- Email: [email protected]
Does the physical environment interact with the sleep process?
Sleep Medicine Reviews (2004) 8, 77–79
www.elsevier.com/locate/jnlabr/ysmrv
GUEST EDITORIAL
Does the physical environment interact with the sleep process? This issue of Sleep Medicine Reviews presents two papers dealing with possible interactions between physical factors of our environment and sleep. This is certainly an interesting and not very usual way of looking at the sleep process, because the sleeping environment is highly variable from one bedroom to the next and because we have no way to escape to our physical environment and its possible influences. There are numerous other environmental factors that can potentially influence sleep which might have been similarly reviewed, for example, a specific paper on influence of ambient noise on sleep could well have also appeared in this issue. In their article ‘Thermoregulation as a sleep signalling system’, Gilbert, van den Heuvel, Ferguson and Dawson discuss the interrelations between the sleep process and the body temperature regulation. We know that thermal homeostasis is achieved by the activation of several physiological processes, which control heat production on the one hand and heat dissipation on the other. Regulation of body temperature depends on thermal sensitivity and thermoregulatory responses to the variations of environmental temperature, and this regulation is under the control of hypothalamic structures. According to general models of thermoregulation, core body temperature is regulated around a given set point, although, during sleep, thermoregulation depends also on variations of the hypothalamic command, as demonstrated in animals.1,2 Heat transfer from core to body surface layers uses blood as vehicle and variation in skin blood flow through vasodilatation and vasoconstriction actions, controlled by the autonomic nervous system. These actions, together with sweating, facilitate or restrict heat exchange between the body and its physical environment. At the beginning of the night, increasing skin blood flow due to vasodilatation induces a greater heat dissipation, which is followed by decrease in blood temperature,
and this leads to the decrease in core body temperature. This effect takes approximately between 25 and 100 min3 and it is largely dependent on the ambient temperature and the establishment of a ‘nest’ climate inside the bed of the sleeper.4 These thermoregulatory mechanisms allow the human body to maintain a core body temperature inside a 1 8C range, around an average temperature of about 37 8C, whatever the local skin temperatures at the extremities, which can vary across a much larger range. Core body temperature fluctuates over the 24-hour period, describing a true circadian rhythm with a maximum reached during the late part of the day and a minimum value observed in the last part of the night. This circadian profile is one of the most recognised circadian rhythms and its stability is quite remarkable. Temporal isolation studies have shown, however, that the period of this rhythm is spontaneously longer than 24 h and that it is clearly under the influence of external synchronisers.5 These isolation studies have also demonstrated that sleep duration depends on the phase-relationship between retiring time and the core body temperature curve.6 This review paper also reports on studies using passive body heating or exercise prior to sleep, which increase sleep propensity and induce increased amount of slow wave sleep (SWS). In fact these findings can be related to the observed increase in sweating rate prior to and during the first part of sleep mainly during SWS. The increase in heat loss, facilitated through sweating, is accentuated in SWS, as sweating appears to be enhanced in this specific sleep state.7 Therefore, core body temperature has its strongest reduction during this first hour of the night and this is contemporaneous with SWS. This decrease in core body temperature occurring prior to sleep onset might play a role in the facilitation of sleep initiation, as underlined by the authors.
1087-0792/$ - see front matter q 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.smrv.2003.12.001
78
In this paper, the main question is to know whether the inverse relationship, across day and night, between sleep propensity and core body temperature rhythms is causative or coincidental? Thus, is the drop in body temperature triggering sleep onset or is sleep onset responsible for the drop in body temperature? In their conclusion, the authors suggest that changes in core body temperature are not simply a consequence of sleep onset but rather that these changes are in fact involved in the regulation of sleep itself. This is a most interesting question as practical implications can be drawn from their conclusions. It is, however, a somewhat limited conclusion as besides the sleep process initiation, we know that ambient temperature has direct effects on sleep architecture, and that sleep stages interact with the thermoregulatory processes.8,9 For instance, several studies have shown that REM sleep and thermoregulation are mutually exclusive in animals,10 while thermoregulatory responses to heat were demonstrated not to be abolished during this particular sleep state in man.11 Therefore, it appears that, in contrast to animals, the hypothalamic thermoregulatory structures are not completely inactivated during REM sleep in humans, but show only changes in threshold of all thermoregulatory responses. Variations in ambient temperature can also be used to modify the nocturnal profile of core body temperature rhythm.12 Thus, ambient temperature has an effect not only on the level but also on the shape of the curve of the rectal temperature during sleep. Under cold conditions body temperature decreases earlier and is sustained longer at a low level than under warm conditions.4 In addition, it is clear that core body temperature starts to rise in the late part of sleep without interrupting it. All these results suggest that, although there are indisputable relationships between thermoregulation and the sleep process, these two phenomena are quite independent. The second paper, entitled ‘Sleep under exposure to high-frequency electromagnetic fields’, by Mann and Ro ¨schke, is concerned with what appears to be a growing exposure to an environmental factor in our everyday life. While low-frequency exposure (1 – 100 GHz) is mostly related to generation, transmission and consumption of electric power, high-frequency electric and magnetic fields (100 – 300 GHz) are mainly due to the increasing use of mobile phones and other telecommunication devices. This paper is a global review on the possible and demonstrated effects of high-frequency electric and magnetic fields on sleep.
A. Muzet
In contrast to low-frequency fields, highfrequency radiation can be absorbed by human tissues with significant increase in local temperature if the intensity of the radiation is high enough. Several studies have looked at this particular effect during the last decade and safety guidelines have been developed to avoid any damaging consequence for the exposed tissues.13,14 Other studies have focussed on direct nonthermal effects, as low-intensity radiation diminishes this particular risk. It appears clearly, from this very extensive review, that only a few epidemiological studies have been carried out in this particular domain and that sleep disturbance does not appear to be a predominant symptom in this kind of exposure. In this area, and certainly because exposure to mobile communication devices has not been of sufficient duration in the general population, it is difficult to assess a specific effect of high-frequency electric and magnetic fields on human health, and more precisely on sleep.
References 1. Parmeggiani PL, Franzini C, Lenzi P, Zamboni G. Threshold of respiratory responses to preoptic heating during sleep in freely moving cats. Brain Res 1973; 52: 189—201. 2. Glotzbach SF, Heller HC. Central nervous regulation of body temperature during sleep. Science 1976; 194: 537—539. 3. Krauchi K, Wirz-Justice A. Circadian rhythm of heat production, heart rate, and skin and core temperature under unmasking conditions in men. Am J Physiol 1994; 267: R819—R829. 4. Candas V, Libert JP, Vogt JJ, Ehrhart J, Muzet A. Body temperature during sleep under different thermal conditions. In: PO Fanger, O Valbjorn (eds.) Indoor climate: effect on human comfort, performance and health. Copenhagen: Danish Building Research Institute 1979; 763—775. 5. Aschoff J, Wever R. Spontanperiodik des Menschen bei Ausschluss aller Zeitgeber. Naturwissenschaften 1962; 49: 337—342. 6. Zulley J, Wever R, Aschoff J. The dependence of onset and duration of sleep on the circadian rhythm of rectal ¨gers Arch 1981; 391: 314—318. temperature. Pflu 7. Sagot JC, Amoros C, Candas V, Libert JP. Sweating responses and body temperature during nocturnal sleep in humans. Am J Physiol 1987; 252: R462—R470. 8. Libert JP, Di Nisi J, Fukuda H, Muzet A, Ehrhart J, Amoros C. Effect of continuous heat exposure on sleep stages in humans. Sleep 1988; 11: 195—209. 9. Muzet A, Libert JP, Candas V. Ambient temperature and human sleep. Experientia 1984; 40: 425—429. 10. Parmeggiani PL, Agnati LF, Zamboni G, Cianci T. Hypothalamic temperature during the sleep cycle at different ambient temperatures. Electroencephalogr Clin Neurophysiol 1975; 38: 589—596. 11. Libert JP, Candas V, Muzet A, Ehrhart J. Thermoregulatory adjustments to thermal transients during slow wave sleep and REM sleep in man. J Physiol 1982; 78: 251—257.
Does the physical environment interact with the sleep process?
12. Dewasmes G, Signoret P, Nicolas A, Ehrhart J, Muzet A. Advances of human core temperature minimum and maximal paradoxical sleep propensity by ambient thermal transients. Neurosc Lett 1996; 215: 25—28. 13. Michaelson SM, Lin JC. Biological effects and health implications of radio frequency radiation. New York: Plenum Press 1987. 14. International Commission on Non-Ionizing Radiation Protection (ICNIRP), Guidelines for limiting exposure to time-varying
79
electric, magnetic, and electromagnetic fields (up to 300 GHz). Health Phys 1998; 74: 494—522.
Alain Muzet Centre of Applied Physiology Studies, CNRS, 21 rue Becquerel, 67087 Strasbourg, France E-mail address: [email protected]
www.elsevier.com/locate/jnlabr/ysmrv
GUEST EDITORIAL
Does the physical environment interact with the sleep process? This issue of Sleep Medicine Reviews presents two papers dealing with possible interactions between physical factors of our environment and sleep. This is certainly an interesting and not very usual way of looking at the sleep process, because the sleeping environment is highly variable from one bedroom to the next and because we have no way to escape to our physical environment and its possible influences. There are numerous other environmental factors that can potentially influence sleep which might have been similarly reviewed, for example, a specific paper on influence of ambient noise on sleep could well have also appeared in this issue. In their article ‘Thermoregulation as a sleep signalling system’, Gilbert, van den Heuvel, Ferguson and Dawson discuss the interrelations between the sleep process and the body temperature regulation. We know that thermal homeostasis is achieved by the activation of several physiological processes, which control heat production on the one hand and heat dissipation on the other. Regulation of body temperature depends on thermal sensitivity and thermoregulatory responses to the variations of environmental temperature, and this regulation is under the control of hypothalamic structures. According to general models of thermoregulation, core body temperature is regulated around a given set point, although, during sleep, thermoregulation depends also on variations of the hypothalamic command, as demonstrated in animals.1,2 Heat transfer from core to body surface layers uses blood as vehicle and variation in skin blood flow through vasodilatation and vasoconstriction actions, controlled by the autonomic nervous system. These actions, together with sweating, facilitate or restrict heat exchange between the body and its physical environment. At the beginning of the night, increasing skin blood flow due to vasodilatation induces a greater heat dissipation, which is followed by decrease in blood temperature,
and this leads to the decrease in core body temperature. This effect takes approximately between 25 and 100 min3 and it is largely dependent on the ambient temperature and the establishment of a ‘nest’ climate inside the bed of the sleeper.4 These thermoregulatory mechanisms allow the human body to maintain a core body temperature inside a 1 8C range, around an average temperature of about 37 8C, whatever the local skin temperatures at the extremities, which can vary across a much larger range. Core body temperature fluctuates over the 24-hour period, describing a true circadian rhythm with a maximum reached during the late part of the day and a minimum value observed in the last part of the night. This circadian profile is one of the most recognised circadian rhythms and its stability is quite remarkable. Temporal isolation studies have shown, however, that the period of this rhythm is spontaneously longer than 24 h and that it is clearly under the influence of external synchronisers.5 These isolation studies have also demonstrated that sleep duration depends on the phase-relationship between retiring time and the core body temperature curve.6 This review paper also reports on studies using passive body heating or exercise prior to sleep, which increase sleep propensity and induce increased amount of slow wave sleep (SWS). In fact these findings can be related to the observed increase in sweating rate prior to and during the first part of sleep mainly during SWS. The increase in heat loss, facilitated through sweating, is accentuated in SWS, as sweating appears to be enhanced in this specific sleep state.7 Therefore, core body temperature has its strongest reduction during this first hour of the night and this is contemporaneous with SWS. This decrease in core body temperature occurring prior to sleep onset might play a role in the facilitation of sleep initiation, as underlined by the authors.
1087-0792/$ - see front matter q 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.smrv.2003.12.001
78
In this paper, the main question is to know whether the inverse relationship, across day and night, between sleep propensity and core body temperature rhythms is causative or coincidental? Thus, is the drop in body temperature triggering sleep onset or is sleep onset responsible for the drop in body temperature? In their conclusion, the authors suggest that changes in core body temperature are not simply a consequence of sleep onset but rather that these changes are in fact involved in the regulation of sleep itself. This is a most interesting question as practical implications can be drawn from their conclusions. It is, however, a somewhat limited conclusion as besides the sleep process initiation, we know that ambient temperature has direct effects on sleep architecture, and that sleep stages interact with the thermoregulatory processes.8,9 For instance, several studies have shown that REM sleep and thermoregulation are mutually exclusive in animals,10 while thermoregulatory responses to heat were demonstrated not to be abolished during this particular sleep state in man.11 Therefore, it appears that, in contrast to animals, the hypothalamic thermoregulatory structures are not completely inactivated during REM sleep in humans, but show only changes in threshold of all thermoregulatory responses. Variations in ambient temperature can also be used to modify the nocturnal profile of core body temperature rhythm.12 Thus, ambient temperature has an effect not only on the level but also on the shape of the curve of the rectal temperature during sleep. Under cold conditions body temperature decreases earlier and is sustained longer at a low level than under warm conditions.4 In addition, it is clear that core body temperature starts to rise in the late part of sleep without interrupting it. All these results suggest that, although there are indisputable relationships between thermoregulation and the sleep process, these two phenomena are quite independent. The second paper, entitled ‘Sleep under exposure to high-frequency electromagnetic fields’, by Mann and Ro ¨schke, is concerned with what appears to be a growing exposure to an environmental factor in our everyday life. While low-frequency exposure (1 – 100 GHz) is mostly related to generation, transmission and consumption of electric power, high-frequency electric and magnetic fields (100 – 300 GHz) are mainly due to the increasing use of mobile phones and other telecommunication devices. This paper is a global review on the possible and demonstrated effects of high-frequency electric and magnetic fields on sleep.
A. Muzet
In contrast to low-frequency fields, highfrequency radiation can be absorbed by human tissues with significant increase in local temperature if the intensity of the radiation is high enough. Several studies have looked at this particular effect during the last decade and safety guidelines have been developed to avoid any damaging consequence for the exposed tissues.13,14 Other studies have focussed on direct nonthermal effects, as low-intensity radiation diminishes this particular risk. It appears clearly, from this very extensive review, that only a few epidemiological studies have been carried out in this particular domain and that sleep disturbance does not appear to be a predominant symptom in this kind of exposure. In this area, and certainly because exposure to mobile communication devices has not been of sufficient duration in the general population, it is difficult to assess a specific effect of high-frequency electric and magnetic fields on human health, and more precisely on sleep.
References 1. Parmeggiani PL, Franzini C, Lenzi P, Zamboni G. Threshold of respiratory responses to preoptic heating during sleep in freely moving cats. Brain Res 1973; 52: 189—201. 2. Glotzbach SF, Heller HC. Central nervous regulation of body temperature during sleep. Science 1976; 194: 537—539. 3. Krauchi K, Wirz-Justice A. Circadian rhythm of heat production, heart rate, and skin and core temperature under unmasking conditions in men. Am J Physiol 1994; 267: R819—R829. 4. Candas V, Libert JP, Vogt JJ, Ehrhart J, Muzet A. Body temperature during sleep under different thermal conditions. In: PO Fanger, O Valbjorn (eds.) Indoor climate: effect on human comfort, performance and health. Copenhagen: Danish Building Research Institute 1979; 763—775. 5. Aschoff J, Wever R. Spontanperiodik des Menschen bei Ausschluss aller Zeitgeber. Naturwissenschaften 1962; 49: 337—342. 6. Zulley J, Wever R, Aschoff J. The dependence of onset and duration of sleep on the circadian rhythm of rectal ¨gers Arch 1981; 391: 314—318. temperature. Pflu 7. Sagot JC, Amoros C, Candas V, Libert JP. Sweating responses and body temperature during nocturnal sleep in humans. Am J Physiol 1987; 252: R462—R470. 8. Libert JP, Di Nisi J, Fukuda H, Muzet A, Ehrhart J, Amoros C. Effect of continuous heat exposure on sleep stages in humans. Sleep 1988; 11: 195—209. 9. Muzet A, Libert JP, Candas V. Ambient temperature and human sleep. Experientia 1984; 40: 425—429. 10. Parmeggiani PL, Agnati LF, Zamboni G, Cianci T. Hypothalamic temperature during the sleep cycle at different ambient temperatures. Electroencephalogr Clin Neurophysiol 1975; 38: 589—596. 11. Libert JP, Candas V, Muzet A, Ehrhart J. Thermoregulatory adjustments to thermal transients during slow wave sleep and REM sleep in man. J Physiol 1982; 78: 251—257.
Does the physical environment interact with the sleep process?
12. Dewasmes G, Signoret P, Nicolas A, Ehrhart J, Muzet A. Advances of human core temperature minimum and maximal paradoxical sleep propensity by ambient thermal transients. Neurosc Lett 1996; 215: 25—28. 13. Michaelson SM, Lin JC. Biological effects and health implications of radio frequency radiation. New York: Plenum Press 1987. 14. International Commission on Non-Ionizing Radiation Protection (ICNIRP), Guidelines for limiting exposure to time-varying
79
electric, magnetic, and electromagnetic fields (up to 300 GHz). Health Phys 1998; 74: 494—522.
Alain Muzet Centre of Applied Physiology Studies, CNRS, 21 rue Becquerel, 67087 Strasbourg, France E-mail address: [email protected]