To gain some insight into how various behavioral (lifestyle) factors influence sleep duration, by investigation of the relationship of sleep time to waking activities using the American Time Use Survey (ATUS). Cross-sectional data from ATUS, an annual telephone survey of a population sample of US citizens who are interviewed regarding how they spent their time during a 24-hour period between 04:00 on the previous day and 04:00 on the interview day. Data were pooled from the 2003, 2004, and 2005 ATUS databases involving N=47,731 respondents older than 14 years of age. N/A Adjusted multiple linear regression models showed that the largest reciprocal relationship to sleep was found for work time, followed by travel time, which included commute time. Only shorter than average sleepers (<7.5 h) spent more time socializing, relaxing, and engaging in leisure activities, while both short (<5.5 h) and long sleepers (≥8.5 h) watched more TV than the average sleeper. The extent to which sleep time was exchanged for waking activities was also shown to depend on age and gender. Sleep time was minimal while work time was maximal in the age group 45-54 yr, and sleep time increased both with lower and higher age. Work time, travel time, and time for socializing, relaxing, and leisure are the primary activities reciprocally related to sleep time among Americans. These activities may be confounding the frequently observed association between short and long sleep on one hand and morbidity and mortality on the other hand and should be controlled for in future studies.

The efficacy of currently recommended treatments is uncertain in patients with mild to moderate obstructive sleep apnea (apnea–hypopnea index [AHI], 5–30). A group of 114 sleep clinic patients with an AHI of 5–30 have participated in a randomized controlled crossover trial of 3 months of treatment with each of nasal continuous positive airway pressure (CPAP), a mandibular advancement splint, and a placebo tablet. Outcomes were sleep fragmentation and hypoxemia, daytime sleepiness, quality of life, neurobehavioral function, and blood pressure. Both active treatments improved sleep outcomes, but positive airway pressure had a greater effect. The quality of life, symptoms, and subjective but not objective sleepiness improved to a similar degree with both treatments; however, many of the improvements seen in neuropsychologic function and mood were not better than the placebo effect. Some aspects of nocturnal blood pressure were improved with the splint but not with CPAP. This study has shown that although both CPAP and mandibular advancement splint effectively treated sleep-disordered breathing and sleepiness, the expected response in neurobehavioral function was incomplete. This may be due to the splint having a lesser therapeutic effect and CPAP being poorly tolerated and therefore used less in this patient group.

Stress often co-occurs with inadequate sleep duration, and both are believed to impact mood and emotion. It is not yet known whether inadequate sleep simply increases the intensity of subsequent stress responses or interacts with stressors in more complicated ways. To address this issue, we investigated the effects of one night of total sleep deprivation on subjective stress and mood in response to low-stress and high-stress cognitive testing conditions in healthy adult volunteers in two separate experiments (total N = 53). Sleep was manipulated in a controlled, laboratory setting and stressor intensity was manipulated by changing difficulty of cognitive tasks, time pressure, and feedback about performance. Sleep-deprived participants reported greater subjective stress, anxiety, and anger than rested controls following exposure to the low-stressor condition, but not in response to the high-stressor condition, which elevated negative mood and stress about equally for both sleep conditions. These results suggest that sleep deprivation lowers the psychological threshold for the perception of stress from cognitive demands but does not selectively increase the magnitude of negative affect in response to high-stress performance demands.

Establish the dose-response relationship between increasing sleep durations in a single night and recovery of neurobehavioral functions following chronic sleep restriction. Intent-to-treat design in which subjects were randomized to 1 of 6 recovery sleep doses (0, 2, 4, 6, 8, or 10 h TIB) for 1 night following 5 nights of sleep restriction to 4 h TIB. Twelve consecutive days in a controlled laboratory environment. N = 159 healthy adults (aged 22–45 y), median = 29 y). Following a week of home monitoring with actigraphy and 2 baseline nights of 10 h TIB, subjects were randomized to either sleep restriction to 4 h TIB per night for 5 nights followed by randomization to 1 of 6 nocturnal acute recovery sleep conditions (N = 142), or to a control condition involving 10 h TIB on all nights (N = 17). Primary neurobehavioral outcomes included lapses on the Psychomotor Vigilance Test (PVT), subjective sleepiness from the Karolinska Sleepiness Scale (KSS), and physiological sleepiness from a modified Maintenance of Wakefulness Test (MWT). Secondary outcomes included psychomotor and cognitive speed as measured by PVT fastest RTs and number correct on the Digit Symbol Substitution Task (DSST), respectively, and subjective fatigue from the Profile of Mood States (POMS). The dynamics of neurobehavioral outcomes following acute recovery sleep were statistically modeled across the 0 h–10 h recovery sleep doses. While TST, stage 2, REM sleep and NREM slow wave energy (SWE) increased linearly across recovery sleep doses, best-fitting neurobehavioral recovery functions were exponential across recovery sleep doses for PVT and KSS outcomes, and linear for the MWT. Analyses based on return to baseline and on estimated intersection with control condition means revealed recovery was incomplete at the 10 h TIB (8.96 h TST) for PVT performance, KSS sleepiness, and POMS fatigue. Both TST and SWE were elevated above baseline at the maximum recovery dose of 10 h TIB. Neurobehavioral deficits induced by 5 nights of sleep restricted to 4 h improved monotonically as acute recovery sleep dose increased, but some deficits remained after 10 h TIB for recovery. Complete recovery from such sleep restriction may require a longer sleep period during 1 night, and/or multiple nights of recovery sleep. It appears that acute recovery from chronic sleep restriction occurs as a result of elevated sleep pressure evident in both increased SWE and TST.