Age‐related Changes in the Circadian and Homeostatic Regulation of Human Sleep

Abstract

The reduction of electroencephalographic (EEG) slow-wave activity (SWA) (EEG power density between 0.75-4.5 Hz) and spindle frequency activity, together with an increase in involuntary awakenings during sleep, represent the hallmarks of human sleep alterations with age. It has been assumed that this decrease in non-rapid eye movement (NREM) sleep consolidation reflects an age-related attenuation of the sleep homeostatic drive. To test this hypothesis, we measured sleep EEG characteristics (i.e., SWA, sleep spindles) in healthy older volunteers in response to high (sleep deprivation protocol) and low sleep pressure (nap protocol) conditions. Despite the fact that the older volunteers had impaired sleep consolidation and reduced SWA levels, their relative SWA response to both high and low sleep pressure conditions was similar to that of younger persons. Only in frontal brain regions did we find an age-related diminished SWA response to high sleep pressure. On the other hand, we have clear evidence that the circadian regulation of sleep during the 40 h nap protocol was changed such that the circadian arousal signal in the evening was weaker in the older study participants. More sleep occurred during the wake maintenance zone, and subjective sleepiness ratings in the late afternoon and evening were higher than in younger participants. In addition, we found a diminished melatonin secretion and a reduced circadian modulation of REM sleep and spindle frequency-the latter was phase-advanced relative to the circadian melatonin profile. Therefore, we favor the hypothesis that age-related changes in sleep are due to weaker circadian regulation of sleep and wakefulness. Our data suggest that manipulations of the circadian timing system, rather than the sleep homeostat, may offer a potential strategy to alleviate age-related decrements in sleep and daytime alertness levels.

Circadian clock resetting in the mouse changes with age

“…Recent data suggest that these disruptions are due to weaker circadian regulation of sleep and wakefulness rather than alterations in the homeostatic mechanisms governing the sleep/wake cycle (Cajochen et al 2006). Our data suggest that at least some of the observed disruption with age may be due to alterations in the activity of neurotransmitters crucial for synchronisation of the circadian clock.…”

Ultradian and circadian modulation of dream recall: EEG correlates and age effects

“…Furthermore, we focused on how the topographic distribution of EEG activity during NREM and REM sleep can underpin potential cortical networks related to dream recall. The methodological rationale was to access dream recall using the sleep mentation questionnaire (Chellappa et al, 2009), which was carried out immediately after awakenings from scheduled 75-min naps during a 40-h multiple nap paradigm (150/75 min of wake-sleep schedule; 10 naps in total), under constant routine conditions (Cajochen et al, 2006). This enabled the estimation of dream recall after multiple sleep episodes, without the experimental bias of awakening participants during, for instance, an 8-h sleep episode, which is the most usual approach in dream research.…”

Interindividual differences in circadian rhythmicity and sleep homeostasis in older people: effect of a PER3 polymorphism

“…Aging is associated with numerous changes in sleep, such as increased number and duration of awakenings, and reduced time spent in slow wave sleep (SWS), as well as earlier wake-up time (Cajochen et al, 2006;Dijk et al, 1999). The decline in sleep consolidation, together with the advance of sleep timing, may reflect age-related changes in the homeostatic and/or circadian aspects of sleep regulation (Cajochen et al, 2006;Dijk et al, 1999).…”

“…The decline in sleep consolidation, together with the advance of sleep timing, may reflect age-related changes in the homeostatic and/or circadian aspects of sleep regulation (Cajochen et al, 2006;Dijk et al, 1999). From the sleep homeostatic perspective, older people display a shallower dissipation of sleep pressure, as indexed by reduced SWS and slow wave activity (SWA) (electroencephalographic [EEG] power density between 0.75 and 4.5 Hz, also referred to as delta activity) dynamics across the night (Dijk and Beersma, 1989;Landolt et al, 1996).…”