Evaluation of a daily facial massage on perceived sleep quality and well-being: A pilot study.

OBJECTIVE: Sleep disorders are widespread and constitute a major public health risk. The present study thus aims to investigate the effect of a facial cosmetic self-massage daily routine on women's sleep and well-being. METHODS: The present pilot study was conducted on 62 middle-aged women declaring daily tiredness and sleep troubles. We examined the effect of a regular facial cosmetic self-massage routine on sleep patterns, daytime sleepiness, and well-being over the course of 2 months. RESULTS: After 1 and 2 months, our results show improved sleep quality (Pittsburgh Sleep Quality Index, PSQI - -20.2% after 2 months), reduced daytime sleepiness (Epworth Sleepiness Scale, ESS, -31.2% after 2 months), and increased well-being measures. The number of participants with abnormal sleep (PSQI >5) decreased over the course of the experiment as well, from 71.9% to 49.2% at the end of the 2 months [odds ratio 95% CI for decrease: 0.38 (0.18-0.81)]. Similarly, the number of participants with excessive daytime sleepiness (>10 on the ESS) decreased over the course of the study from 44.3% to 21% after 1 month [95% CI: 0.33 (0.15-0.73)] and to 16.1% after 2 months [95% CI: 0.24 (0.10-0.56)]. CONCLUSIONS: These results suggest that a facial cosmetic self-massage routine may improve sleep patterns and is likely to be a useful addition to a standard sleep hygiene routine.

OBJECTIF: Les troubles du sommeil sont répandus et constituent un risque majeur pour la santé publique. La présente étude vise donc à examiner l'effet d'une routine quotidienne d'auto­massage cosmétique du visage sur le sommeil et le bien­être des femmes. MÉTHODES: La présente étude pilote a été menée auprès de 62 femmes d'âge moyen déclarant une fatigue quotidienne et des troubles du sommeil. Nous avons examiné l'effet d'une routine régulière d'auto­massage cosmétique du visage sur les habitudes de sommeil, la somnolence diurne et le bien­être sur une période de deux mois. RÉSULTATS: Après un et deux mois, nos résultats montrent une amélioration de la qualité du sommeil (échelle de qualité du sommeil de Pittsburgh [Pittsburgh Sleep Quality Index, PSQI]: −20.2% après deux mois), une diminution de la somnolence diurne (échelle de somnolence d'Epworth [Epworth Sleepiness Scale, ESS]: −31.2% après deux mois) et une augmentation des valeurs dans les mesures du bien­être. Le nombre de participantes présentant un sommeil anormal (PSQI > 5) a également diminué au cours de l'expérience, passant de 71.9% à 49.2% à la fin des deux mois [rapport de cotes avec IC à 95% pour la diminution: 0.38 (0.18­0.81)]. De même, le nombre de participantes présentant une somnolence diurne excessive (>10 sur l'échelle ESS) a diminué au cours de l'étude passant de 44.3% à 21% après un mois [IC à 95%: 0.33 (0.15­0.73)] et à 16.1% après 2 mois [IC à 95%: 0.24 (0.10­0.56)]. CONCLUSIONS: Ces résultats indiquent qu'incorporer une routine d'auto­massage cosmétique du visage peut favoriser de meilleures habitudes de sommeil, et qu'elle pourrait être bénéfique en complément d'une routine d'hygiène du sommeil habituelle.

Sleep Inertia in Aviation.

INTRODUCTION: Sleep inertia is the transition state during which alertness and cognitive performance are temporarily impaired after awakening. Magnitude and time course of sleep inertia are characterized by high individual variability with large differences between the cognitive functions affected. This period of impairment is of concern to pilots, who take sleep or nap periods during on-call work hours or in-flight rest, then need to perform safety-critical tasks soon after waking. This review analyzes literature related to sleep inertia and countermeasures applicable for aviation.METHODS: The large part of scientific literature that focuses on sleep inertia is based on studies in patients with chronic sleep inertia. We analyzed 8 narrative reviews and 64 papers related to acute sleep inertia in healthy subjects.DISCUSSION: Sleep inertia is a multifactorial, complex process, and many different protocols have been conducted, with a low number of subjects, in noncontrolled laboratory designs, with questionnaires or cognitive tests that have not been replicated. Evidence suggests that waking after sleep loss, or from deeper stages of sleep, can exacerbate sleep inertia through complex interactions between awakening and sleep-promoting brain structures. Nevertheless, no meta-analyses are possible and extrapolation to pilots' performances is hypothetical. Studies in real life or simulated operational situations must be conducted to improve the description of the impact of sleep inertia and kinetics on pilots' performances. Taking rest or sleep time remains the main method for pilots to fight against fatigue and related decreases in performance. We propose proactive strategies to mitigate sleep inertia and improve alertness.Sauvet F, Beauchamps V, Cabon P. Sleep inertia in aviation. Aerosp Med Hum Perform. 2024; 95(4):206-213.

The Impact of Multisession Sleep-Hygiene Strategies on Sleep Parameters in Elite Swimmers.

PURPOSE: Short sleep duration and poor sleep quality are common in swimmers. Sleep-hygiene strategies demonstrated beneficial effects on several sleep parameters. The present study assessed the impact of a multisession sleep-hygiene training course on sleep in elite swimmers. METHODS: Twenty-eight elite swimmers (17 [2] y) participated. The sleep-hygiene strategy consisted of 3 interventions. Sleep was measured by actigraphy for 7 days before the beginning of the intervention (baseline), after the first collective intervention (postintervention), after the second collective intervention (postintervention 2), and, finally, after the individual intervention (postintervention 3). The Epworth Sleepiness Scale (ESS) was completed concurrently. Swimmers were classified into 2 groups: nonsomnolent (baseline ESS score ≤ 10, n = 13) and somnolent (baseline ESS score ≥ 11, n = 15). RESULTS: All swimmers had a total sleep time of <8 hours per night. Sixty percent of swimmers were moderately morning type. Later bedtime, less time in bed, and total sleep time were observed in the somnolent group compared with the nonsomnolent group at baseline. An interaction between training course and group factors was observed for bedtime, with a significant advance in bedtime between baseline, postintervention 2, and postintervention 3 for the somnolent group. CONCLUSIONS: The present study confirms the importance of implementing sleep-hygiene strategies, particularly in athletes with an ESS score ≥11. A conjunction of individual and collective measures (eg, earlier bedtime, napping, and delaying morning training session) could favor the total sleep time achieved.

Effects of Acute Caffeine Intake on Insulin-Like Growth Factor-1 Responses to Total Sleep Deprivation: Interactions with COMT Polymorphism - A Randomized, Crossover Study.

INTRODUCTION: Genes encoding catechol-O-methyl-transferase (COMT) and adenosine A2A receptor (ADORA2A) have been shown to influence cognitive performances and responses to caffeine intake during prolonged wakefulness. The rs4680 single-nucleotide polymorphism (SNP) of COMT differentiates on memory score and circulating levels of the neurotrophic factor IGF-1. This study aimed to determine the kinetics of IGF-1, testosterone, and cortisol concentrations during prolonged wakefulness under caffeine or placebo intake in 37 healthy participants, and to analyze whether the responses are dependent on COMT rs4680 or ADORA2A rs5751876 SNPs. METHODS: In caffeine (2.5 mg/kg, twice over 24 h) or placebo-controlled condition, blood sampling was performed at 1 h (08:00, baseline), 11 h, 13 h, 25 h (08:00 next day), 35 h, and 37 h of prolonged wakefulness, and at 08:00 after one night of recovery sleep, to assess hormonal concentrations. Genotyping was performed on blood cells. RESULTS: Results indicated a significant increase in IGF-1 levels after 25, 35, and 37 h of prolonged wakefulness in the placebo condition, in subjects carrying the homozygous COMT A/A genotype only (expressed in absolute values [±SEM]: 118 ± 8, 121 ± 10, and 121 ± 10 vs. 105 ± 7 ng/mL for A/A, 127 ± 11, 128 ± 12, and 129 ± 13 vs. 120 ± 11 ng/mL for G/G, and 106 ± 9, 110 ± 10, and 106 ± 10 vs. 101 ± 8 ng/mL for G/A, after 25, 35, and 37 h of wakefulness versus 1 h; p < 0.05, condition X time X SNP). Acute caffeine intake exerted a COMT genotype-dependent reducing effect on IGF-1 kinetic response (104 ± 26, 107 ± 27, and 106 ± 26 vs. 100 ± 25 ng/mL for A/A genotype, at 25, 35, and 37 h of wakefulness vs. 1 h; p < 0.05 condition X time X SNP), plus on resting levels after overnight recovery (102 ± 5 vs. 113 ± 6 ng/mL) (p < 0.05, condition X SNP). Testosterone and cortisol concentrations decreased during wakefulness, and caffeine alleviated the testosterone reduction, unrelated to the COMT polymorphism. No significant main effect of the ADORA2A SNP was shown regardless of hormonal responses. CONCLUSION: Our results indicated that the COMT polymorphism interaction is important in determining the IGF-1 neurotrophic response to sleep deprivation with caffeine intake (NCT03859882).

Effects of a Sleep Hygiene Strategy on Parameters of Sleep Quality and Quantity in Youth Elite Rugby Union Players.

PURPOSE: To assess the effects of a sleep hygiene strategy on parameters of sleep quality and quantity in youth elite rugby union players. METHOD: Eleven male players (age: 19.0 [1.4] y) undertook a sleep hygiene strategy composed of 2 theoretical sessions and 3 practical sessions over a 4-week period. Sleeping time, time in bed, total sleep time, sleep latency (SL), sleep efficiency (SE), wake after sleep onset, and wake bouts were recorded with an actigraphic device during the 4-week sleep hygiene strategy (baseline) and during 4 weeks after the last intervention (postintervention). RESULTS: At baseline, the overall group reported poor sleep quantity (total sleep time = 6:27 [0:30] min), but sleep quality was considered acceptable (SL = 0:18 [0:08] min and SE = 77.8% [5.8%]). Postintervention, the overall group showed a small improvement in SL (d = -0.23 [-0.42 to -0.04], P = .003) and SE (d = 0.30 [0.03 to 0.57], P = .0004). For individual responses, sleeping time, time in bed, and total sleep time were positively influenced in only 4, 3, and 5 players, respectively. For parameters of sleep quality, SL and SE were positively influenced in a majority of players (n = 7 and 8, respectively). The magnitude of difference between baseline and postintervention was strongly associated with baseline values in SE (r = -.86; P = .0005) and wake after sleep onset (r = -.87; P = .0007). CONCLUSION: A sleep hygiene strategy is efficient to improve sleep quality but not sleep quantity in young rugby union players. The strategy was more efficient in players with lower initial sleep quality and should be implemented prior to a high cumulative fatigue period.

Relationship between Habitual Caffeine Consumption, Attentional Performance, and Individual Alpha Frequency during Total Sleep Deprivation.

(1) Background: Caffeine is a psychostimulant that is well known to mitigate the deleterious effects of sleep debt. Our aim was to assess the effects of acute caffeine intake on cognitive vulnerability and brain activity during total sleep deprivation (TSD), taking into account habitual caffeine consumption. (2) Methods: Thirty-seven subjects were evaluated in a double-blind, crossover, total sleep deprivation protocol with caffeine or placebo treatment. Vigilant attention was evaluated every six hours during TSD using the psychomotor vigilance test (PVT) with EEG recordings. The influence of habitual caffeine consumption was analyzed by categorizing subjects into low, moderate, and high consumers. (3) Results: The PVT reaction time (RT) increased during TSD and was lower in the caffeine condition vs. the placebo condition. The RT was shorter in the low-caffeine consumers compared to moderate and high consumers, regardless of conditions and treatments. The TSD-related increase in EEG power was attenuated by acute caffeine intake independently of habitual caffeine consumption, and the individual alpha frequency (IAF) was lower in the high-consumption group. The IAF was negatively correlated with daytime sleepiness. Moreover, a correlation analysis showed that the higher the daily caffeine consumption, the higher the RT and the lower the IAF. (4) Conclusions: A high level of habitual caffeine consumption decreases attentional performance and alpha frequencies, decreasing tolerance to sleep deprivation.

Relationship between genetic polymorphisms of cytokines and self-reported sleep complaints and habitual caffeine consumption.

Pro-inflammatory cytokines are involved in sleep-wake regulation and are associated with caffeine consumption. This is a cross-sectional study in 1023 active French workers investigating associations between self-reported sleep complaints (>3months) and total sleep time (TST) with nine single-nucleotide-polymorphisms (SNPs) including pro-inflammatory cytokines, according to caffeine consumption. Participants were characterized as low, moderate and high (0-50, 51-300, and >300 mg/day) caffeine consumers. After adjusting the odd ratios (OR) for age, gender, and smoking, the risk of sleep complaints was higher in subjects with genetic mutations in tumor necrosis factor alpha (TNF-α, rs 1800629) (ORa [95%CI] = 1.43 [1.07-1.92] for both G/A and A/A aggregate genotypes) or interleukin-1 beta (IL-1ß, rs1143627) (ORa = 1.61 [1.08-2.44] for homozygous A/A genotype), and the risk was higher when subjects carry the mutations in TNF-α plus IL-1ß regardless of caffeine consumption. When stratified with caffeine consumption, the risk of sleep complaints was higher in TNF-α A allele carriers in high caffeine consumers, and in homozygous A/A genotype of IL-1ß in moderate and high consumers. None of the nine SNPs influence TST, with the exception of the mutation on CYP1A2 and only when stratified with caffeine consumption. Our results also indicated more caffeine side-effects when carrying mutation on IL1ß. This study showed that polymorphisms in TNF-α and/or IL-1ß influenced sleep complaints but did not influence total sleep time. This suggests that management of sleep complaints, which can be addressed by clinical interventions, should consider the influence of the genetic profile of pro-inflammatory cytokines.

Sleep loss effects on physiological and cognitive responses to systemic environmental hypoxia.

In the course of their missions or training, alpinists, but also mountain combat forces and mountain security services, professional miners, aircrew, aircraft and glider pilots and helicopter crews are regularly exposed to altitude without oxygen supplementation. At altitude, humans are exposed to systemic environmental hypoxia induced by the decrease in barometric pressure (<1,013 hPa) which decreases the inspired partial pressure of oxygen (PIO2), while the oxygen fraction is constant (equal to approximately 20.9%). Effects of altitude on humans occur gradually and depend on the duration of exposure and the altitude level. From 1,500 m altitude (response threshold), several adaptive responses offset the effects of hypoxia, involving the respiratory and the cardiovascular systems, and the oxygen transport capacity of the blood. Fatigue and cognitive and sensory disorders are usually observed from 2,500 m (threshold of prolonged hypoxia). Above 3,500 m (the threshold for disorders), the effects are not completely compensated and maladaptive responses occur and individuals develop altitude headache or acute altitude illness [Acute Mountain Sickness (AMS)]. The magnitude of effects varies considerably between different physiological systems and exhibits significant inter-individual variability. In addition to comorbidities, the factors of vulnerability are still little known. They can be constitutive (genetic) or circumstantial (sleep deprivation, fatigue, speed of ascent.). In particular, sleep loss, a condition that is often encountered in real-life settings, could have an impact on the physiological and cognitive responses to hypoxia. In this review, we report the current state of knowledge on the impact of sleep loss on responses to environmental hypoxia in humans, with the aim of identifying possible consequences for AMS risk and cognition, as well as the value of behavioral and non-pharmacological countermeasures.

The HMOX2 polymorphism contributes to the carotid body chemoreflex in European sea-level residents by regulating hypoxic ventilatory responses.

This study investigates whether a functional single nucleotide polymorphism of HMOX2 (heme oxygenase-2) (rs4786504 T>C) is involved in individual chemosensitivity to acute hypoxia, as assessed by ventilatory responses, in European individuals. These responses were obtained at rest and during submaximal exercise, using a standardized and validated protocol for exposure to acute normobaric hypoxia. Carriers of the ancestral T allele (n = 44) have significantly lower resting and exercise hypoxic ventilatory responses than C/C homozygous carriers (n = 40). In the literature, a hypoxic ventilatory response threshold to exercise has been identified as an independent predictor of severe high altitude-illness (SHAI). Our study shows that carriers of the T allele have a higher risk of SHAI than carriers of the mutated C/C genotype. Secondarily, we were also interested in COMT (rs4680 G > A) polymorphism, which may be indirectly involved in the chemoreflex response through modulation of autonomic nervous system activity. Significant differences are present between COMT genotypes for oxygen saturation and ventilatory responses to hypoxia at rest. In conclusion, this study adds information on genetic factors involved in individual vulnerability to acute hypoxia and supports the critical role of the ≪ O2 sensor ≫ - heme oxygenase-2 - in the chemosensitivity of carotid bodies in Humans.

Immune disruptions and night shift work in hospital healthcare professionals: The intricate effects of social jet-lag and sleep debt.

Objectives: We aimed to examine the effects of circadian and sleep rhythm disruptions on immune biomarkers among hospital healthcare professionals working night shifts and rotating day shifts. Methods: Hospital nurses working either as permanent night shifters (n=95) or as day shifters rotating between morning and afternoon shifts (n=96) kept a daily diary on their sleep and work schedules over a full working week. Blood samples were collected at the beginning and end of the last shift during the week, and participants were categorized into three groups based on work shift: morning shift (39 day shifters sampled at 7:00 and 14:00), afternoon shift (57 day shifters sampled at 14:00 and 21:00), and night shift (95 night shifters sampled at 21:00 and 7:00). Circulating blood counts in immune cells, interleukin-6 and C-reactive protein concentrations as well as total sleep time per 24 hours during work days (TST24w) and free days (TST24f), sleep debt (TST24f - TST24w) and social jet-lag (a behavioral proxy of circadian misalignment) were assessed. Results: Compared with day shifters, night shifters had shorter sleep duration (TST24w=5.4 ± 1.4h), greater sleep debt (3.2 ± 1.4 h) and social jet-lag (6.7 ± 2.4 h). Variations of immune biomarkers concentrations were consistent with the expected diurnal variations among day shifters (i.e., low level in the morning, increase during the day, peak value in the evening). By contrast, in night shifters, blood concentrations of total lymphocytes, T-helper cells, cytotoxic T-cells, memory B-cells and interleukin-6 were lower at 21:00, increased during the night, and reached higher values at 7:00. Multivariate analyses ruled out significant impact of TST24w, sleep debt, and social jet-lag on immune biomarkers concentrations among day shifters. In contrast, among night shifters, multivariate analyses indicated a combined effect of total sleep time (TST24w), sleep debt and social jet-lag for total lymphocytes and T-helper cells but only a social jet-lag effect for interleukin-6 and a single total sleep time effect for neutrophil and B-Cells. Conclusions: Altogether, our results point to intricate response patterns of immune rhythms to circadian misalignment and sleep debt in night shifters. Specifically, these altered pattern expressions of immune cells may increase vulnerability to infections and reduce vaccination efficiency in night workers.

Impact of tapering and proactive recovery on young elite rugby union players' repeated high intensity effort ability.

To assess the effects of a taper combined with proactive recovery on the repeated high intensity effort (RHIE) of elite rugby union players, and the possible interaction of pre-taper fatigue and sleep. Eighteen players performed a 3-week intensive training block followed by a 7-day exponential taper combined with a multicomponent recovery strategy. Following the intervention, players were divided into 3 groups (Normal Training: NT, Acute Fatigue: AF or Functional Overreaching: F-OR) based on their readiness to perform prior to the taper. Total sprint time [TST], percentage decrement [%D] and the number of sprints ≥90% of the best [N90] were analyzed to assess performance during a RHIE test. Subjective sleep quality was assessed through the Pittsburg Sleep Quality Index (PSQI) and the Epworth Sleepiness Scale (ESS). No improvement in TST was reported in either NT or F-OR after the taper, whereas AF tended to improve (-1.58 ± 1.95%; p > 0.05; g = -0.20). F-OR players reported baseline PSQI and ESS indicative of sleep disturbance (6.2 ± 2.2 and 10.6 ± 5.4, respectively). AF displayed a small impairment in PSQI during intensive training (11.5 ± 80.6%; p > 0.05; g = 0.20), which was reversed following the taper (-34.6 ± 62.1%; p > 0.05; g = -0.73). Pre-taper fatigue precluded the expected performance benefits of the combined taper and recovery intervention, likely associated with a lack of strictly controlled intensive training block. Poor sleep quality before the intensive training period appeared to predispose the players to developing functional overreaching.

The impact of 16-h heat exposure on appetite and food reward in adults.

Heat exposure is thought to reduce energy intake (EI) but studies are sparse and results not always concordant. The aim of this study was to examine whether a 16-h exposure to 32 °C leads to reduced EI compared to a control session (22 °C) and whether modifications in appetite sensations or food reward are implied. Sixteen healthy, lean, and active participants (9 women and 7 men, 25 ± 5 yo, body mass index: 22.0 ± 2.4 kg m-2) were passively exposed to two different thermal temperatures from 4:00 p.m. to 8:00 a.m. under controlled conditions. Hunger and thirst scores were regularly assessed using visual analogue scales. A fixed dinner meal (3670 ± 255 kJ) was consumed at 7:30 p.m. and an ad libitum breakfast buffet (20 foods/drinks varying in temperature, fat, and carbohydrate content) at 7:30 a.m. Components of reward (explicit liking [EL] and implicit wanting [EI]) for fat and sweet properties of food were assessed before each meal using the Leeds Food Preference Questionnaire (LFPQ). Ad libitum EI at breakfast did not differ between sessions (2319 ± 1108 vs 2329 ± 1141 kJ, in 22 and 32 °C sessions, respectively; p = 0.955). While thirst scores were higher in the 32 than the 22 °C session (p < 0.001), hunger scores did not differ (p = 0.580). EL and IW for high fat foods relative to low fat foods were decreased in 32 compared to 22 °C before dinner and breakfast (p < 0.001 for all). Although EI and hunger were not affected by a 16-h exposure to heat, modifications in food reward suggested a reduction in the preference of high-fat foods. Future research should investigate whether reduced EI in response to heat exposure is due to spontaneous selection of low-fat foods rather than altered appetite sensations.

Effects of Caffeine Intake on Cognitive Performance Related to Total Sleep Deprivation and Time on Task: A Randomized Cross-Over Double-Blind Study.

Introduction: It is widely admitted that both total sleep deprivation (TSD) and extended task engagement (Time-On-Task, TOT) induce a cognitive fatigue state in healthy subjects. Even if EEG theta activity and adenosine both increase with cognitive fatigue, it remains unclear if these modifications are common mechanisms for both sustained attention and executive processes. Methods: We performed a double-blind counter-balanced (placebo (PCBO) and caffeine (CAF) - 2×2.5 mg/kg/24 h)) study on 24 healthy subjects (33.7 ± 5.9 y). Subjects participated in an experimental protocol including an habituation/training day followed by a baseline day (D0 and D1) and a total sleep deprivation (TSD) day beginning on D1 at 23:00 until D2 at 21:00. Subjects performed the psychomotor vigilance test (PVT) assessing sustained attention, followed by the executive Go-NoGo inhibition task and the 2-NBack working memory task at 09:15 on D1 and D2. Results: We showed differential contributions of TSD and TOT on deficits in sustained attention and both executive processes. An alleviating effect of caffeine intake is only observed on sustained attention deficits related to TSD and not at all on TOT effect. The caffeine dose slows down the triggering of sustained attention deficits related to TOT effect. Discussion: These results suggest that sustained attention deficits induced by TSD rely on the adenosinergic mechanism whereas TOT effect observed for both sustained attention and executive would not.

Strategies to Limit Cognitive Impairments under Sleep Restriction: Relationship to Stress Biomarkers.

Adding relaxation techniques during nap or auditory stimulation of EEG slow oscillation (SO) during nighttime sleep may limit cognitive impairments in sleep-deprived subjects, potentially through alleviating stress-releasing effects. We compared daytime sleepiness, cognitive performances, and salivary stress biomarker responses in 11 volunteers (aged 18-36) who underwent 5 days of sleep restriction (SR, 3 h per night, with 30 min of daily nap) under three successive conditions: control (SR-CT), relaxation techniques added to daily nap (SR-RT), and auditory stimulation of sleep slow oscillations (SO) during nighttime sleep (SR-NS). Test evaluation was performed at baseline (BASE), the fifth day of chronic SR (SR5), and the third and fifth days after sleep recovery (REC3, REC5, respectively). At SR5, less degradation was observed for percentage of commission errors in the executive Go-noGo inhibition task in SR-RT condition compared to SR-CT, and for sleepiness score in SR-NS condition compared both to SR-CT and SR-RT. Beneficial effects of SR-RT and SR-NS were additionally observed on these two parameters and on salivary α-amylase (sAA) at REC3 and REC5. Adding relaxation techniques to naps may help performance in inhibition response, and adding nocturnal auditory stimulation of SO sleep may benefit daytime sleepiness during sleep restriction with persistent effects during recovery. The two strategies activated the autonomic nervous system, as shown by the sAA response.

Order matters: sleep spindles contribute to memory consolidation only when followed by rapid-eye-movement sleep.

Sleep is known to benefit memory consolidation, but little is known about the contribution of sleep stages within the sleep cycle. The sequential hypothesis proposes that memories are first replayed during nonrapid-eye-movement (NREM or N) sleep and then integrated into existing networks during rapid-eye-movement (REM or R) sleep, two successive critical steps for memory consolidation. However, it lacks experimental evidence as N always precedes R sleep in physiological conditions. We tested this sequential hypothesis in patients with central hypersomnolence disorder, including patients with narcolepsy who present the unique, anti-physiological peculiarity of frequently falling asleep in R sleep before entering N sleep. Patients performed a visual perceptual learning task before and after daytime naps stopped after one sleep cycle, starting in N or R sleep and followed by the other stage (i.e. N-R vs. R-N sleep sequence). We compared over-nap changes in performance, reflecting memory consolidation, depending on the sleep sequence during the nap. Thirty-six patients who slept for a total of 67 naps were included in the analysis. Results show that sleep spindles are associated with memory consolidation only when N is followed by R sleep, that is in physiologically ordered N-R naps, thus providing support to the sequential hypothesis in humans. In addition, we found a negative effect of rapid-eye-movements in R sleep on perceptual consolidation, highlighting the complex role of sleep stages in the balance to remember and to forget.

Sleep and COVID-19. A Case Report of a Mild COVID-19 Patient Monitored by Consumer-Targeted Sleep Wearables.

Since its first description in Wuhan, China, the novel Coronavirus (SARS-CoV-2) has spread rapidly around the world. The management of this major pandemic requires a close coordination between clinicians, scientists, and public health services in order to detect and promptly treat patients needing intensive care. The development of consumer wearable monitoring devices offers physicians new opportunities for the continuous monitoring of patients at home. This clinical case presents an original description of 55 days of SARS-CoV-2-induced physiological changes in a patient who routinely uses sleep-monitoring devices. We observed that sleep was specifically affected during COVID-19 (Total Sleep time, TST, and Wake after sleep onset, WASO), within a seemingly bidirectional manner. Sleep status prior to infection (e.g., chronic sleep deprivation or sleep disorders) may affect disease progression, and sleep could be considered as a biomarker of interest for monitoring COVID-19 progression. The use of habitual data represents an opportunity to evaluate pathologic states and improve clinical care.

Sleep and PTSD in the Military Forces: A Reciprocal Relationship and a Psychiatric Approach.

Sleep disturbances are well-recognised symptoms of Post-Traumatic Stress Disorder (PTSD). This review updates knowledge regarding the relationship between sleep during deployment, combat-related trauma, and PTSD in military personnel, from which the importance of restorative sleep results. The description of the characteristics of sleep in military forces with the considerable roles of the operational and training contexts highlights the important consequences of degraded sleep. Indeed, a lot of data suggest a dynamic link between sleep and the onset and chronicity of PTSD. We propose a reciprocal relationship model with strategies strongly recommended or already adopted by the military to promote restorative sleep before and after combat exposure. Among the alterations in a variety of sleep architecture and sleep patterns described in PTSD, the physiological hypothesis of REM sleep fragmentation in the development of PTSD symptoms may be important because REM sleep is generally associated with emotional memory. Finally, we address clinical and research perspectives that could be used to detect or restore sleep continuity before and during military deployment to possibly alleviate nightmares and insomnia related to combat exposure and PTSD occurrence and improve our understanding of sleep in PTSD.

Genetics and Cognitive Vulnerability to Sleep Deprivation in Healthy Subjects: Interaction of ADORA2A, TNF-α and COMT Polymorphisms.

Several genetic polymorphisms differentiate between healthy individuals who are more cognitively vulnerable or resistant during total sleep deprivation (TSD). Common metrics of cognitive functioning for classifying vulnerable and resilient individuals include the Psychomotor Vigilance Test (PVT), Go/noGo executive inhibition task, and subjective daytime sleepiness. We evaluated the influence of 14 single-nucleotide polymorphisms (SNPs) on cognitive responses during total sleep deprivation (continuous wakefulness for 38 h) in 47 healthy subjects (age 37.0 ± 1.1 years). SNPs selected after a literature review included SNPs of the adenosine-A2A receptor gene (including the most studied rs5751876), pro-inflammatory cytokines (TNF-α, IL1-ß, IL-6), catechol-O-methyl-transferase (COMT), and PER3. Subjects performed a psychomotor vigilance test (PVT) and a Go/noGo-inhibition task, and completed the Karolinska Sleepiness Scale (KSS) every 6 h during TSD. For PVT lapses (reaction time >500 ms), an interaction between SNP and SDT (p < 0.05) was observed for ADORA2A (rs5751862 and rs2236624) and TNF-α (rs1800629). During TSD, carriers of the A allele for ADORA2A (rs5751862) and TNF-α were significantly more impaired for cognitive responses than their respective ancestral G/G genotypes. Carriers of the ancestral G/G genotype of ADORA2A rs5751862 were found to be very similar to the most resilient subjects for PVT lapses and Go/noGo commission errors. Carriers of the ancestral G/G genotype of COMT were close to the most vulnerable subjects. ADORA2A (rs5751862) was significantly associated with COMT (rs4680) (p = 0.001). In conclusion, we show that genetic polymorphisms in ADORA2A (rs5751862), TNF-α (rs1800629), and COMT (rs4680) are involved in creating profiles of high vulnerability or high resilience to sleep deprivation. (NCT03859882).

Impact of total sleep deprivation and related mood changes on approach-avoidance decisions to threat-related facial displays.

STUDY OBJECTIVES: Total sleep deprivation is known to have significant detrimental effects on cognitive and socio-emotional functioning. Nonetheless, the mechanisms by which total sleep loss disturbs decision-making in social contexts are poorly understood. Here, we investigated the impact of total sleep deprivation on approach/avoidance decisions when faced with threatening individuals, as well as the potential moderating role of sleep-related mood changes. METHODS: Participants (n = 34) made spontaneous approach/avoidance decisions in the presence of task-irrelevant angry or fearful individuals, while rested or totally sleep deprived (27 h of continuous wakefulness). Sleep-related changes in mood and sustained attention were assessed using the Positive and Negative Affective Scale and the psychomotor vigilance task, respectively. RESULTS: Rested participants avoided both fearful and angry individuals, with stronger avoidance for angry individuals, in line with previous results. On the contrary, totally sleep deprived participants favored neither approach nor avoidance of fearful individuals, while they still comparably avoided angry individuals. Drift-diffusion models showed that this effect was accounted for by the fact that total sleep deprivation reduced value-based evidence accumulation toward avoidance during decision making. Finally, the reduction of positive mood after total sleep deprivation positively correlated with the reduction of fearful display avoidance. Importantly, this correlation was not mediated by a sleep-related reduction in sustained attention. CONCLUSIONS: All together, these findings support the underestimated role of positive mood-state alterations caused by total sleep loss on approach/avoidance decisions when facing ambiguous socio-emotional displays, such as fear.