Study Objectives: Daytime napping is frequently reported among the older population and has attracted increasing attention due to its association with multiple health conditions. Here, we tested whether napping in the aged is associated with altered circadian regulation of sleep, sleepiness, and vigilance performance. Methods: Sixty healthy older individuals (mean age: 69 years, 39 women) were recruited with respect to their napping habits (30 nappers, 30 non-nappers). All participants underwent an in-lab 40-hour multiple nap protocol (10 cycles of 80 minutes of sleep opportunity alternating with 160 minutes of wakefulness), preceded and followed by a baseline and recovery sleep period. Saliva samples for melatonin assessment, sleepiness, and vigilance performance were collected during wakefulness and electrophysiological data were recorded to derive sleep parameters during scheduled sleep opportunities. Results: The circadian amplitude of melatonin secretion was reduced in nappers, compared to non-nappers. Furthermore, nappers were characterized by higher sleep efficiencies and REM sleep proportion during day- compared to nighttime naps. The nap group also presented altered modulation in sleepiness and vigilance performance at specific circadian phases. Discussion: Our data indicate that napping is associated with an altered circadian sleep–wake propensity rhythm. They thereby contribute to the understanding of the biological correlates underlying napping and/or sleep–wake cycle fragmentation during healthy aging. Altered circadian sleep–wake promotion can lead to a less distinct allocation of sleep into nighttime and/or a reduced wakefulness drive during the day, thereby potentially triggering the need to sleep at adverse circadian phase.
Study objectives: Daytime napping is frequently reported among the older population and has attracted increasing attention due to its association with multiple health conditions. Here, we tested whether napping in the aged is associated with altered circadian regulation of sleep, sleepiness and vigilance performance. Methods: Sixty healthy older individuals (mean age: 69y., 39 women) were recruited with respect to their napping habits (30 nappers, 30 non-nappers). All participants underwent an in-lab 40-h multiple nap protocol (10 cycles of 80 mins of sleep opportunity alternating with 160 mins of wakefulness), preceded and followed by a baseline and recovery sleep period. Saliva samples for melatonin assessment, sleepiness and vigilance performance were collected during wakefulness and electrophysiological data were recorded to derive sleep parameters during scheduled sleep opportunities. Results: The circadian amplitude of melatonin secretion was reduced in nappers, compared to non-nappers. Furthermore, nappers were characterized by higher sleep efficiencies and REM sleep proportion during day-compared to night-time naps. The nap group also presented altered modulation in sleepiness and vigilance performance at specific circadian phases. Discussion: Our data indicate that napping is associated with an altered circadian sleep-wake propensity rhythm and thereby contribute to the understanding of the biological correlates underlying napping and/or sleep-wake cycle fragmentation during healthy aging. Altered circadian sleep-wake promotion can lead to a less distinct allocation of sleep into night-time and/or a reduced wakefulness drive during the day, thereby potentially triggering the need to sleep at adverse circadian phase. SIGNIFICANCE STATEMENT: While napping has raised increasing interest as a health risk factor in epidemiological studies, its underlying regulation processes in the aged remain largely elusive. Here we assessed whether napping in the older population is associated with physiological and behavioral changes in circadian sleep-wake characteristics. Our data indicate that, concomitant to a reduced circadian amplitude in melatonin secretion, healthy older nappers are characterized by reduced day-night differences in sleep efficiency and more particularly in REM sleep, compared to their non-napping counterparts. These results suggest altered circadian response as a cause or consequence of chronic napping in the aged and thereby contribute to the understanding of nap regulation during healthy aging.
Whether light exposure during the day reduces non-visual light effects later in the evening has not been studied in adolescents. We investigate whether afternoon-early evening (AEE) light interventions (130 lx, 2500 lx, 4.5 hours, compared to 6.5 lx) would increase melatonin levels during later evening light exposure (130 lx) in a counterbalanced crossover study with 22 adolescents (14-17 years, 11 female). Contrary to our hypothesis, evening melatonin levels decreased after AEE bright light exposure, while sleepiness and vigilance were unaffected, and skin temperature showed no clear changes. The AEE light had acute alerting effects and bright light exposure in the 32 hours before laboratory entry was associated with higher evening melatonin and sleepiness. These findings suggest that bright AEE light increases alertness but may delay melatonin production by interfering with circadian rhythms. The study highlights the complex effects of light timing and its implications for managing adolescents' light exposure.
Fixed sleep schedules with an 8 h time in bed (TIB) are used to ensure participants are well-rested before laboratory studies. However, such schedules may lead to cumulative excess wakefulness in young individuals. Effects on older individuals are unknown. We combine modelling and experimental data to quantify the effects of sleep debt on sleep propensity in healthy younger and older participants. A model of arousal dynamics was fitted to sleep data from 22 young (20–31 y.o.) and 26 older (61–82 y.o.) individuals (25 male) undertaking 10 short sleep–wake cycles during a 40 h napping protocol, following >1 week of fixed 8 h TIB schedules. Homeostatic sleep drive at the study start was varied systematically to identify best fits between observed and predicted sleep profiles for individuals and group averages. Daytime sleep duration was the same on the two days of the protocol within the groups but different between the groups (young: 3.14 ± 0.98 h vs. 3.06 ± 0.75 h, older: 2.60 ± 0.98 h vs. 2.37 ± 0.64 h). The model predicted an initial homeostatic drive of 11.2 ± 3.5% (young) and 10.1 ± 3.5% (older) above well-rested. Individual variability in first-day, but not second-day, sleep patterns was explained by the differences in the initial homeostatic drive for both age groups. Our study suggests that both younger and older participants arrive at the laboratory with cumulative sleep debt, despite 8 h TiB schedules, which dissipates after the first four sleep opportunities on the protocol. This has implications for protocol design and the interpretation of laboratory studies.
Ageing is associated with alterations in circadian rhythms and thermoregulation, contributing to a fragmentation of the sleep–wake cycle and possibly age-related changes in cognitive performance. In this study, we investigated the relationship between visuo-spatial working memory (vsWM) performance and thermoregulation in young (18–34 years) and old (64–84 years) healthy human adults. Variations in the distal–proximal skin temperature gradient (DPG) were continuously monitored over the 24 h cycle in a field setting. vsWM was assessed during morning (09:00) and evening sessions (17:00) using an object–location binding task. As expected, a reduced circadian DPG amplitude was observed in old as compared to young participants. Likewise, old participants produced more errors than the young ones in object identification and location, suggesting reduced vsWM ability. Notwithstanding this, no significant association was found between circadian DPG modulation and vsWM performance, nor between testing time-of-day and cognitive performance. Further research is needed to explore environmental factors and the timing of peak circadian rhythms to better understand the interplay between circadian biology and cognitive ageing.