ABSTRACT
La estrecha relación entre el ciclo de sueño vigilia y el ritmo de temperatura corporal es un hecho que se conoce desde hace tiempo, de tal forma que aumenta la propensión al sueño cuando la temperatura corporal central se acerca a su mínimo valor. No obstante, y dadas los inconvenientes metodológicos que plantea la medida del ritmo de temperatura corporal central (TCC) de forma continua, ha ido ganando interés la medida del ritmo de temperatura periférica (TP) como índice de somnolencia. El comportamiento de esta nueva variable en relación con el sueño es opuesto al del ritmo de TCC, de modo que son las elevaciones de TP las que van asociadas a una mayor propensión a dormir, mientras que los descensos inducen estados de vigilia. La TP no sólo se anticipa a los cambios que suceden en el ritmo de TCC, lo que subraya su carácter endógeno, sino que además constituye una señal que actúa sobre los centros reguladores del sueño, modificando la propensión al sueño. Es más, los datos más recientes apuntan a que la caída en la TCC, que se encuentra bajo el control del sistema circadiano, estaría fundamentalmente causada por un aumento en la disipación de calor, gracias a la vasodilatación de la piel y su calentamiento, y sería por lo tanto, la elevación de la temperatura distal, y no tanto la caída en la TCC, la señal que desencadena el inicio y mantenimiento del sueño. Este hecho permite introducir modificaciones en los patrones de comportamiento previos al sueño orientados a mejorar los cambios termorreguladores que facilitan el mismo (AU)
It has long been known that the sleep-wake cycle is closely related to the body temperature rhythm, in such a way that sleep propensity increases when the core body temperature (CBT) reaches a minimun value. However, the unpleasantness associated with the methods used for continuous CBT recordings has recently increased the interest for peripheral temperature (PT) measurements as an index of sleepeness. The peripheral temperature pattern is opposed to that of CBT with respect to sleep, since the propensity to fall asleep increases along with PT, while PT decrements are associated with alertness. Changes in peripheral temperature rhythm precede those of CBT, highlighting its endogenous component, and demonstrating that PT acts as a signal for sleep regulating centers. In addition, more recent data indicates that, under the circadian sistem control, CBT lowering is specially dependent on heat loss by skin vasodilation and heating, which means that it is the PT increment, rather than the CBT drop, which triggers sleep onset and its consolidation. Based on this assumption a number of behavioral pattern modifications can be suggested to improve those thermoregutranslatory changes that could facilitate sleep (AU)
Subject(s)
Humans , Male , Female , Body Temperature/physiology , Wakefulness/physiology , Sleep Initiation and Maintenance Disorders/complications , Sleep Initiation and Maintenance Disorders/diagnosis , Disorders of Excessive Somnolence/complications , Sleep-Wake Transition Disorders/complications , Sleep-Wake Transition Disorders/diagnosis , Circadian Rhythm/physiology , Sleep Disorders, Circadian Rhythm/complications , Sleep Disorders, Circadian Rhythm/diagnosis , Thermography , Sleep Disorders, Circadian Rhythm/physiopathologyABSTRACT
Most circadian rhythms are under the control of a major pacemaker located in the hypothalamic suprachiasmatic nucleus. Some of these rhythms, called marker rhythms, serve to characterize the timing of the internal temporal order. A marker rhythm, (e.g., one used in chronotherapy) has to be periodic and easy to measure over long periods using non-invasive methods. The most frequent reference variables for human chronotherapy include salivary melatonin or cortisol, urinary 6-sulfatoximelatonin, actimetry and core body temperature (CBT). Recent evidence suggests that sleepiness may be more closely linked to increased peripheral skin temperature than to a core temperature drop, and that distal skin temperature seems to be correlated and phase-advanced with respect to CBT, suggesting that heat loss from the extremities may drive the circadian CBT rhythm. The aim of the present study was to evaluate whether the wrist skin temperature rhythm could be used as a possible index of the human circadian system. To this end, wrist skin temperature (WT1), as determined by a wireless data logger in healthy normal living subjects, was correlated with sleep-wake diaries and oral temperature (OT) recordings. WT and sleep habits were studied in 99 university students. Each subject wore a wireless iButton sensor attached to the inner side of a sport wristband. Our results show that the WT rhythm exhibits an inverse phase relationship with OT, and it is phase-advanced by 60 min with respect to OT. WT started to increase in association to bed time and dropped sharply after awakening. A secondary WT increase, independent of feeding, was observed in the early afternoon. In conclusion, WT wireless recording can be considered a reliable procedure to evaluate circadian rhythmicity, and an index to establish and follow the effects of chronotherapy in normal living subjects.