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.

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.

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.

Determination of the sleep-wake pattern and feasibility of NREM/REM discrimination using the non-invasive piezoelectric system in rats.

The piezoelectric cage-floor sensors have been used to successfully dissect sleep patterns in mice based on signal features related to respiration and body movements. We studied performance of the piezoelectric system to quantify the sleep-wake pattern in the rat over 7 days of recording compared with a visual electroencephalogram/electromyogram scoring, and under two light/dark (LD12:12 and LD16:8) photoperiods leading to change in the 24-hr sleep characteristics (N = 7 per group). The total sleep time (%/24 hr) over the 7 days recording and hourly sleep time over the last 24-hr recording were not statistically different between methods under the two photoperiods. Both methods detected higher total sleep time with the LD16:8 photoperiod compared with LD12:12 (p < .05), and correlated significantly (p < .001) at light and dark periods during each photoperiod. The accuracies for discrimination of sleep-wake patterns between methods were 81.9% and 84.9% for LD12:12 and LD16:8, respectively. In addition, spectral analysis of the respiratory signal given by piezo during all 10-s periods of the corresponding non-rapid eye movement and rapid eye movement sleep periods recorded by electroencephalogram/electromyogram resulted in selection of 36 features that could be inserted in an automated non-rapid eye movement sleep and rapid eye movement sleep classification, with 90% accuracy with the electroencephalogram/electromyogram visual scoring. The piezo system proved to be a reliable non-invasive alternative to electroencephalogram recording to study total sleep time in rat, with feasibility to discriminate between non-rapid eye movement and rapid eye movement sleep stages. This will be interesting in pharmacological or bio-behavioural studies evaluating sleep patterns or the restorative functions of sleep in the body and the brain.

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.

Lengthening of the photoperiod influences sleep characteristics before and during total sleep deprivation in rat.

The photoperiod has been evidenced to influence sleep regulation in the rat. Nevertheless, lengthening of the photoperiod beyond 30 days seems to have little effect on the 24-hr baseline level of sleep and the response to total sleep deprivation. We studied the effects of 12:12 (habitual) and 16:8 (long) light-dark photoperiods on sleep, locomotor activity and body core temperature, before and after 24 hr of total sleep deprivation. Eight rats were submitted for 14 days to light-dark 12:12 (lights on: 08:00 hours-20:00 hours) followed by total sleep deprivation, and then for 14 days to light-dark 16:8 (light extended to 24:00 hours) followed by total sleep deprivation. Rats were simultaneously recorded for electroencephalogram, locomotor activity and body core temperature for 24 hr before and after total sleep deprivation. At baseline before total sleep deprivation, total sleep time and non-rapid eye movement sleep per 24 hr and during extended light hours (20:00 hours-24:00 hours) were higher (13% for total sleep time) after light-dark exposure compared with habitual photoperiod, while percentage delta power in non-rapid eye movements and rapid eye movements were unchanged. Locomotor activity and body core temperature were lower, particularly during extended light hours (20:00 hours-24:00 hours). Following total sleep deprivation, total sleep time and non-rapid eye movements were significantly lower after long photoperiod between 20:00 hours and 24:00 hours, and between 10:00 hours and 12:00 hours, and unchanged per 24 hr. The percentage delta power in non-rapid eye movements was lower between 08:00 hours and 11:00 hours. Total sleep deprivation decreased locomotor activity and body core temperature after habitual photoperiod exposure only. Fourteen days under long photoperiod (light-dark 16:8) increased non-rapid eye movements sleep, and decreased sleep rebound related to total sleep deprivation (lower non-rapid eye movements duration and delta power). This may create a model of sleep extension for the rat that has been found to favour anabolism in the brain and the periphery.

Daytime microsleeps during 7 days of sleep restriction followed by 13 days of sleep recovery in healthy young adults.

We investigated the consequences of sleep restriction (SR) on maintenance of wakefulness capacities and diurnal sleepiness through microsleeps monitoring. 12 healthy males (20-36 years old) were sleep restricted (4 h per night) during 7 nights followed by 13 nights of recovery sleep. Participants completed Karolinska Sleepiness Scale (KSS) and Maintenance of Wakefulness Test (MWT) at baseline (B), during SR (SR1, SR4 and SR7) and during recovery (R3 and R13), while continuously recorded for EEG analysis. During SR, MWT latencies decreased (SR7: -24.4%), whereas the number, the cumulative duration of microsleeps and KSS scores increased. Recovery nights allowed MWT latencies, KSS scores and all sleep values to return to baseline levels, while a rebound in N3, N3% and REM% sleep stages occurred. During SR, the maintenance of N3 sleep duration seems not sufficient to reduce daytime sleepiness and MWT results did not reflect the sleepiness levels characterized by persistent sleep attacks.

Hyperactivity of the Sympatho-Adrenomedullary System Without Any Modification of the Hypothalamic-Pituitary-Adrenal Axis After Food Restriction Among High-Level Weightlifters.

Durguerian, A, Filaire, E, Drogou, C, Sauvet, F, Bougard, C, and Chennaoui, M. Hyperactivity of the sympatho-adrenomedullary system without any modification of the hypothalamic-pituitary-adrenal axis after food restriction among high-level weightlifters. J Strength Cond Res 32(6): 1643-1655, 2018-We examined the effects of 6 days of food restriction on salivary α-amylase (sAA), cortisol and dehydroepiandrostenedione (DHEA) awakening responses, psychological parameters and performance among 11 international weightlifters. Assessments were made at baseline (T1) and 6 days after a normal period of training while maintaining body weight (T2). Then, participants were assigned to 2 groups depending on whether they lost (Diet group) or maintained (Control group) their body mass. Anthropometric, psychological, physical, and physiological assessments were also realized 6 days (T3) after the restricted dietary period for the Diet group. Food restriction (T3) induced a significant rise of sAA awakening response (364.6%, p ≤ 0.05), whereas no significant variations were observed among the hypothalamic-pituitary-adrenal axis (cortisol and DHEA). Significant alterations of the general Recovery Score and General stress Score, evaluated through the Recovery-Stress Questionnaire for athletes, were noted after food restriction. Weightlifting performance, evaluated during a simulated weightlifting competition, was maintained after the 6-day food restriction; we even noted an increased weightlifting performance related to body mass (Sinclair coefficient). Our findings support the hypothesis that food restriction induces a challenging situation to the organism, resulting in an asymmetry between the 2 stress systems activation. These results reinforce the necessity to cautiously plan and monitor the weight regulation process before competition to avoid potential negative outcomes on psychophysiological parameters. In this regard, the psychobiological approach, especially the awakening responses, seems a useful tool.

The homeostatic and circadian sleep recovery responses after total sleep deprivation in mice.

Many studies on sleep deprivation effects lack data regarding the recovery period. We investigated the 2-day homeostatic and circadian sleep recovery response to 24 h of total sleep deprivation (TSD) induced by brief rotation of an activity wheel. Eight mice were implanted with telemetry transmitters (DSI F40-EET) that recorded simultaneously their electroencephalography (EEG), locomotor activity and temperature during 24 h of baseline (BSL), TSD and 2 days of recovery (D1 and D2). In a second experiment, two groups of five non-implanted mice underwent TSD or ad libitum sleep, after which they were killed, adrenal glands were weighed and blood was collected for analysis of corticosterone concentration. During TSD mice were awake at least 97% of the time, with a consecutive sleep rebound during D1 that persisted during D2. This was characterized by increases of non-rapid eye movement (NREM) sleep (44.2 ± 6.9% for D1 and 43.0 ± 7.7% for D2 versus 33.8 ± 9.2% for BSL) and the relative delta band power (179.2 ± 34.4% for D1 and 81.9 ± 11.2% for D2). Greater NREM and REM sleep amounts were observed during the 'light' periods. Temperature and locomotor activity characteristics were unchanged during D1 and D2 versus BSL. In non-implanted mice, corticosterone levels as well as adrenal gland and overall body weights did not differ between TSD and ad libitum sleep groups. In conclusion, 24 h of TSD in an activity wheel without stress responses influence homeostatic sleep regulation with no effect on the circadian regulation over at least 2 days of recovery in mice.

Changes of Cerebral and/or Peripheral Adenosine A1 Receptor and IGF-I Concentrations under Extended Sleep Duration in Rats.

Extended sleep improves sustained attention and reduces sleep pressure in humans. Downregulation of adenosine A1 receptor (A1R) and modulation of the neurotrophic factor insulin growth factor-1 (IGF-I) in brain structures controlling attentional capacities could be involved. In the frontal cortex and hippocampus of rats, we measured adenosine A1R and IGF-I protein concentrations after photoperiod-induced sleep extension. Two groups of twelve rats were adapted over 14 days to a habitual (CON) 12:12 light-dark (LD) schedule and an extended (EXT) 16:8 LD schedule. IGF-I content was also measured in plasma, liver, and skeletal muscle. In EXT, compared to CON rats, A1R content in the frontal cortex was significantly lower (p < 0.05), while IGF-I content was higher (p < 0.001), and no significant change was observed in the hippocampus. IGF-I content in plasma and muscle was higher (p < 0.001 and p < 0.01), while it was lower in liver (p < 0.001). The absolute weight and weight gain were higher in EXT rats (p < 0.01). These data suggest that 14 days under a 16:8 LD photoperiod respectively down- and upregulated cortical A1R and IGF-I levels. This photoperiod induced an anabolic profile with increased weight gain and circulating and muscular IGF-I levels. An extension of sleep duration might favor cerebral and peripheral anabolism, which may help attentional and physical capacities.

Efficacy of THN102 (a combination of modafinil and flecainide) on vigilance and cognition during 40-hour total sleep deprivation in healthy subjects: Glial connexins as a therapeutic target.

AIMS: THN102 is a novel combination of modafinil and low-dose flecainide, targeting glial connexin activity to modulate modafinil effects. We investigated THN102 efficacy compared to modafinil and to placebo on vigilance and cognitive function during 40-hour total sleep deprivation (TSD). METHODS: Twenty healthy men participated in a double-blind, randomized, incomplete-block 3-period cross-over trial with 5 treatments (n = 12 per group): placebo (PBO), modafinil 100 mg (MOD100), THN102 100/1, 100/3, 100/9 (modafinil 100 mg and flecainide 1, 3 or 9 mg). Each period included a baseline day and a TSD day with treatments administered 3 times (01:00, 09:00 and 19:00). Reaction time in psychomotor vigilance test, subjective somnolence and vital signs were assessed before and during treatment. Working memory (2-Back) and executive processes (Go/noGo for vigilance and inhibition, Wisconsin card sorting task for mental flexibility, and Tower of London test for planning) were evaluated at 16:30. RESULTS: At 5 hours postdose−1 (after 23 hours TSD, primary endpoint), THN102 100/1 resulted in statistically higher psychomotor vigilance test speed vs MOD100 (3.97 ± 0.09 vs 3.74 ± 0.14, P < .05). No increase in effect was observed with higher flecainide doses in combinations. Most THN102 doses vs MOD100 also improved the number of correct responses in 2-Back and Go errors in Go/noGo (P < .05 for all doses), and perseverative responses in Wisconsin card sorting task (for 100/1 and 100/9). No impact on cardiac conduction was noted with THN102, and safety was similar to MOD100. CONCLUSIONS: THN102 seems more efficient than modafinil on vigilance, working memory and executive functions, opening new perspectives in management of hypersomnolence disorders.

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 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.

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).

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.

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.

Effects of 29-h total sleep deprivation on local cold tolerance in humans.

To study the effects of a 29-h total sleep deprivation (TSD) on local cold tolerance, 10 healthy men immersed their right hand for 30 min in a 5°C water bath (CWI) after a 30-min rest period in a thermoneutral environment (Control), after a normal night (NN) and after a 29-h TSD. CWI was followed by a 30-min passive rewarming (Recovery). Finger 2 and 4 skin temperatures (Tfi2, Tfi4) and finger 2 cutaneous vascular conductance (CVC) were monitored to study cold-induced vasodilation (CIVD). Rectal temperature (Tre), mean skin temperature ([Formula: see text]), heart rate (HR) and blood pressure (BP) were also measured. Blood samples were collected at the end of the Control, at the lower and at the first maximal Tfi2 values during CWI and at Recovery. Tfi2, Tfi4 and CVC did not differ after TSD at Control, whereas they were reduced during CWI (-2.6 ± 0.7°C for Tfi2; -2 ± 0.8°C for Tfi4, -79 ± 25% for relative CVC, P < 0.05) as during Recovery (-4.9 ± 1.9°C for Tfi2, -2.6 ± 1.8°C for Tfi4, -70 ± 22% for relative CVC, P < 0.05). After TSD, the lower CVC values appeared earlier during CWI (-59 ± 19.6 s, P < 0.05). After TSD at Control and CWI, plasma endothelin levels were higher and negatively correlated with Tfi2, Tfi4 and CVC. However, no effect of TSD was found on the number and amplitude of CIVD and in Tre, HR, BP and catecholamines, for all periods. We concluded that TSD induced thermal and vascular changes in the hand which impair the local cold tolerance, suggesting that TSD increases the risk of local cold injuries.

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.

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.