Okamoto-Mizuno and Mizuno Journal of Physiological Anthropology 2012, 31:14
http://www.jphysiolanthropol.com/content/31/1/14

REVIEW

Open Access

Effects of thermal environment on sleep andcircadian rhythm
Kazue Okamoto-Mizuno1* and Koh Mizuno2
Abstract
The thermal environment is one of the most important factors that can affect human sleep. The stereotypicaleffects 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 anddecreases 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 affectsleep stages, though the use of beddings and clothing during sleep is critical in supporting thermoregulation andsleep 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 thanthat 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

Review
The thermal environment is a key determinant of sleep
because thermoregulation is strongly linked to themechanism regulating sleep [1]. Excessively high or low
ambient temperature (Ta) may affect sleep even inhealthy humans without insomnia. Furthermore, disturbed nocturnal sleep affects not only daytime activities,
but is also related to various adverse health effects, suchas obesity [2], quality of life, and even mortality [3,4].
These findings indicate that maintaining a comfortable
thermal sleep environment is important for sleep maintenance as well as daytime activities and health status.
Among the various thermal environmental factors, the relationship between Ta and the use of clothing and beddings 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, making it difficult to extrapolate the results of animal studies* Correspondence: kazue@tfu-mail.tfu.ac.jp
1
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

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 avariety of environments by providing thermal resistancefor the human body from its environment [5]. In this review, based on our studies related to thermoregulationand sleep in humans, the effects of the thermal environment on sleep and circadian rhythm are discussed. The
effects of heat and cold exposure, including bedding andclothing conditions along with their effects in the elderly,
are of special interest, because these are the important factors that most impact sleep and thermoregulation.
Sleep and thermoregulation

Many previous studies in humans indicate that sleep isstrongly 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 bodytemperature (Tcore), which also cycles along with thesleep-wake rhythm, decreases during the nocturnal sleep
phase and increases during the wake phase repeatedly in a

© 2012 Okamoto-Mizuno and Mizuno; licensee BioMed Central Ltd. This is an Open Access article distributed under the termsof 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
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24-hour circadian rhythm. Sleep is most likely to occur
when Tcore decreases, while it hardly occurs during theincreasing phases [7]. This relationship between the sleepwake rhythm and the circadian rhythm of Tcore is important 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 [8].
The driving force behind this Tcore decrease is the peripheral skin temperature (Tsk), which is rich in arteriovenous
anastomoses and plays a central role in thermoregulation
by adjusting blood flow to the skin [9]. Increased peripheral Tsk is largely due to reduced activation of noradrenergic vasoconstrictor tone, allowing greater inflow of heatedblood from the core, thus facilitating heat loss to the environment through the skin surface [10]. The selective
vasodilation of distal skin regions promotes the rapid
onset of sleep [9] and is strongly associated with melatonin secretion [11]. Indeed, foot Tsk warming has beenshown to reduce sleep onset latency [12], indicating that
normal sleep onset is accomplished by increased peripheral heat loss and/or Tcore decrease [13]. The Tcore decrease in the sleep onset period is also strongly associatedwith cardiac autonomic activity. It has been suggested thatchanges in the cardiac autonomic nervous system precede
sleep onset, which is strongly associated with changes inbody temperature [14].
After sleep onset, Tcore gradually decreases further[8], while distal and proximal Tsk remain high [15]. The
importance of maintaining Tsk at physiological range forsleep maintenance has been suggested [6]. 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 comparedwith the young, with increased insomnia [18]. The sleep
parameters measured by actigraphy correlate only withchest Tsk, and decreased chest Tsk is associated with adecrease in the sleep efficiency index [19]. Interestingly,
even a slight increase in proximal Tsk increases theamount of SWS and decreases the early-morning awakening in the elderly [20]. Sleep-related areas in thebrain are associated with an increased Tsk within thephysiological range during sleep [21]. Moreover, Tsk
might act as an input signal to sleep-regulating systems[6]. These results indicate that slightly increasing theproximal Tsk may help alleviate sleep problems, especially in the elderly. The temperature and humidity ofthe microclimate between humans and bed covers (bedclimate) also play crucial roles in creating a warm bed
climate temperature to support increased Tsk and sleep[6]. 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 climate range suggested by Yanase [24].

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Another important aspect to consider is that thethermoregulatory response during sleep differs depending on sleep stages. In animal studies, the thermoregulatory system is abolished during rapid eye movement
sleep (REM) [25], due to a loss of thermosensitivity inthe majority of the hypothalamic preoptic neurons [26].
In humans, thermosensitivity during REM is not completely depressed; however, sensitivity to hot or cold
stimulation is reduced in REM compared to non-REM
and wakefulness [27,28]. In addition, the sweat rateincreases during SWS compared to other sleep stages[29], while delayed onset of sweating [30] and adecreased sweat rate [31] decrease evaporative heat dissipation and reduce heat tolerance during REM. Interestingly, the decreased sweat rate during REM isobserved prior to REM stage onset [32]. Consideringthat skin sympathetic nerve activity (SSNA) contains
sudomotor activity synchronous with vasodilator activity[33], this result indicates that SSNA might precede thesleep stage shift corresponding with heart rate variability(HRV) preceding the sleep stage shift at the sleep onset
period [14]. Changes in the sensitivity of the sweat response depending on sleep stages are considered to be acentral drive effect, since no peripheral change in sweat
gland levels has been observed [34]. In cold exposure,
shivering during sleep is confined to stages 1 and 2 andis not observed in SWS and REM [35], while the Tsk ofthe extremities is decreased during REM compared tothat at control conditions [36]. These results indicatethat 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 tosleep 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 decreaseor increase, respectively, the areas of the body coveredby bed covers, with the neck, shoulder and upper extremities showing higher sensitivity than lower extremities and the trunk [37]. In heat exposure, lateral body
position increases compared to the supine position, possibly because this position may decrease the contact area
between the body and the mattress [38]. 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 sleepers spend more time on their backs with their heads
straight, sleep positions may be related to sleep quality[39]. It is interesting to consider these behaviors in various 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
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understanding of thermoregulation during sleep inhumans.
Effects of heat exposure

Increases in wakefulness are greater in cold Ta than inheat , suggesting that the impact of cold exposure isgreater than that of heat exposure. Ta higher or lower
than the thermal neutral temperature (29°C) have beenshown to increase wakefulness and decrease REM and
SWS in semi-nude subjects [40]. However, these results
are based on semi-nude subjects and exclude the effectsof bed covers and clothing. In real-life situations where
bed covers and clothing are used, sleep is actually disturbed during heat exposure rather than cold exposurein the young [41], as well as in the elderly [19]. The
increased wakefulness and decreased SWS and REM are
stereotypical effects that are observed in heat exposure[42]. 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 disruption in the initial sleep segment leads to an increased
demand, which may overcome the thermal stress in thelater segment of sleep [42,43]. Heat-related sleep disruptions do not adapt even after 5 days of continuous daytime and nocturnal heat exposure [44]. Furthermore, theeffect on SWS does not change after partial sleep
deprivation where sleep pressure is increased [45]. 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 copewith an increased thermal load [26] and that wakefulness
replaces SWS and REM to maintain homeothermy.
Heat load suppresses the decrease in Tcore andincreases 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 throughthe 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 islargely due to increased skin blood flow, which is regulated primarily through two pathways in the sympathetic
nervous system: the noradrenergic vasoconstrictor system and the active vasodilator system. Increased Tsk
during sleep in heat exposure may be largely due to anincreased active vasodilator system. In subjects that are
awake, an active vasodilator system is responsible formost of the vasodilatory responses to heat stress [47].
The SSNA contains vasodilator activity synchronouswith sudomotor activity [33] and may lead to an increasein whole body sweat loss. Taken together, these results
suggest the possibility that increased vasodilator activity
may be related to increased Tsk and wakefulness due toheat exposure during sleep. Because sleep distribution iscontrolled by both peripheral and central driving effects

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[13,48], it is possible that increased active vasodilation
and Tcore both increase wakefulness during heat exposure. These results support the notion that, although
sleep states affect thermoregulation, thermoregulation
equally affects the mechanism governing sleep [1].
One of the most important factors that increase heatstress 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[43]. Humid heat exposure most probably increases heatstress 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 toevaporate, causing the skin to remain wet. The dripping
sweat and increased skin wetness decrease the sweat response 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 exposure in the initial segment decreases SWS in that segment and increases wakefulness in both segments [50].
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 [50]. These
effects on sleep stages can be explained by thermoregulation and microclimate temperature (temperature andhumidity of the microclimate between skin and theclothing) (Figure 1). Humid heat exposure in the later
segment causes a decrease in Tcore in the initial segment, followed by an increase in Tcore, Tsk and microclimate temperature in the later segment. Humid heat
exposure in the initial segment suppresses the decreasein 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 segment of sleep may also increase wakefulness. The chilling effects of a decrease in Ta and humidity and areduction in clothing insulation due to wetness [51]caused by sweating at initial humid heat exposure may
also be a possibility for the increase in wakefulness. Another possible contributing factor for decreased Tsk andTcore in the later segment of sleep could be that a decrease in Ta coincides with a time when REM sleep generally increases, since Tsk decreases are greater in REM
compared to other sleep stages [36]. In Japan, a majority

Okamoto-Mizuno and Mizuno Journal of Physiological Anthropology 2012, 31:14
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Page 4 of 9

Experiment 1

Experiment 2
37.6

37.6
Rectal temperature

37.4

37.2
37

36.8

36.8

36.6

36.6

36.4
36.2

36.4
36.2

26
26-32

36

Rectal temperature

37.4

37.2
37

26
32-26

36

Temperature ( )

35.8
37

Mean Tsk

37

36

36

35

35

Mean Tsk

34

34
26

33

26
32-26

33

26-32

32

32

37

37

Clothing Microclimate

36

36

35

35

34

34

33

33

Clothing Microclimate

32

32
31

26

31

26

30

26-32

30

32-26

29

29
0

1

2

3

4

5

6

7

Time (Hr)

0

1

2

3

4

5

6

7

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 bodytemperature. Physiol Behav 2005, 83:759–765 with kind permission from Elsevier.

use air conditioning only for a few hours after going tosleep [52] due to the notion that being exposed to air
conditioning is unhealthy [53], and 90% of Japanesepeople are interested in saving energy [54]. These results
indicate that if air conditioning use is limited, then it
should be used during the initial segment of sleep. Furthermore, when air conditioning is used in the later segment 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 [55]. 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[56], which in turn increases susceptibility to externalarousal stimuli during sleep [57]. These changes in sleep
may decrease the thermal awakening threshold. Anotherreason for this could be reduced heat tolerance in oldermen, since most heat exposure studies have found a
reduced ability to regulate Tcore in subjects who areawake (for example, see [58]). Mild heat exposure

further suppresses the decline in Tcore, increases Tsk,and increases whole body sweat loss by two-fold in theelderly [55]. The increase in nocturnal Tcore [59] andthe attenuation of the nocturnal drop in Tcore [60] may
underlie age-related declines in sleep maintenance andsleep quality. Furthermore, the period of overnight fasting
results in mild dehydration in older men even undernormal conditions [61], suggesting that increased wholebody sweat loss during sleep in mild heat exposure may
be related to dehydration in the elderly. Although further study to directly compare older and younger men isneeded, it appears quite likely that sleep in older men ismore affected by heat exposure than in younger men.
These results indicate that the Ta during sleep warrants
particularly careful consideration in older men, especially since decreased sleep duration in the older men isrelated 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 twolayers of underwear under nightwear even in summer[62].

Okamoto-Mizuno and Mizuno Journal of Physiological Anthropology 2012, 31:14
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Effects of cold exposure

Heart rate

Beats/min

70

3
10
17

60

50

40

HF

3000
2500
msec2

The difference between cold exposure and heat exposureis that cold exposure mainly affects the later segment of
sleep, where REM is dominant [63]. In semi-nude subjects, cold exposure mainly affects REM due to suppression of the thermoregulatory response [35,40]. SWS is
not affected because it predominates in the initial segment of sleep [64]. In thermoregulation during sleep,
Tcore decreases through the night [36] as the Ta
decreases [65]. However, in real-life situations people
generally use clothing and bed covers during sleep incold 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 [66] and 3°C to 17°C [67]. Also,no significant difference in sleep quality measured by
actigraphy was observed between 9°C and 20°C in theelderly [19]. These results indicate that, in real-life situations, 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 [66]. The use of
bed covers allows for the development of an isolated highbed climate temperature, which is critical for maintaining
sleep [6] as well as determining sleep quality [68].
However, our study indicates that cold exposure significantly changes cardiac autonomic activity during
sleep, without affecting the sleep stages (Figure 2) [67].
With regard to cardiac autonomic activity based on the
HRV index, the ratio of the low frequency (LF) to highfrequency (HF) band (LF/HF) significantly decreases
during stage 2 and SWS, while the percentage of the LF
component (LF/(LF + HF)) significantly decreases during
SWS as the Ta decreases from 17°C to 3°C. In contrast,
no significant effect is observed during REM or wakefulness. These results may indicate that cardiac parasympathetic 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 andSWS may be related to at least three factors: cold stimulation 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 stimulation of the face, a unique reflex referred to as cold facetest, increases the cardiac parasympathetic activity andthe peripheral skin SSNA simultaneously and integrates
the trigeminal brain stem reflex arc in wakeful subjects[69]. 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 bloodpressure [70-72] and a significant increase in the HF
component [69,73]. Second, inhalation of cold air may
increase muscle sympathetic nervous activity and bloodpressure in wakeful subjects [74]. Third, whole body

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2000
1500
1000
500

LF/(LF+HF)

1.0
0.8
0.6

*
*

*
*

0.4
0.2
0.0

LF/HF

6
5
4

*
*

3
2
1
0
Stage2

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 thestandard error. *indicates the significant level after Friedman test;
P <0.05. †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 ratevariability during sleep in humans. Eur J Appl Physiol 2009,
105:191–197 with kind permission from Springer Science andBusiness Media.

cooling may also be related to increases in systolic anddiastolic blood pressure and decreases in heart rate in
wakeful subjects [75]. Considering that approximately
70% of sleep time comprises stage 2 and SWS, the cardiac parasympathetic activity may be dominant during
sleep in cold exposure.

Okamoto-Mizuno and Mizuno Journal of Physiological Anthropology 2012, 31:14
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These findings could partly explain the adverse cardiac
events that peak during the colder periods in the winterseason [76,77]. Mortality due to ischemic heart disease is
not related to low outside temperature, but to low living-room temperatures and limited bedroom heating in
the winter [78]. Cold climates increase blood pressure[75] as well as the levels of hematological factors thatfavor arterial thrombosis [79] and fibrinogen synthesis[80]. It has been suggested that the onset of major cardiovascular events is triggered by sleep stage-dependent
fluctuations in the autonomic nervous system [81]. Significantly 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 duringtransition from non-REM to awakening and REM favors
adverse cardiac events [82]. Further study considering
the relationship between the increased incidence of adverse cardiac events and marked variations in HRV during transition from non-REM to wakefulness and REM
may provide insights into understanding the increase in
cardiac events peaking in winter. Besides HRV, the lackof 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 thatsleep is not disturbed. The impact on the cardiovascularresponse may be occurring without subjective sensation,suggesting that cold exposure may have more impact thanheat exposure. In Japan, bedroom Ta falls to as low as 3°C
in the suburbs [53]. Excessive layers of underwear undernight wear and bed covers are common observations inelderly Japanese people [85] and this behavior supports
sleep in cold exposure. Indeed, about 50% of elderly Japanese people use two to six layers of underwear and three
to five layers of bed covers [85]. The most important aspect 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 environmental synchronizer of the circadian pacemaker inhumans as well as other species [7]; however, the effects
of social cues and other nonphotic entrainment, including Ta, on human circadian system are less understood.

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Twenty-four hours of warm Ta increases activity, suggesting that Ta has a masking effect on circadian activity
rhythms in animal studies [86]. In high and cool Ta
cycles, Ta acts as a weak synchronizer in laboratory rats[87] and mice [88]. These results suggest that, at theleast, Ta may have masking effects on circadian activity
rhythms in homeothermic animals. In humans, manystudies 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 cyclic Ta changes do not significantly affect sleep stages[89], or increase SWS compared to constant Ta [90].
These results indicate that cyclic Ta changes do not
induce any adverse effects on sleep stages at least
within the thermoneutral temperature range. Interestingly, studies by Dewasmes et al. [89,93] showed thatcyclic Ta, as opposed to constant Ta, advanced theminimum Tcore by 143 minutes and the propensity
for REM. The REM cycle length changes dependingon Ta with a delayed REM cycle in low Ta comparedwith high Ta [94], and the REM propensity has a close
relationship with body temperature rhythm [95].
These results indicate that Ta itself as well as cyclic Tachange may advance circadian Tcore and/or REM andthat the thermoregulatory system may have effects onphase advancing mechanisms.
One possible explanation for these effects of cyclic Tachange on Tcore may be the reduced thermoregulation
during sleep compared to wakefulness [28]. No significant
difference between sleep stages at Ta of 13°C to 23°C isobserved, although Tcore clearly decreases as the Ta
decreases [66]. Not only Ta but also bed mattress properties with decreased thermal insulation result in significantly decreased Tcore without affecting sleep stages [96].
Although sleep stages were not measured, effects of different types of quilts [97] and clothing [98] during sleep
decreased Tcore under decreased thermal insulation conditions. The effects of heat exposure during sleep are also
greater compared to the waking state with an increase of afew degrees in Ta above the thermal neutral zone affecting
Tcore during sleep [31]. These results indicate that Tcore
during sleep may be sensitive to Ta change as well as
clothing and bedding thermal insulation. It is important tonote that these effects on Tcore do not always affect sleep
stages in parallel. During cyclic Ta changes, Tcore may beaffected by peripheral skin blood flow that regulates thecircadian rhythm of Tcore [99]. Increased and decreased
dry heat loss from changes in the peripheral Tsk has beensuggested as one possible effect of cyclic Ta change on
Tcore during sleep [100]. However, further precise study

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on peripheral Tsk under cyclic Ta changes together withsleep stages, especially with REM propensity and cycle,
melatonin secretion and bed climate, is needed.
Interestingly, it has been suggested that time memoryfor heat exposure exists in the human thermoregulatory
system, and that autonomic thermoregulation in Tcorechanges during the previous heat exposure period without actual temperature stimuli [101]. It would be interesting to know whether continuous phase shifting effectof cyclic Ta changes during sleep may keep time memory
and whether this phase shifting effect continues evenunder constant Ta. Furthermore, effects of cyclic Tachange on Tcore are limited during sleep, and further
study is warranted to determine its effects on the wakeful state. Results from blind individuals indicate that, although nonphotic stimuli can exert a small, but
significant resetting response, these effects are weaker
than light stimuli in affecting the human circadian pacemaker [102]. Indeed, cyclic Ta change combined with a
gradual light-dark intensity cycle indicates a stronger effect of light compared with Ta [103]. In real-life situations, Ta and light change in a 24-hour cycle may
involve the circadian system in humans. It has been suggested that in, addition to light, the daily rise and fall inenvironmental temperature could be an essential input
to the circadian clock [104]. Since thermoregulatory
mechanisms are strongly related with the circadian timing system, the Ta change may be an essential entrainment input additional to light environment, or at leastexert masking effects on the circadian system.

Conclusions
Heat exposure affects SWS and REM, whereas cold exposure does not affect sleep stages. Considering that a
Ta of 32°C with 80% relative humidity affects only SWS
without affecting REM [46], heat affects SWS first,
whereas REM may be well-preserved in real-life situations. Sleep disturbance during heat exposure may lead
to behavioral thermoregulation in humans, for example,
using an air conditioner to decrease Ta. However, duringcold exposure, the cardiac autonomic response may beaffected without affecting sleep stages and subjective
sensations, and so not trigger behavioral thermoregulation 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 exposure on sleep and other physiological parameters.
Competing interests
The authors declare that they have no competing interests.
Authors’ contributions
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.

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Author details
1
Kansei Fukushi Research Center, Tohoku Fukushi University, 1-149-6
Kunimigaoka Aoba Sendai, Miyagi, 981-0935, Japan. 2Department 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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doi:10.1186/1880-6805-31-14
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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