R E V I E W Open Access
Effects of thermal environment on sleep and
and Koh Mizuno
The thermal environment is one of the most important factors that can affect human sleep. The stereotypical
effects of heat or cold exposure are increased wakefulness and decreased rapid eye movement sleep and slow
wave sleep. These effects of the thermal environment on sleep stages are strongly linked to thermoregulation,
which affects the mechanism regulating sleep. The effects on sleep stages also differ depending on the use of
bedding and/or clothing. In semi-nude subjects, sleep stages are more affected by cold exposure than heat
exposure. In real-life situations where bedding and clothing are used, heat exposure increases wakefulness and
decreases slow wave sleep and rapid eye movement sleep. Humid heat exposure further increases thermal load
during sleep and affects sleep stages and thermoregulation. On the other hand, cold exposure does not affect
sleep stages, though the use of beddings and clothing during sleep is critical in supporting thermoregulation and
sleep in cold exposure. However, cold exposure affects cardiac autonomic response during sleep without affecting
sleep stages and subjective sensations. These results indicate that the impact of cold exposure may be greater than
that of heat exposure in real-life situations; thus, further studies are warranted that consider the effect of cold
exposure on sleep and other physiological parameters.
Keywords: Cold, Heat, Sleep, Thermal environment, Thermoregulation
The thermal environment is a key determinant of sleep
because thermoregulation is strongly linked to the
mechanism regulating sleep . Excessively high or low
ambient temperature (Ta) may affect sleep even in
healthy humans without insomnia. Furthermore, dis-
turbed nocturnal sleep affects not only daytime activities,
but is also related to various adverse health effects, such
as obesity , quality of life, and even mortality [3,4].
These findings indicate that maintaining a comfortable
thermal sleep environment is important for sleep main-
tenance as well as daytime activities and health status.
Among the various thermal environmental factors, the re-
lationship between Ta and the use of clothing and bed-
dings differs greatly between humans and animals. The
effects of Ta on sleep stages differ depending on whether
subjects are semi-nude or use bedding and clothing, mak-
ing it difficult to extrapolate the results of animal studies
related to thermal environment and sleep to humans. The
use of clothing and beddings greatly aid in maintaining
the body temperature at an acceptable thermal state in a
variety of environments by providing thermal resistance
for the human body from its environment . In this re-
view, based on our studies related to thermoregulation
and sleep in humans, the effects of the thermal environ-
ment on sleep and circadian rhythm are discussed. The
effects of heat and cold exposure, including bedding and
clothing conditions along with their effects in the elderly,
are of special interest, because these are the important fac-
tors that most impact sleep and thermoregulation.
Sleep and thermoregulation
Many previous studies in humans indicate that sleep is
strongly linked to thermoregulation (For examples, see
[1,6]), which is primarily controlled by circadian rhythm
and sleep regulation. Humans have a sleep-wake rhythm
that is repeated in a 24-hour cycle. The core body
temperature (Tcore), which also cycles along with the
sleep-wake rhythm, decreases during the nocturnal sleep
phase and increases during the wake phase repeatedly in a
* Correspondence: firstname.lastname@example.org
Kansei Fukushi Research Center, Tohoku Fukushi University, 1-149-6
Kunimigaoka Aoba Sendai, Miyagi, 981-0935, Japan
Full list of author information is available at the end of the article
© 2012 Okamoto-Mizuno and Mizuno; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms
of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use,
distribution, and reproduction in any medium, provided the original work is properly cited.
Okamoto-Mizuno and Mizuno Journal of Physiological Anthropology 2012, 31:14
24-hour circadian rhythm. Sleep is most likely to occur
when Tcore decreases, while it hardly occurs during the
increasing phases . This relationship between the sleep-
wake rhythm and the circadian rhythm of Tcore is import-
ant for maintaining sleep. At the normal sleep onset
period in humans, Tcore decreases due to an underlying
circadian rhythm, and sleep further induces this effect .
The driving force behind this Tcore decrease is the periph-
eral skin temperature (Tsk), which is rich in arteriovenous
anastomoses and plays a central role in thermoregulation
by adjusting blood flow to the skin . Increased periph-
eral Tsk is largely due to reduced activation of noradrener-
gic vasoconstrictor tone, allowing greater inflow of heated
blood from the core, thus facilitating heat loss to the en-
vironment through the skin surface . The selective
vasodilation of distal skin regions promotes the rapid
onset of sleep  and is strongly associated with mela-
tonin secretion . Indeed, foot Tsk warming has been
shown to reduce sleep onset latency , indicating that
normal sleep onset is accomplished by increased periph-
eral heat loss and/or Tcore decrease . The Tcore de-
crease in the sleep onset period is also strongly associated
with cardiac autonomic activity. It has been suggested that
changes in the cardiac autonomic nervous system precede
sleep onset, which is strongly associated with changes in
body temperature .
After sleep onset, Tcore gradually decreases further
, while distal and proximal Tsk remain high . The
importance of maintaining Tsk at physiological range for
sleep maintenance has been suggested . In the elderly,
only chest Tsk shows a significant decrease during sleep
compared with the young [16,17], and slow wave sleep
(SWS) decreases and wakefulness increases compared
with the young, with increased insomnia . The sleep
parameters measured by actigraphy correlate only with
chest Tsk, and decreased chest Tsk is associated with a
decrease in the sleep efficiency index . Interestingly,
even a slight increase in proximal Tsk increases the
amount of SWS and decreases the early-morning awa-
kening in the elderly . Sleep-related areas in the
brain are associated with an increased Tsk within the
physiological range during sleep . Moreover, Tsk
might act as an input signal to sleep-regulating systems
. These results indicate that slightly increasing the
proximal Tsk may help alleviate sleep problems, espe-
cially in the elderly. The temperature and humidity of
the microclimate between humans and bed covers (bed
climate) also play crucial roles in creating a warm bed
climate temperature to support increased Tsk and sleep
. The bed climate temperature and relative humidity
are generally maintained around 32°C to 34°C, 40% to
60% relative humidity when normal sleep is obtained
[22,23], which is in agreement with the comfort bed cli-
mate range suggested by Yanase .
Another important aspect to consider is that the
thermoregulatory response during sleep differs depend-
ing on sleep stages. In animal studies, the thermoregula-
tory system is abolished during rapid eye movement
sleep (REM) , due to a loss of thermosensitivity in
the majority of the hypothalamic preoptic neurons .
In humans, thermosensitivity during REM is not com-
pletely depressed; however, sensitivity to hot or cold
stimulation is reduced in REM compared to non-REM
and wakefulness [27,28]. In addition, the sweat rate
increases during SWS compared to other sleep stages
, while delayed onset of sweating  and a
decreased sweat rate  decrease evaporative heat dis-
sipation and reduce heat tolerance during REM. Inter-
estingly, the decreased sweat rate during REM is
observed prior to REM stage onset . Considering
that skin sympathetic nerve activity (SSNA) contains
sudomotor activity synchronous with vasodilator activity
, this result indicates that SSNA might precede the
sleep stage shift corresponding with heart rate variability
(HRV) preceding the sleep stage shift at the sleep onset
period . Changes in the sensitivity of the sweat re-
sponse depending on sleep stages are considered to be a
central drive effect, since no peripheral change in sweat
gland levels has been observed . In cold exposure,
shivering during sleep is confined to stages 1 and 2 and
is not observed in SWS and REM , while the Tsk of
the extremities is decreased during REM compared to
that at control conditions . These results indicate
that REM and thermoregulation are mutually exclusive
and partly explain the decrease in REM observed during
heat or cold exposure, bearing in mind that REM is
more sensitive to Ta than other sleep stages.
Although physiological thermoregulation related to
sleep has been well defined, behavioral thermoregulation
during sleep remains unclear. Limited behavioral
thermoregulation reduces the thermoregulatory response
during sleep compared to wakefulness. However, Ta
increases or decreases during sleep significantly decrease
or increase, respectively, the areas of the body covered
by bed covers, with the neck, shoulder and upper ex-
tremities showing higher sensitivity than lower extrem-
ities and the trunk . In heat exposure, lateral body
position increases compared to the supine position, pos-
sibly because this position may decrease the contact area
between the body and the mattress . These results
suggest that behavioral thermoregulation is active during
sleep and that bed cover behaviors and body position
may have an important role. Considering that poor slee-
pers spend more time on their backs with their heads
straight, sleep positions may be related to sleep quality
. It is interesting to consider these behaviors in vari-
ous thermal environments during sleep, since it may be
an important sleep variable that would aid in our further
Okamoto-Mizuno and Mizuno Journal of Physiological Anthropology 2012, 31:14 Page 2 of 9
understanding of thermoregulation during sleep in
Effects of heat exposure
Increases in wakefulness are greater in cold Ta than in
heat , suggesting that the impact of cold exposure is
greater than that of heat exposure. Ta higher or lower
than the thermal neutral temperature (29°C) have been
shown to increase wakefulness and decrease REM and
SWS in semi-nude subjects . However, these results
are based on semi-nude subjects and exclude the effects
of bed covers and clothing. In real-life situations where
bed covers and clothing are used, sleep is actually dis-
turbed during heat exposure rather than cold exposure
in the young , as well as in the elderly . The
increased wakefulness and decreased SWS and REM are
stereotypical effects that are observed in heat exposure
. These effects on sleep stages are concentrated in
the initial segment rather than the later segment of
sleep. One possible explanation for this is that sleep dis-
ruption in the initial sleep segment leads to an increased
demand, which may overcome the thermal stress in the
later segment of sleep [42,43]. Heat-related sleep disrup-
tions do not adapt even after 5 days of continuous day-
time and nocturnal heat exposure . Furthermore, the
effect on SWS does not change after partial sleep
deprivation where sleep pressure is increased . These
results suggest a strong effect of heat load on sleep
stages, which is related to thermoregulation during
sleep. Thus, wakefulness is the only stage that can cope
with an increased thermal load  and that wakefulness
replaces SWS and REM to maintain homeothermy.
Heat load suppresses the decrease in Tcore and
increases Tsk and whole body sweat loss during sleep
[43,46]. Although Tsk increases at the onset of sleep,
high Ta suppresses heat loss to the environment through
the skin surface, thereby suppressing the decrease in
Tcore. This suppressed decrease in Tcore may disturb
sleep at the initial segment of sleep. The increased Tsk is
largely due to increased skin blood flow, which is regu-
lated primarily through two pathways in the sympathetic
nervous system: the noradrenergic vasoconstrictor sys-
tem and the active vasodilator system. Increased Tsk
during sleep in heat exposure may be largely due to an
increased active vasodilator system. In subjects that are
awake, an active vasodilator system is responsible for
most of the vasodilatory responses to heat stress .
The SSNA contains vasodilator activity synchronous
with sudomotor activity  and may lead to an increase
in whole body sweat loss. Taken together, these results
suggest the possibility that increased vasodilator activity
may be related to increased Tsk and wakefulness due to
heat exposure during sleep. Because sleep distribution is
controlled by both peripheral and central driving effects
[13,48], it is possible that increased active vasodilation
and Tcore both increase wakefulness during heat expos-
ure. These results support the notion that, although
sleep states affect thermoregulation, thermoregulation
equally affects the mechanism governing sleep .
One of the most important factors that increase heat
stress during sleep is the humidity. Humid heat exposure
further increases wakefulness, decreases REM and SWS,
and excessively suppresses the decrease in Tcore,
whereas Tsk and whole body sweat loss are not affected
. Humid heat exposure most probably increases heat
stress because of the difference in the sweat response
caused by the humidity. Decreased ambient humidity
allows sweat to evaporate, thereby dissipating the heat,
whereas increased humidity does not allow the sweat to
evaporate, causing the skin to remain wet. The dripping
sweat and increased skin wetness decrease the sweat re-
sponse due to hidromeiosis preventing dehydration.
These results indicate the importance of taking humidity
into account, especially in Japan and many other Asian
countries that experience humid heat in the summer.
Interestingly, although the exposure time is the same,
the effect of humid heat is greater in the initial segment
than in the later segment of sleep. Humid heat exposure
during the later segment of sleep increases wakefulness
in that segment [49,50]. In contrast, humid heat expos-
ure in the initial segment decreases SWS in that seg-
ment and increases wakefulness in both segments .
Furthermore, decreased SWS in the initial segment of
sleep tends to increase it in the later segment of sleep.
Thus, humid heat exposure in the initial segment of
sleep appears to change the polarity of SWS . These
effects on sleep stages can be explained by thermoregu-
lation and microclimate temperature (temperature and
humidity of the microclimate between skin and the
clothing) (Figure 1). Humid heat exposure in the later
segment causes a decrease in Tcore in the initial seg-
ment, followed by an increase in Tcore, Tsk and micro-
climate temperature in the later segment. Humid heat
exposure in the initial segment suppresses the decrease
in Tcore, whereas Tsk and the microclimate temperature
increase lead to a decrease in SWS and an increase in
wakefulness. Furthermore, the sharp decrease in Tcore,
Tsk and the microclimate temperature in the later seg-
ment of sleep may also increase wakefulness. The chil-
ling effects of a decrease in Ta and humidity and a
reduction in clothing insulation due to wetness 
caused by sweating at initial humid heat exposure may
also be a possibility for the increase in wakefulness. An-
other possible contributing factor for decreased Tsk and
Tcore in the later segment of sleep could be that a de-
crease in Ta coincides with a time when REM sleep gen-
erally increases, since Tsk decreases are greater in REM
compared to other sleep stages . In Japan, a majority
Okamoto-Mizuno and Mizuno Journal of Physiological Anthropology 2012, 31:14 Page 3 of 9
use air conditioning only for a few hours after going to
sleep  due to the notion that being exposed to air
conditioning is unhealthy , and 90% of Japanese
people are interested in saving energy . These results
indicate that if air conditioning use is limited, then it
should be used during the initial segment of sleep. Fur-
thermore, when air conditioning is used in the later seg-
ment of sleep, drying off the sweat and changing clothing
are essential to avoid chilling effects.
In the elderly, even mild heat exposure increases
wakefulness and decreases REM . Since the elderly
exhibit a decreased amount of SWS even under normal
conditions, SWS is not thought to be affected by heat
exposure. Sleep consolidation decreases in older men
, which in turn increases susceptibility to external
arousal stimuli during sleep . These changes in sleep
may decrease the thermal awakening threshold. Another
reason for this could be reduced heat tolerance in older
men, since most heat exposure studies have found a
reduced ability to regulate Tcore in subjects who are
awake (for example, see ). Mild heat exposure
further suppresses the decline in Tcore, increases Tsk,
and increases whole body sweat loss by two-fold in the
elderly . The increase in nocturnal Tcore  and
the attenuation of the nocturnal drop in Tcore  may
underlie age-related declines in sleep maintenance and
sleep quality. Furthermore, the period of overnight fasting
results in mild dehydration in older men even under
normal conditions , suggesting that increased whole
body sweat loss during sleep in mild heat exposure may
be related to dehydration in the elderly. Although fur-
needed, it appears quite likely that sleep in older men is
more affected by heat exposure than in younger men.
These results indicate that the Ta during sleep warrants
particularly careful consideration in older men, espe-
cially since decreased sleep duration in the older men is
related to reduced quality of life and mortality [3,4]. Ta
for the elderly should also take into account clothing
conditions; elderly Japanese people wear more than two
layers of underwear under nightwear even in summer
Experiment 1 Experiment 2
Temperature ( )
37 Clothing Microclimate
01234567 01 23 45 67
Time (Hr) Time (Hr)
Figure 1 Effects of humid heat exposure at different segment of sleep on thermoregulation. Experiments 1 (26°C 60%RH stable (26),
compared with 26°C 60% in the initial segment and 32°C 80%RH in the later segment of sleep (26 !32)) and experiments 2 (26°C60%RH stable
(26), compared with 32°C 80%RH in the initial segment and 26°C60%RH in the later segment of sleep (32 !26)).. Reprinted from Okamoto-Mizuno
K, Tsuzuki K, MizunoK, Iwaki T: Effects of partial humid heat exposure during different segments of sleep on human sleep stages and body
temperature. Physiol Behav 2005, 83:759–765 with kind permission from Elsevier.
Okamoto-Mizuno and Mizuno Journal of Physiological Anthropology 2012, 31:14 Page 4 of 9
Effects of cold exposure
The difference between cold exposure and heat exposure
is that cold exposure mainly affects the later segment of
sleep, where REM is dominant . In semi-nude sub-
jects, cold exposure mainly affects REM due to suppres-
sion of the thermoregulatory response [35,40]. SWS is
not affected because it predominates in the initial seg-
ment of sleep . In thermoregulation during sleep,
Tcore decreases through the night  as the Ta
decreases . However, in real-life situations people
generally use clothing and bed covers during sleep in
cold exposure. In studies using clothing and/or bedding,
no significant difference was observed in sleep in a Ta
range of 13°C to 23°C  and 3°C to 17°C . Also,
no significant difference in sleep quality measured by
actigraphy was observed between 9°C and 20°C in the
elderly . These results indicate that, in real-life situa-
tions, cold exposure does not affect sleep. This is related
to the fact that despite large changes in Ta the bed climate
temperature remained relatively constant . The use of
bed covers allows for the development of an isolated high
bed climate temperature, which is critical for maintaining
sleep  as well as determining sleep quality .
However, our study indicates that cold exposure sig-
nificantly changes cardiac autonomic activity during
sleep, without affecting the sleep stages (Figure 2) .
With regard to cardiac autonomic activity based on the
HRV index, the ratio of the low frequency (LF) to high
frequency (HF) band (LF/HF) significantly decreases
during stage 2 and SWS, while the percentage of the LF
component (LF/(LF + HF)) significantly decrea ses during
SWS as the Ta decreases from 17°C to 3°C. In contrast,
no significant effect is observed during REM or wakeful-
ness. These results may indicate that cardiac parasympa-
thetic activity predominates under cold exposure during
stage 2 and SWS, although the results of the LF/HF and
LF/(LF + HF) should be interpreted with caution. The
dominant parasympathetic activity during stage 2 and
SWS may be related to at least three factors: cold stimu-
lation of the head since sufficient thermal insulation of
the body is obtained from bedding and clothing; cold air
inhalation; and whole body cooling. First, cold stimula-
tion of the face, a unique reflex referred to as cold face
test, increases the cardiac parasympathetic activity and
the peripheral skin SSNA simultaneously and integrates
the trigeminal brain stem reflex arc in wakeful subjects
. Additionally, this reflex activates reflex centers
located in the medullary region and induces bradycardia
[70-72]. Furthermore, the concomitant increase in the
SSNA leads to vasoconstriction, an increase in blood
pressure [70-72] and a significant increase in the HF
component [69,73]. Second, inhalation of cold air may
increase muscle sympathetic nervous activity and blood
pressure in wakeful subjects . Third, whole body
cooling may also be related to increases in systolic and
diastolic blood pressure and decreases in heart rate in
wakeful subjects . Considering that approximately
70% of sleep time comprises stage 2 and SWS, the car-
diac parasympathetic activity may be dominant during
sleep in cold exposure.
e2 SWS REM Wake
Figure 2 Changes of heart rate and high frequency, percentage
of low frequency and ratio of low frequency to high frequency
components in three conditions. The vertical line represents the
standard error. *indicates the significant level after Friedman test;
indicates the significant level after Scheffe’s post-hoc test;
P<0.05. Reprinted from Okamoto-Mizuno K, Tsuzuki K, Mizuno K,
Ohshiro Y: Effects of low ambient temperature on heart rate
variability during sleep in humans. Eur J Appl Physiol 2009,
105:191–197 with kind permission from Springer Science and
Okamoto-Mizuno and Mizuno Journal of Physiological Anthropology 2012, 31:14 Page 5 of 9
These findings could partly explain the adverse cardiac
events that peak during the colder periods in the winter
season [76,77]. Mortality due to ischemic heart disease is
not related to low outside temperature, but to low liv-
ing-room temperatures and limited bedroom heating in
the winter . Cold climates increase blood pressure
 as well as the levels of hematological factors that
favor arterial thrombosis  and fibrinogen synthesis
. It has been suggested that the onset of major car-
diovascular events is triggered by sleep stage-dependent
fluctuations in the autonomic nervous system . Sig-
nificantly dominant cardiac parasympathetic activity
during stage 2 and SWS, which is not observed during
REM and wakefulness in cold exposure, suggests marked
variations in HRV during the transition from stage 2 to
REM and wakefulness. The marked rise in HRV during
transition from non-REM to awakening and REM favors
adverse cardiac events . Further study considering
the relationship between the increased incidence of ad-
verse cardiac events and marked variations in HRV dur-
ing transition from non-REM to wakefulness and REM
may provide insights into understanding the increase in
cardiac events peaking in winter. Besides HRV, the lack
of nocturnal decline in blood pressure is also related to
an increase in end-organ damage and cardiovascular
events [83,84]. Considering that the cold face test, inhaling
cold air and whole body cooling accompany increased
blood pressure, it would be interesting to investigate
whether cold exposure suppresses blood pressure decline
during sleep. It is extremely important to note that Ta in
winter should be maintained at a level higher than 10°C.
However, the most difficult aspect of cold exposure is that
sleep is not disturbed. The impact on the cardiovascular
response may be occurring without subjective sensation,
suggesting that cold exposure may have more impact than
heat exposure. In Japan, bedroom Ta falls to as low as 3°C
in the suburbs . Excessive layers of underwear under
night wear and bed covers are common observations in
elderly Japanese people  and this behavior supports
sleep in cold exposure. Indeed, about 50% of elderly Japa-
nese people use two to six layers of underwear and three
to five layers of bed covers . The most important as-
pect of this is whether HRV during sleep in elderly people
habitually sleeping in cold Ta is affected by cold exposure
or is somewhat adapted to it. Further study on measuring
HRV in the elderly habitually sleeping in cold Ta at home
may thus be required.
Ambient temperature and circadian rhythm
The environmental light-dark cycle is the principal en-
vironmental synchronizer of the circadian pacemaker in
humans as well as other species ; however, the effects
of social cues and other nonphotic entrainment, includ-
ing Ta, on human circadian system are less understood.
Twenty-four hours of warm Ta increases activity, sug-
gesting that Ta has a masking effect on circadian activity
rhythms in animal studies . In high and cool Ta
cycles, Ta acts as a weak synchronizer in laboratory rats
 and mice . These results suggest that, at the
least, Ta may have masking effects on circadian activity
rhythms in homeothermic animals. In humans, many
studies indicate that different Ta cycles during sleep
within the thermoneutral Ta range can affect Tcore.
Decreased Ta occurring a few hours before and after
sleep onset and increased Ta occurring around wake-up
time increases the decline in Tcore and advances the
Tcore nadir compared to constant Ta [89,90] and/or
the opposite Ta cycle [91,92]. The effects of these cyc-
lic Ta changes do not significantly affect sleep stages
, or increase SWS compared to constant Ta .
These results indicate that cyclic Ta changes do not
induce any adverse effects on sleep stages at least
within the thermoneutral temperature range. Interest-
ingly, studies by Dewasmes et al. [89,93] showed that
cyclic Ta, as opposed to constant Ta, advanced the
minimum Tcore by 143 minutes and the propensity
for REM. The REM cycle length changes depending
on Ta with a delayed REM cycle in low Ta compared
with high Ta , and the REM propensity has a close
relationship with body temperature rhythm .
These results indicate that Ta itself as well as cyclic Ta
change may advance circadian Tcore and/or REM and
that the thermoregulatory system may have effects on
phase advancing mechanisms.
One possible explanation for these effects of cyclic Ta
change on Tcore may be the reduced thermoregulation
during sleep compared to wakefulness . No significant
difference between sleep stages at Ta of 13°C to 23°C is
observed, although Tcore clearly decreases as the Ta
decreases . Not only Ta but also bed mattress proper-
ties with decreased thermal insulation result in signifi-
cantly decreased Tcore without affecting sleep stages .
Although sleep stages were not measured, effects of differ-
ent types of quilts  and clothing  during sleep
decreased Tcore under decreased thermal insulation con-
ditions. The effects of heat exposure during sleep are also
greater compared to the waking state with an increase of a
few degrees in Ta above the thermal neutral zone affecting
Tcore during sleep . These results indicate that Tcore
during sleep may be sensitive to Ta change as well as
clothing and bedding thermal insulation. It is important to
note that these effects on Tcore do not always affect sleep
stages in parallel. During cyclic Ta changes, Tcore may be
affected by peripheral skin blood flow that regulates the
circadian rhythm of Tcore . Increased and decreased
dry heat loss from changes in the peripheral Tsk has been
suggested as one possible effect of cyclic Ta change on
Tcore during sleep . However, further precise study
Okamoto-Mizuno and Mizuno Journal of Physiological Anthropology 2012, 31:14 Page 6 of 9
on peripheral Tsk under cyclic Ta changes together with
sleep stages, especially with REM propensity and cycle,
melatonin secretion and bed climate, is needed.
Interestingly, it has been suggested that time memory
for heat exposure exists in the human thermoregulatory
system, and that autonomic thermoregulation in Tcore
changes during the previous heat exposure period with-
out actual temperature stimuli . It would be inter-
esting to know whether continuous phase shifting effect
of cyclic Ta changes during sleep may keep time memory
and whether this phase shifting effect continues even
under constant Ta. Furthermore, effects of cyclic Ta
change on Tcore are limited during sleep, and further
study is warranted to determine its effects on the wake-
ful state. Results from blind individuals indicate that, al-
though nonphotic stimuli can exert a small, but
significant resetting response, these effects are weaker
than light stimuli in affecting the human circadian pace-
maker . Indeed, cyclic Ta change combined with a
gradual light-dark intensity cycle indicates a stronger ef-
fect of light compared with Ta . In real-life situa-
tions, Ta and light change in a 24-hour cycle may
involve the circadian system in humans. It has been sug-
gested that in, addition to light, the daily rise and fall in
environmental temperature could be an essential input
to the circadian clock . Since thermoregulatory
mechanisms are strongly related with the circadian tim-
ing system, the Ta change may be an essential entrain-
ment input additional to light environment, or at least
exert masking effects on the circadian system.
Heat exposure affects SWS and REM, whereas cold ex-
posure does not affect sleep stages. Considering that a
Ta of 32°C with 80% relative humidity affects only SWS
without affecting REM , heat affects SWS first,
whereas REM may be well-preserved in real-life situa-
tions. Sleep disturbance during heat exposure may lead
to behavioral thermoregulation in humans, for example,
using an air conditioner to decrease Ta. However, during
cold exposure, the cardiac autonomic response may be
affected without affecting sleep stages and subjective
sensations, and so not trigger behavioral thermoregula-
tion to control Ta. This indicates that the impact of cold
exposure may be greater than that of heat; thus, further
studies are warranted to consider the effect of cold ex-
posure on sleep and other physiological parameters.
The authors declare that they have no competing interests.
KO-M has made substantial contributions to the manuscript. KM has been
involved in drafting the manuscript and revising it critically for important
intellectual content. Both authors read and approved the final manuscript.
Kansei Fukushi Research Center, Tohoku Fukushi University, 1-149-6
Kunimigaoka Aoba Sendai, Miyagi, 981-0935, Japan.
Department of Early
Childhood and Primary Education, Tohoku Fukushi University, 6-149-1
Kunimi, Aoba-ku, Sendai, Miyagi, 989-3201, Japan.
Received: 22 March 2012 Accepted: 31 May 2012
Published: 31 May 2012
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Cite this article as: Okamoto-Mizuno and Mizuno: Effects of thermal
environment on sleep and circadian rhythm. Journal of Physiological
Anthropology 2012 31:14.
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