Total sleep deprivation alters cardiovascular reactivity to acute stressors in humans

Exaggerated cardiovascular reactivity to mental stress (MS) and cold pressor test (CPT) has been linked to increased risk of cardiovascular disease. Recent epidemiological studies identify sleep deprivation as an important risk factor for hypertension, yet the relations between sleep deprivation and cardiovascular reactivity remain equivocal. We hypothesized that 24-h total sleep deprivation (TSD) would augment cardiovascular reactivity to MS and CPT and blunt the MS-induced forearm vasodilation. Because the associations between TSD and hypertension appear to be stronger in women, a secondary aim was to probe for sex differences. Mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity (MSNA) were recorded during MS and CPT in 28 young, healthy subjects (14 men and 14 women) after normal sleep (NS) and 24-h TSD (randomized, crossover design). Forearm vascular conductance (FVC) was recorded during MS. MAP, FVC, and MSNA (n = 10) responses to MS were not different between NS and TSD (condition × time, P > 0.05). Likewise, MAP and MSNA (n = 6) responses to CPT were not different between NS and TSD (condition × time, P > 0.05). In contrast, increases in HR during both MS and CPT were augmented after TSD (condition × time, P ≤ 0.05), and these augmented HR responses persisted during both recoveries. When analyzed for sex differences, cardiovascular reactivity to MS and CPT was not different between sexes (condition × time × sex, P > 0.05). We conclude that TSD does not significantly alter MAP, MSNA, or forearm vascular responses to MS and CPT. The augmented tachycardia responses during and after both acute stressors provide new insight regarding the emerging links among sleep deprivation, stress, and cardiovascular risk.     

Meta-Analysis of the Relationship Between Total Sleep Deprivation and Performance

Studies consistently show that total sleep deprivation (TSD) and measures of performance are negatively correlated. However, an accurate quantitative summary of the relationship between these variables has not yet been reported. After collection of the data from 27 relevant studies, meta-analytic techniques were used to test several hypotheses. The correlations were found to be highest for TSD of ≥45 h, speed rather than accuracy measures of performance, and work-paced rather than self-paced tasks. These findings are consistent with the “lapse hypothesis” that posits microsleeps during long hours of sleep deprivation.     

Meta-Analysis of the Relationship Between Total Sleep Deprivation and Performance

Studies consistently show that total sleep deprivation (TSD) and measures of performance are negatively correlated. However, an accurate quantitative summary of the relationship between these variables has not yet been reported. After collection of the data from 27 relevant studies, meta-analytic techniques were used to test several hypotheses. The correlations were found to be highest for TSD of ≥45 h, speed rather than accuracy measures of performance, and work-paced rather than self-paced tasks. These findings are consistent with the “lapse hypothesis” that posits microsleeps during long hours of sleep deprivation.     

Total sleep deprivation does not significantly degrade semantic encoding

ABSTRACT

Sleep deprivation impairs performance on cognitive tasks, but it is unclear which cognitive processes it degrades. We administered a semantic matching task with variable stimulus onset asynchrony (SOA) and both speeded and self-paced trial blocks. The task was administered at the baseline and 24 hours later after 30.8 hours of total sleep deprivation (TSD) or matching well-rested control. After sleep deprivation, the 20% slowest response times (RTs) were significantly increased. However, the semantic encoding time component of the RTs remained at baseline level. Thus, the performance impairment induced by sleep deprivation on this task occurred in cognitive processes downstream of semantic encoding.     

Sympathetic neural responses to 24-hour sleep deprivation in humans: sex differences

Sleep deprivation has been linked to hypertension, and recent evidence suggests that associations between short sleep duration and hypertension are stronger in women. In the present study we hypothesized that 24 h of total sleep deprivation (TSD) would elicit an augmented pressor and sympathetic neural response in women compared with men. Resting heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) were measured in 30 healthy subjects (age, 22 ± 1; 15 men and 15 women). Relations between spontaneous fluctuations of diastolic arterial pressure and MSNA were used to assess sympathetic baroreflex function. Subjects were studied twice, once after normal sleep and once after TSD (randomized, crossover design). TSD elicited similar increases in systolic, diastolic, and mean BP in men and women (time, P < 0.05; time × sex, P > 0.05). TSD reduced MSNA in men (25 ± 2 to 16 ± 3 bursts/100 heart beats; P = 0.02), but not women. TSD did not alter spontaneous sympathetic or cardiovagal baroreflex sensitivities in either sex. However, TSD shifted the spontaneous sympathetic baroreflex operating point downward and rightward in men only. TSD reduced testosterone in men, and these changes were correlated to changes in resting MSNA (r = 0.59; P = 0.04). Resting HR, respiratory rate, and estradiol were not altered by TSD in either sex. In conclusion, TSD-induced hypertension occurs in both sexes, but only men demonstrate altered resting MSNA. The sex differences in MSNA are associated with sex differences in sympathetic baroreflex function (i.e., operating point) and testosterone. These findings may help explain why associations between sleep deprivation and hypertension appear to be sex dependent.     

Prediction of Vigilant Attention and Cognitive Performance Using Self-Reported Alertness,Circadian Phase,Hours since Awakening,and Accumulated Sleep Loss

Sleep restriction causes impaired cognitive performance that can result in adverse consequences in many occupational settings. Individuals may rely on self-perceived alertness to decide if they are able to adequately perform a task. It is therefore important to determine the relationship between an individual’s self-assessed alertness and their objective performance, and how this relationship depends on circadian phase, hours since awakening, and cumulative lost hours of sleep. Healthy young adults (aged 18–34) completed an inpatient schedule that included forced desynchrony of sleep/wake and circadian rhythms with twelve 42.85-hour “days” and either a 1:2 (n = 8) or 1:3.3 (n = 9) ratio of sleep-opportunity:enforced-wakefulness. We investigated whether subjective alertness (visual analog scale), circadian phase (melatonin), hours since awakening, and cumulative sleep loss could predict objective performance on the Psychomotor Vigilance Task (PVT), an Addition/Calculation Test (ADD) and the Digit Symbol Substitution Test (DSST). Mathematical models that allowed nonlinear interactions between explanatory variables were evaluated using the Akaike Information Criterion (AIC). Subjective alertness was the single best predictor of PVT, ADD, and DSST performance. Subjective alertness alone, however, was not an accurate predictor of PVT performance. The best AIC scores for PVT and DSST were achieved when all explanatory variables were included in the model. The best AIC score for ADD was achieved with circadian phase and subjective alertness variables. We conclude that subjective alertness alone is a weak predictor of objective vigilant or cognitive performance. Predictions can, however, be improved by knowing an individual’s circadian phase, current wake duration, and cumulative sleep loss.     

Restricted sleep regime in rhesus monkeys: differential effect of one night's sleep loss and selective REM deprivation.

The differential effect of either one night's total sleep deprivation (TSD) or of selective REM deprivation (REMD) was examined on post-deprivation daytime EEG patterns with respect to control, in the same group of rhesus monkeys. TSD resulted in significantly decreased wakefulness and increased amounts of NREM and REM on the first day following TSD. In contrast, highly significant REM elevation without alteration of other EEG states occurred for 3 days after REMD. Post-deprivation behavioural and photic-induced neural changes were minor. The results obtained after sleep deprivation in simians are comparable with similar findings in human subjects.     

Inter-Individual Differences in Neurobehavioural Impairment following Sleep Restriction Are Associated with Circadian Rhythm Phase

Although sleep restriction is associated with decrements in daytime alertness and neurobehavioural performance, there are considerable inter-individual differences in the degree of impairment. This study examined the effects of short-term sleep restriction on neurobehavioural performance and sleepiness, and the associations between individual differences in impairments and circadian rhythm phase. Healthy adults (n = 43; 22 M) aged 22.5 ± 3.1 (mean ± SD) years maintained a regular 8:16 h sleep:wake routine for at least three weeks prior to laboratory admission. Sleep opportunity was restricted to 5 hours time-in-bed at home the night before admission and 3 hours time-in-bed in the laboratory, aligned by wake time. Hourly saliva samples were collected from 5.5 h before until 5 h after the pre-laboratory scheduled bedtime to assess dim light melatonin onset (DLMO) as a marker of circadian phase. Participants completed a 10-min auditory Psychomotor Vigilance Task (PVT), the Karolinska Sleepiness Scale (KSS) and had slow eye movements (SEM) measured by electrooculography two hours after waking. We observed substantial inter-individual variability in neurobehavioural performance, particularly in the number of PVT lapses. Increased PVT lapses (r = -0.468, p < 0.01), greater sleepiness (r = 0.510, p < 0.0001), and more slow eye movements (r = 0.375, p = 0.022) were significantly associated with later DLMO, consistent with participants waking at an earlier circadian phase. When the difference between DLMO and sleep onset was less than 2 hours, individuals were significantly more likely to have at least three attentional lapses the following morning. This study demonstrates that the phase of an individual’s circadian system is an important variable in predicting the degree of neurobehavioural performance impairment in the hours after waking following sleep restriction, and confirms that other factors influencing performance decrements require further investigation.     

Can a shorter psychomotor vigilance task be used as a reasonable substitute for the ten-minute psychomotor vigilance task?

The 10 min psychomotor vigilance task (PVT) is commonly used in laboratory studies to assess the impact of sleep loss, sustained wakefulness, and/or time of day on neurobehavioral performance. In field settings, though, it may be impractical for participants to perform a test of this length. The aim of this study was to identify a performance measure that is sensitive to the effects of fatigue but less burdensome than a 10 min test. Sixteen participants (11 female, 5 male; mean age = 21.7 years) slept in the sleep laboratory overnight then remained awake for 28 h from 08:00 h. During every second hour, participants completed three PVTs of differing duration (10 min, 5 min, 90 sec). For the 5 min/10 min comparison, ANOVA indicated that response time was significantly affected by test length (F1,14 = 26.9, p < .001) and hours of wakefulness (F13,182 = 46.1, p < .001) but not by their interaction (F13,182 = 1.7, ns). There was a strong correlation between response time on the 5 and 10 min PVTs (r = .88, p < .001). For the 90 sec/10 min comparison, ANOVA indicated that response time was significantly affected by test length (F1,14 = 65.9, p < .001) and hours of wakefulness (F13,182 = 29.7, p < .001) as well as by their interaction (F13,182 = 6.0, p < .001). There was a strong correlation between response time on the 90 sec and 10 min PVTs (r = .77, p < .001). The effects of hours of wakefulness on neurobehavioral performance were similar for the 5 min and 10 min PVTs. In contrast, performance on the 90 sec PVT was less affected by hours of wakefulness than on the 10 min PVT. In addition, performance on the 10 min PVT was more highly correlated with the 5 min PVT than the 90 sec PVT. These data indicate that the 5 min PVT may provide a reasonable substitute for the 10 min PVT in circumstances where a test shorter than 10 min is required.     

完全睡眠剥夺对大脑注意网络冲突效应和脑电样本熵的影响*

目的: 本研究分析睡眠剥夺对个体选择性注意网络冲突效应和脑电样本熵的影响,探讨睡眠剥夺对大脑注意网络的影响。方法: 25名健康受试者参与36 h完全睡眠剥夺试验。试验于当天9:00开始,于次日21:00结束,试验采用自身前后对照设计。受试者在睡眠剥夺前后分别完成注意网络任务,同步采集受试者的脑电图。用脑电样本熵算法分析脑电图的delta、theta、alpha、beta和gamma频率段的脑电复杂度并对比各频段脑电样本熵在睡眠剥夺前、后的变化。结果: 同睡眠剥夺前比较,睡眠剥夺后与受试者的注意网络冲突效应密切相关的反应时显著下降(P＜0.01),正确率显著增加(P＜0.01)。脑电样本熵分析发现在beta频率段,与注意网络冲突控制相关的脑电样本熵值在睡眠剥夺后明显增大(P＜0.01)。其余脑电频率段脑电样本熵未发现显著差异。结论: 表明完全睡眠剥夺后大脑的注意网络冲突效应降低,表明睡眠剥夺后执行冲突控制能力的下降。     

Sensitivity and Validity of Psychometric Tests for Assessing Driving Impairment: Effects of Sleep Deprivation

ObjectiveTo assess drug induced driving impairment, initial screening is needed. However, no consensus has been reached about which initial screening tools have to be used. The present study aims to determine the ability of a battery of psychometric tests to detect performance impairing effects of clinically relevant levels of drowsiness as induced by one night of sleep deprivation.MethodsTwenty four healthy volunteers participated in a 2-period crossover study in which the highway driving test was conducted twice: once after normal sleep and once after one night of sleep deprivation. The psychometric tests were conducted on 4 occasions: once after normal sleep (at 11 am) and three times during a single night of sleep deprivation (at 1 am, 5 am, and 11 am).ResultsOn-the-road driving performance was significantly impaired after sleep deprivation, as measured by an increase in Standard Deviation of Lateral Position (SDLP) of 3.1 cm compared to performance after a normal night of sleep. At 5 am, performance in most psychometric tests showed significant impairment. As expected, largest effect sizes were found on performance in the Psychomotor Vigilance Test (PVT). Large effects sizes were also found in the Divided Attention Test (DAT), the Attention Network Test (ANT), and the test for Useful Field of View (UFOV) at 5 and 11 am during sleep deprivation. Effects of sleep deprivation on SDLP correlated significantly with performance changes in the PVT and the DAT, but not with performance changes in the UFOV.ConclusionFrom the psychometric tests used in this study, the PVT and DAT seem most promising for initial evaluation of drug impairment based on sensitivity and correlations with driving impairment. Further studies are needed to assess the sensitivity and validity of these psychometric tests after benchmark sedative drug use.     

Decreased Thalamocortical Functional Connectivity after 36 Hours of Total Sleep Deprivation: Evidence from Resting State fMRI

Objectives

The thalamus and cerebral cortex are connected via topographically organized, reciprocal connections, which hold a key function in segregating internally and externally directed awareness information. Previous task-related studies have revealed altered activities of the thalamus after total sleep deprivation (TSD). However, it is still unclear how TSD impacts on the communication between the thalamus and cerebral cortex. In this study, we examined changes of thalamocortical functional connectivity after 36 hours of total sleep deprivation by using resting state function MRI (fMRI).

Materials and Methods

Fourteen healthy volunteers were recruited and performed fMRI scans before and after 36 hours of TSD. Seed-based functional connectivity analysis was employed and differences of thalamocortical functional connectivity were tested between the rested wakefulness (RW) and TSD conditions.

Results

We found that the right thalamus showed decreased functional connectivity with the right parahippocampal gyrus, right middle temporal gyrus and right superior frontal gyrus in the resting brain after TSD when compared with that after normal sleep. As to the left thalamus, decreased connectivity was found with the right medial frontal gyrus, bilateral middle temporal gyri and left superior frontal gyrus.

Conclusion

These findings suggest disruptive changes of the thalamocortical functional connectivity after TSD, which may lead to the decline of the arousal level and information integration, and subsequently, influence the human cognitive functions.     

Effect of one night of sleep loss on changes in tumor necrosis factor alpha (TNF-α) levels in healthy men

Total sleep deprivation in humans is associated with increased daytime sleepiness, decreased performance, elevations in inflammatory cytokines, and hormonal/metabolic disturbances.To assess the effects of 40 h of total sleep deprivation (TSD) under constant and well controlled conditions, on plasma levels of TNF-α and its receptor (TNFR1), interleukin-6 (IL-6), cortisol and C-reactive protein (CRP), sleepiness and performance, 12 healthy men (29 ± 3 years) participated in a 5-days sleep deprivation experiment (two control nights followed by a night of sleep loss and one recovery night). Between 0800 and 2300 (i.e. between 25 and 40 h of sleep deprivation), a serial of blood sampling, multiple sleep latency, subjective levels of sleepiness and reaction time tests were completed before (day 2: D2) and after (day 4: D4) one night of sleep loss. We showed that an acute sleep deprivation (i.e. after 34 and 37 h of sleep deprivation) induced a significant increase in TNF-α (P < 0.01), but there were no significant changes in TNFR1, IL-6, cortisol and CRP. In conclusion, our study in which constant and controlled experimental conditions were realized with healthy subjects and in absence of psychological or physical stressors, an acute total sleep deprivation (from 34 h) was sufficient to induce secretion of pro-inflammatory cytokine such as TNF-α, a marker more described in chronic sleep restriction or deprivation and as mediators of excessive sleepiness in humans in pathological conditions.     

CHRONIC SLEEP DEFICIT AND PERFORMANCE OF A SUSTAINED ATTENTION TASK—AN ELECTROOCULOGRAPHY STUDY

Electrooculography (EOG) was used to explore performance differences in a sustained attention task during rested wakefulness (RW) and after 7 days of partial sleep deprivation (SD). The RW condition was based on obtaining regular sleep, and the SD condition involved sleep restriction of 3?h/night for a week resulting in a total sleep debt of 21?h. The study used a counterbalanced design with a 2-wk gap between the conditions. Participants performed a sustained attention task for 45?min on four occasions: 10:00–11:00, 14:00–15:00, 18:00–19:00, and 22:00–23:00?h. The task required moving gaze and attention as fast as possible from a fixation point to a target. In each session, 120 congruent and 34 incongruent stimuli were presented, totaling 1232 observations/participant. Correct responses plus errors of omission (lapses) and commission (false responses) were recorded, and the effect of time-of-day on sustained attention following SD was investigated. The analysis of variance (ANOVA) model showed that SD affected performance on a sustained attention task and manifested itself in a higher number of omission errors: congruent stimuli (F_(1,64)?=?13.3, p?<?.001) and incongruent stimuli (F_(1,64)?=?14.0, p?<?.001). Reaction times for saccadic eye movements did not differ significantly between experimental conditions or by time-of-day. Commission errors, however, exhibited a decreasing trend during the day. The visible prevalence of omissions in SD versus RW was observed during the mid-afternoon hours (the so-called post-lunch dip) for both congruent and incongruent stimuli (F_(1,16)?=?5.3, p?=?.04 and F_(1,16)?=?5.6, p?=?.03, respectively), and at 18:00?h for incongruent stimuli (F_(1,13)?=?5.7, p?=?.03). (Author correspondence: magda.fafrowicz@uj.edu.pl)     

Tradeoffs of different types of species occurrence data for use in systematic conservation planning

Data on the occurrence of species are widely used to inform the design of reserve networks. These data contain commission errors (when a species is mistakenly thought to be present) and omission errors (when a species is mistakenly thought to be absent), and the rates of the two types of error are inversely related. Point locality data can minimize commission errors, but those obtained from museum collections are generally sparse, suffer from substantial spatial bias and contain large omission errors. Geographic ranges generate large commission errors because they assume homogenous species distributions. Predicted distribution data make explicit inferences on species occurrence and their commission and omission errors depend on model structure, on the omission of variables that determine species distribution and on data resolution. Omission errors lead to identifying networks of areas for conservation action that are smaller than required and centred on known species occurrences, thus affecting the comprehensiveness, representativeness and efficiency of selected areas. Commission errors lead to selecting areas not relevant to conservation, thus affecting the representativeness and adequacy of reserve networks. Conservation plans should include an estimation of commission and omission errors in underlying species data and explicitly use this information to influence conservation planning outcomes.     

Effect of acute sleep deprivation and recovery on Insulin-like Growth Factor-I responses and inflammatory gene expression in healthy men

Acute sleep deprivation in humans has been found to increase inflammatory markers and signaling pathways in the periphery through a possible Toll-like receptor 4 (TLR-4). In addition, short duration sleep has been associated with low circulating total Insulin-like Growth Factor-I (IGF-I) concentrations.We aimed to determine whether a total sleep deprivation (TSD) protocol with recovery altered whole-blood gene expression of the proinflammatory cytokines TNF-α and IL-6, as well as TLR-4 expression, and to examine the relationship with circulating concentrations of the IGF-I system. Twelve healthy men participated in a five-day TSD (two control nights followed by one night of sleep deprivation and one night of recovery). Blood was sampled at 0800, before and after sleep deprivation (D2 and D4), and after recovery (D5). It is shown that 25h of sleep deprivation (D4) induced significant increases in mRNA levels of TNF-α and its soluble receptor R1 (P<0.01 respectively), as well as TLR-4 (P<0.05), while IL-6 mRNA levels remained unchanged. Circulating concentrations of free IGF-I were decreased at D4 (P<0.001). One night of recovery was sufficient to restore basal expression levels for TNF-α, sTNF-R1, TLR-4 and circulating IGF-I. Changes in TLR-4 mRNA levels during the protocol correlated positively with those of TNF-α and sTNF-R1 (r = 0.393 and r = 0.490 respectively), and negatively with circulating free IGF-I (r = ?0.494). In conclusion, 25h of sleep deprivation in healthy subjects is sufficient to induce transient and reversible genomic expression of the pro-inflammatory cytokine TNF-α and its R1 receptor, and its mediator TLR-4, with a possible link to IGF-I axis inhibition.     

Daytime napping after a night of sleep loss decreases sleepiness, improves performance, and causes beneficial changes in cortisol and interleukin-6 secretion

Sleep loss has been associated with increased sleepiness, decreased performance, elevations in inflammatory cytokines, and insulin resistance. Daytime napping has been promoted as a countermeasure to sleep loss. To assess the effects of a 2-h midafternoon nap following a night of sleep loss on postnap sleepiness, performance, cortisol, and IL-6, 41 young healthy individuals (20 men, 21 women) participated in a 7-day sleep deprivation experiment (4 consecutive nights followed by a night of sleep loss and 2 recovery nights). One-half of the subjects were randomly assigned to take a midafternoon nap (1400-1600) the day following the night of total sleep loss. Serial 24-h blood sampling, multiple sleep latency test (MSLT), subjective levels of sleepiness, and psychomotor vigilance task (PVT) were completed on the fourth (predeprivation) and sixth days (postdeprivation). During the nap, subjects had a significant drop in cortisol and IL-6 levels (P < 0.05). After the nap they experienced significantly less sleepiness (MSLT and subjective, P < 0.05) and a smaller improvement on the PVT (P < 0.1). At that time, they had a significant transient increase in their cortisol levels (P < 0.05). In contrast, the levels of IL-6 tended to remain decreased for approximately 8 h (P = 0.1). We conclude that a 2-h midafternoon nap improves alertness, and to a lesser degree performance, and reverses the effects of one night of sleep loss on cortisol and IL-6. The redistribution of cortisol secretion and the prolonged suppression of IL-6 secretion are beneficial, as they improve alertness and performance.     

36 h完全睡眠剥夺对客体工作记忆相关电位的影响*

目的:采用事件相关电位(ERP)技术探讨36 h完全睡眠剥夺对客体工作记忆的影响。方法:本研究采用自身前后对照设计,16名睡眠质量良好的健康大学生(平均年龄为23岁,年龄范围21～28岁)分别在清醒状态下及36 h完全睡眠剥夺后接受2-back客体工作记忆任务,同时采集脑电数据。选用重复测量方差分析的方法比较睡眠剥夺前后与客体工作记忆有关的P2、N2、P3成分的波幅和潜伏期的差异。结果:在36 h完全睡眠剥夺后,与客体工作记忆加工相关的N2波的潜伏期显著延长(P＜0.05),波幅减少但未见统计学差异(P＞0.05); P2波潜伏期显著延长(P＜0.05),波幅未见明显变化(P＞0.05)。P3波波幅、潜伏期未见统计学差异(P＞0.05)。结论:36 h的完全睡眠剥夺影响了客体工作记忆相关电位,损害了个体的客体工作记忆加工能力。     

Mood, alertness, and performance in response to sleep deprivation and recovery sleep in experienced shiftworkers versus non-shiftworkers

Previous studies have shown increased sleepiness and mood changes in shiftworkers, which may be due to sleep deprivation or circadian disruption. Few studies, however, have compared responses of experienced shiftworkers and non-shiftworkers to sleep deprivation in an identical laboratory setting. The aim of this laboratory study, therefore, was to compare long-term shiftworkers and non-shiftworkers and to investigate the effects of one night of total sleep deprivation (30.5 h of continuous wakefulness) and recovery sleep on psychomotor vigilance, self-rated alertness, and mood. Eleven experienced male shiftworkers (shiftwork ≥5 yrs) were matched with 14 non-shiftworkers for age (mean ± SD: 35.7 ± 7.2 and 32.5 ± 6.2 yrs, respectively) and body mass index (BMI) (28.7 ± 3.8 and 26.6 ± 3.4 kg/m(2), respectively). After keeping a 7-d self-selected sleep/wake cycle (7.5/8 h nocturnal sleep), both groups entered a laboratory session consisting of a night of adaptation sleep and a baseline sleep (each 7.5/8 h), a sleep deprivation night, and recovery sleep (4-h nap plus 7.5/8 h nighttime sleep). Subjective alertness and mood were assessed with the Karolinska Sleepiness Scale (KSS) and 9-digit rating scales, and vigilance was measured by the visual psychomotor vigilance test (PVT). A mixed-model regression analysis was carried out on data collected every hour during the sleep deprivation night and on all days (except for the adaptation day), at .25, 4.25, 5.25, 11.5, 12.5, and 13.5 h after habitual wake-up time. Despite similar circadian phase (melatonin onset), demographics, food intake, body posture, and environmental light, shiftworkers felt significantly more alert, more cheerful, more elated, and calmer than non-shiftworkers throughout the laboratory study. In addition, shiftworkers showed a faster median reaction time (RT) compared to non-shiftworkers, although four other PVT parameters did not differ between the groups. As expected, both groups showed a decrease in subjective alertness and PVT performance during and following the sleep deprivation night. Subjective sleepiness and most aspects of PVT performance returned to baseline levels after a nap and recovery sleep. The mechanisms underlying the observed differences between shiftworkers and non-shiftworkers require further study, but may be related to the absence of shiftwork the week prior to and during the laboratory study as well as selection into and out of shiftwork.     

Sleep deprivation sensitizes human craniofacial muscles

It is unknown whether and how sleep deprivation influences craniofacial muscle sensitivity in healthy humans. We investigated whether total sleep deprivation (TSD) and one night of recovery sleep (RS) can alter mechanical pain sensitivity in temporal and masseter muscles. Fifteen healthy volunteers participated in three consecutive sessions. Pressure pain thresholds were measured on the temporal and masseter muscles. Both temporal and masseter muscles became sensitized after 24?h of TSD. RS reversed the muscle sensitization.