Daniel Filipini

Sleep slow wave changes during the middle years of life

Slow waves (SW; < 4 Hz and > 75 μV) during non‐rapid eye movement (NREM) sleep in humans are characterized by hyperpolarization [surface electroencephalogram (EEG) SW negative phase], during which cortical neurons are silent, and depolarization (surface EEG positive phase), during which the cortical neurons fire intensively. We assessed the effects of age, sex and topography on the dynamics of SW characteristics in a large population (n = 87) of healthy young (23.3 ± 2.4 years) and middle‐aged (51.9 ± 4.6 years) volunteers. Older subjects showed lower SW density and amplitude than young subjects. Age‐related lower SW density in men was especially marked in prefrontal/frontal brain areas, where they originate more frequently. Older subjects also showed longer SW positive and negative phase durations. These last results indicate that, in young subjects, cortical neurons would synchronously enter the SW hyperpolarization and depolarization phases, whereas this process would take longer in older subjects, leading to lower slope and longer SW positive and negative phases. Importantly, after controlling for SW amplitude, middle‐aged subjects still showed lower slope than young subjects in prefrontal, frontal, parietal and occipital derivations. Age‐related effects on SW density, frequency and positive phase duration were more prominent at the beginning of the night, when homeostatic sleep pressure is at its highest. Age‐related SW changes may be associated with changes in synaptic density and white matter integrity and may underlie greater sleep fragmentation and difficulty in recuperating and maintaining sleep under challenges in older subjects.

Challenging sleep in aging: the effects of 200 mg of caffeine during the evening in young and middle-aged moderate caffeine consumers

The aim of this study was to evaluate the effects of a 200‐mg administration of caffeine on polysomnographic sleep variables and quantitative sleep electroencephalography (EEG) in 12 young (20–30 years) and 12 middle‐aged (40–60 years) moderate caffeine consumers (one to three cups of coffee per day). All subjects were submitted to both a caffeine (200 mg) and placebo (lactose) condition in a double‐blind cross‐over design. The conditions were separated by 1 week. Compared with the placebo condition, the evening ingestion of caffeine lengthened sleep latency, reduced sleep efficiency, and decreased sleep duration and amount of stage 2 sleep in both age groups. Caffeine also reduced spectral power in delta frequencies in frontal, central and parietal brain areas, but not in prefrontal (PF) and occipital regions. Moreover, caffeine increased spectral power in beta frequencies in frontal and central brain areas in both age groups. A suppression of spectral power in the PF area in low delta frequencies (0.5–1.00 Hz) and a rise in spectral power in the parietal region in high alpha (10.00–12.00 Hz) and beta frequencies (17.00–21.00, 23.00–25.00, 27.00–29.00 Hz) occurred solely in middle‐aged subjects. No such changes were noticeable in young subjects. Generally, caffeine produced similar effects in young and middle‐aged subjects. Only a few frequency bins showed more effects of caffeine in middle‐aged subjects compared with young subjects. Furthermore, sleep EEG results do not entirely support the hypothesis that caffeine fully mimics the effects of a reduction of homeostatic sleep propensity when following a normal sleep–wake cycle.

Effects of Caffeine are more Marked on Daytime Recovery Sleep than on Nocturnal Sleep

Caffeine is often used to counteract sleepiness generated by sleep deprivation, jet lag, and shift-work, and is consumed at different times of day. Caffeine also has effects on sleep. However, little is known about the interaction between sleep deprivation, circadian timing, and caffeine consumption on sleep. In this study, we compared the effects of caffeine on nocturnal sleep initiated at habitual circadian time and on daytime recovery sleep. Thirty-four moderate caffeine consumers participated in both caffeine (200 mg) and placebo (lactose) conditions in a double-blind crossover design. Seventeen subjects followed their habitual sleep–wake cycle and slept in the laboratory during the night (Night), while 17 subjects were sleep deprived for one night and recovery sleep started in the morning (DayRec). All subjects received a capsule of 100 mg of caffeine (or placebo) 3 h before bedtime, and the remaining dose 1 h before bedtime. Compared to placebo, caffeine lengthened sleep latency, increased stage 1, and reduced stage 2 and slow-wave sleep (SWS) in both groups. However, caffeine reduced sleep efficiency more strongly in the DayRec group, and decreased sleep duration and REM sleep only in that group. The stronger effects of caffeine on daytime recovery sleep compared to nocturnal sleep are probably the consequence of the combined influence of increasing circadian wake propensity drive and the dissipation of homeostatic sleep pressure. We propose that the reduction of SWS by caffeine during daytime sleep increases the impact of the circadian wake signal on sleep. These results have implications for individuals using caffeine during night time.

Effects of caffeine on daytime recovery sleep: A double challenge to the sleep–wake cycle in aging

BACKGROUND AND OBJECTIVE Caffeine is the most widely used stimulant to counteract the effects of sleepiness, but it also produces important detrimental effects on subsequent sleep, especially when sleep is initiated at a time when the biological clock sends a strong waking signal such as during daytime. This study compares the effects of caffeine on daytime recovery sleep in young (20-30 y.) and middle-aged subjects (45-60 y.). METHODS Subjects participated in both caffeine (200mg) and placebo conditions (double-blind cross-over design), spaced one month apart. For each condition, subjects initially came to the laboratory for a nocturnal sleep episode. Daytime recovery sleep started in the morning after 25h of wakefulness. Subjects were administered either one caffeine (100mg) or placebo capsule three hours before daytime recovery sleep and the remaining dose one hour before daytime recovery sleep. RESULTS Middle-aged subjects showed greater decrements of sleep duration and sleep efficiency than young subjects during daytime recovery under placebo compared to nocturnal sleep. Caffeine decreased sleep efficiency, sleep duration, slow-wave sleep (SWS) and REM sleep during daytime recovery sleep similarly in both age groups. Caffeine also reduced N-REM sleep EEG synchronization during daytime recovery sleep (reduced delta, theta, and alpha power, and greater beta power). CONCLUSIONS The combined influence of age and caffeine made the sleep of middle-aged subjects particularly vulnerable to the circadian waking signal. We propose that lower brain synchronization due to age and caffeine produces greater difficulty in overriding the circadian waking signal during daytime sleep and leads to fragmented sleep. These results have implications for the high proportion of the population using caffeine to cope with night work and jet lag, particularly the middle-aged.

Aging Worsens the Effects of Sleep Deprivation on Postural Control

Falls increase with age and cause significant injuries in the elderly. This study aimed to determine whether age modulates the interactions between sleep deprivation and postural control and to evaluate how attention influences these interactions in the elderly. Fifteen young (24±2.7 y.o.) and 15 older adults (64±3.2 y.o.) stood still on a force plate after a night of sleep and after total sleep deprivation. Center of pressure range and velocity were measured with eyes open and with eyes closed while participants performed an interference task, a control task, and no cognitive task. Sleep deprivation increased the antero-posterior range of center of pressure in both age groups and center of pressure speed in older participants only. In elderly participants, the destabilizing effects of sleep deprivation were more pronounced with eyes closed. The interference task did not alter postural control beyond the destabilization induced by sleep loss in older subjects. It was concluded that sleep loss has greater destabilizing effects on postural control in older than in younger participants, and may therefore increase the risk of falls in the elderly.

Effects of increased homeostatic sleep pressure on postural control and their modulation by attentional resources

OBJECTIVE This study aimed to determine how increased sleep pressure interferes with postural control according to the availability of attentional resources and visual input. METHODS Thirteen healthy young adults performed a psychomotor vigilance task and postural tasks after a night of sleep and after 25 h of sleep deprivation. Primary outcome variables were calculated from the center of pressure (CoP) displacement measured by two force plates in various cognitive load and visual state conditions. RESULTS Sleep deprivation increased CoP anterior-posterior range in the no cognitive load condition and decreased CoP mediolateral range and velocity in the high cognitive load conditions. Sleep deprivation effects on the mediolateral range in the eyes open high cognitive load condition were significantly correlated with its effects on the psychomotor vigilance task. CONCLUSIONS Sleep deprivation destabilizes postural control when attentional and sensory resources are not challenged. In high cognitive load condition, sleep loss induces a general freezing effect that seems to be modulated by the degree of impairment in psychomotor speed. SIGNIFICANCE This study demonstrates that sleep pressure has a destabilizing effect on postural control independently of circadian factors, therefore suggesting that sleep debt may be a significant risk factor for falls.

Reduced Slow-Wave Rebound during Daytime Recovery Sleep in Middle-Aged Subjects

Cortical synchronization during NREM sleep, characterized by electroencephalographic slow waves (SW <4Hz and >75 µV), is strongly related to the number of hours of wakefulness prior to sleep and to the quality of the waking experience. Whether a similar increase in wakefulness length leads to a comparable enhancement in NREM sleep cortical synchronization in young and older subjects is still a matter of debate in the literature. Here we evaluated the impact of 25-hours of wakefulness on SW during a daytime recovery sleep episode in 29 young (27y ±5), and 34 middle-aged (51y ±5) subjects. We also assessed whether age-related changes in NREM sleep cortical synchronization predicts the ability to maintain sleep during daytime recovery sleep. Compared to baseline sleep, sleep efficiency was lower during daytime recovery sleep in both age-groups but the effect was more prominent in the middle-aged than in the young subjects. In both age groups, SW density, amplitude, and slope increased whereas SW positive and negative phase duration decreased during daytime recovery sleep compared to baseline sleep, particularly in anterior brain areas. Importantly, compared to young subjects, middle-aged participants showed lower SW density rebound and SW positive phase duration enhancement after sleep deprivation during daytime recovery sleep. Furthermore, middle-aged subjects showed lower SW amplitude and slope enhancements after sleep deprivation than young subjects in frontal and prefrontal derivations only. None of the SW characteristics at baseline were associated with daytime recovery sleep efficiency. Our results support the notion that anterior brain areas elicit and may necessitate more intense recovery and that aging reduces enhancement of cortical synchronization after sleep loss, particularly in these areas. Age-related changes in the quality of wake experience may underlie age-related reduction in markers of cortical synchronization enhancement after sustained wakefulness.