.5 (1.9)
0.0 (2.4)
6.7 (2.7)
2.4 (2.9)
1.6 (3.4)
1.5 (2.4)
81.4 (11.5)
94.8 (12.9)
20.8 (4.6)
19.9 (5.1)
39.0 (3.1)*
51.7 (6.0)*
° Mean SWAin NREMS.
b Mean SWAin the first 30 minutes of the NREMS episode.
e The interindividual mean of the intraindividual median valUl! of the differences in SWA over consecutive 5-minute intervals in the
first 30 minutes of a NREMS episode.
d Mean rectal temperature ("C) per cycle.
20
e Change in rectal temperature over the first 30 minutes of the NREMS episode (1O- C); difference between the mean 5-minute value
preceding the episode and the mean value of the 25-30-minute interval.
All SWA parameters are expressed as a percentage of the mean SWA in NREMS (100%). Significant differences between BL and DL are
indicated by *p < 0.05 and **p < 0.01 (paired t test).
REMS cycle, power density in a frequency bin within
the delta range was lower in BL than in DL. Conversely, an increase in delta activity was present in the fourth
cycle. This shift in the distribution ofSWA could have
been caused by a slight suppression in the first cycle
as a consequence of BL and a rebound during later
parts of sleep. A similar intra sleep rebound has been
induced after the selective suppression of SWAby
acoustic stimuli in the first 3 hours of sleep (28). The
higher rise rate of SWA in the fourth NREMS episode
is an indication that "sleep pressure" in the later part
of sleep was higher in BL than in DL (24). On the other
hand, it is more difficult to specify the factor that led
to the slight initial suppression of SWAin BL. Although the longer sleep latency is consistent with a
sleep-disturbing aftereffect of BL, the rise rate in the
first NREMS episode was not altered (Table 3). It may
be the somewhat earlier initiation ofREMS in BL (Fig.
2) that gave rise to a curtailment of SWAin the first
cycle and a compensatory increase in cycle 4.
The present study provided the opportunity of comparing the dynamics of SWA and rectal temperature.
It had been reported that the elevation of body temperature during waking to values that are at the limit
or above values that occur under physiological conditions enhance SWS (17-19). Other authors proposed
that a regulated rapid decline in core body temperature
after sleep onset is a necessary prerequisite for sustained SWS (29). The present data do not support the
assumption of a close relationship between body temperature on the one hand and either SWS or SWA on
the other hand. The higher body temperature in BL
during the hours preceding sleep (16) did not affect
Sleep, Vol. 15, No.4, 1992
SWS, and, if anything, reduced SWA in the first
NREMS-REMS cycle. As has been mentioned, the
slight increase of SWAin cycle 4 constituted probably
a compensatory response. However, the possibility that
it may have been due to a delayed effect of the heat
load cannot be excluded. There was no indication that
the rate of initial temperature decline was related to
SWS or SWA. If anything, the slight reduction ofSW A
in the first cycle of BL was associated with a steeper
decline of rectal temperature (Table 3). This weak relationship between SWS/SWA and body temperature
is in accordance with Dijk et al. (30) who found a
dissociation between the time course ofSW A and body
temperature.
In conclusion, exposure to BL prior to sleep constitutes a subtle method for elevating body temperature
at sleep onset and during the first part of sleep. This
effect is mediated via the eyes rather than by the radiant
heat of light (16) and must be due to an action on
mechanisms subserving thermoregulation and/or circadian rhythmicity. Processes underlying sleep homeostasis are apparently little affected when body temperature is manipulated within a physiological range.
Acknowledgements: We thank Dr. I. Tobler and Dr. P.
Achermann for their comments and Dr. M. MUnch for her
assistance in data acquisition. The study was supported by
the Swiss National Science Foundation, grant no. 3125634.88.
REFERENCES
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