IntroductionSleep deprivation is known to induce cardiovascular responses. Several studies have shown the beneficial effect of caffeine on neurobehavioral performance during sleep deprivation, but less is known about its influence on the cardiovascular and inflammatory responses associated with sleep deprivation. The aim of this study is to evaluate the impact of acute caffeine intake on (1) peripheral blood pressures, and (2) heart rate, and cutaneous vascular conductance (CVC) and related biomarkers of endothelial activation, during total sleep deprivation (TSD), considering habitual caffeine consumption.Methods41 subjects followed a randomized, placebo-controlled, cross-over study and underwent 2 conditions of TSD (38 h), one with caffeine intake at 09:00 and 14:00 (2.5 mg/kg), and the other with placebo intake.ResultsWe confirm that TSD increases systolic and diastolic arterial pressures (p = 0.001 and p = 0.002 for main effects respectively) and heart rate (p = 0.001), and decreases endothelium-dependent and -independent CVC (p = 0.001). Acute caffeine intake inflates the increase in arterial pressures and IL-6 levels, while it does not affect CVC and levels of E-selectin and monocyte chemotaxis protein-1 (MCP-1). Moreover, chronic caffeine consumption had significant main effects on systolic arterial pressure (p = 0.03), heart rate (p = 0.02), IL-6 levels (p = 0.02), and acetylcholine (ACh)-induced CVC (p = 0.02), and interacted with TSD on E-selectin levels and ACh-induced CVC (p = 0.02 respectively).ConclusionAcute caffeine intake provokes immuno-inflammatory and cardiovascular responses, and chronic caffeine consumption should be limited to the lowest efficient doses.Clinical Trial Registrationhttps://clinicaltrials.gov/study/NCT03859882, identifier NCT03859882.

Background and Objective Aircraft pilots can be faced with a high mental workload (MW) combined with moderate hypoxia and sleep restriction. We aimed to assess the cross-validation of a machine learning-based MW predictive model under hypoxia and/or sleep restriction. Secondly, we developed a robust predictive model using multimodal physiological parameters to improve the validity across different physiological conditions. Methods Seventeen healthy participants were randomly exposed to three 12-minute periods of increased MW (low, medium, and high) in a 4-condition crossover design: sleep restriction (SR, <3h Total Sleep Time, TST) vs. habitual sleep (HS, >6h TST), hypoxia (HY, 2h, FIO2=13.6%, ∼3,500 m) vs. normoxia (NO, FIO2=21%). MW levels were designed using the Multi-Attribute Test Battery (MATB)-II with an additional auditory Oddball-like task. Six machine learning classifiers were compared. Features selection (from EEG, ECG, respiratory and eye tracking sensors) was performed using backward Recursive Feature Elimination (RFE). Results The best models for 1-minute MW levels classification on HSNO were K-Nearest Neighbors (KNN, F1 score = 80.3±8.9%), Support Vector Machine (SVM, 77.8±10.3%) and Random Forest (RF, 75.7±9.1%). Exposure to sleep restriction and/or hypoxia decreased models’ performance (F1 <35%). KNN and RF models, in particular those including EEG and eye tracking, trained on All-Conditions performed well across conditions (F1 scores = 77.4±7.8% and 70.7±10.2%). Conclusion Our results highlight the need for training MW models under different physiological constraints and using multimodal datasets to improve robustness. (NCT05563688)

Background: Exercise duration at maximum oxygen uptake (V˙O2max) appears to be influenced not only by metabolic factors but also by the interplay between brain dynamics and ventilatory regulation. This study examined how cortical activity, assessed via electroencephalography (EEG), relates to performance and acute fatigue regulation during a constant-load cycling test. We hypothesized that oscillatory activity in the theta, alpha, and beta bands would be associated with ventilatory coordination and endurance capacity. Methods: Thirty trained participants performed a cycling test to exhaustion at 90% maximal aerobic power. EEG and gas exchange were continuously recorded; ratings of perceived exertion were assessed immediately after exhaustion. Results: Beta power was negatively correlated with time spent at V˙O2max (r = −0.542, p = 0.002). Theta and Alpha power alone showed no direct associations with endurance, but EEG–metabolic ratios revealed significant correlations. Specifically, the time to reach V˙O2max correlated with Alpha/V˙O2 (p < 0.001), Alpha/V˙CO2 (p < 0.001), and Beta/V˙CO2 (p = 0.002). The time spent at V˙O2max correlated with Theta/V˙O2 (p = 0.002) and Theta/V˙CO2 (p < 0.001). The time-to-exhaustion was correlated with Theta/V˙CO2 (p < 0.001) and Alpha/V˙CO2 (p < 0.001). Conclusions: These findings indicate that cortical oscillations were associated with different aspects of acute fatigue regulation. Beta activity was associated with fatigue-related neural strain, whereas Theta and Alpha bands, when normalized to metabolic load, were consistent with a role in ventilatory coordination and motor control. EEG–metabolic ratios may provide exploratory indicators of brain–metabolism interplay during high-intensity exercise and could help guide future brain-body interactions in endurance performance.

Sleep disturbances, including insomnia and trauma‐related nightmares (TRNs), are the core symptoms of post‐traumatic stress disorder (PTSD) in military personnel. Furthermore these nocturnal manifestations are directly related to the persistence of daytime PTSD symptoms and are known to exacerbate comorbid conditions such as depression, suicidality, and daytime impairments. This prospective study examined the variability of PTSD‐related sleep disruptions and its relationship to symptom severity using ecological recordings over several nights. One hundred thirty PTSD‐diagnosed service members and 65 healthy military controls recorded sleep data at home for five nights using a polysomnographic headband to measure total sleep time (TST), sleep onset latency (SOL), wake after sleep onset (WASO), sleep efficiency index (SEI), and sleep stages. PTSD severity and comorbid symptoms were assessed by clinical evaluations. Compared to controls, PTSD participants had higher SOL and WASO (+14.1 min and +9.1 min, p < 0.001, respectively), reduced SEI (−6.6%, p < 0.001), and lower N3 and rapid eye movement (REM) sleep durations. In addition, night‐to‐night variability (NNV) in SOL and WASO was higher in the PTSD group. The sleep fragmentation index (FI)—and more specifically non‐REM (NREM) sleep fragmentation—was significantly correlated with PTSD severity, particularly the intrusive and avoidance symptoms clusters in the PCL‐5 score. The results highlight the need for customized multinight assessments to study sleep variability in military patients with combat‐related PTSD, in order to advance therapeutic strategies for military populations. Trial Registration: ClinicalTrials.gov Identifier: NCT04581850

Total sleep deprivation (TSD) alters local cold tolerance and could thus increase the risk of cold injury. We evaluated the impact of acute caffeine intake, the main countermeasure to TSD-related deleterious effects, on local cold tolerance before and after TSD. Thirty-six healthy subjects underwent two TSD protocols (i.e., continuous wakefulness), with randomized crossover intake of acute caffeine or placebo (2.5 mg/kg) administered twice during wakefulness. Before and after 33 h of TSD, finger (index and annular) temperature and skin blood flow were assessed during cold-water immersion (CWI, 5°C, 20 min) followed by 20 min of rewarming in ambient air. We showed no significant effects of TSD on mean finger temperature during CWI in the placebo condition, but a significant reduction of the minimal temperature (8.86°C ± 0.35°C vs. 8.64°C ± 0.27°C, p = 0.02). During rewarming, we showed a reduction in temperature in the placebo condition (p = 0.02 for the mean temperature and p = 0.03 for the maximal) and an increase in the skin blood flow disparity between fingers at the four points of laser speckle rewarming measurements (p = 0.03). After TSD, acute caffeine intake (vs. placebo) increased mean (+2.11°C ± 0.21°C, p = 0.01) and minimal (+0.61°C ± 0.10°C, p = 0.02) finger temperatures during CWI, and improved rewarming after CWI (mean and maximal temperatures) (+2.28°C ± 0.08°C, p = 0.01, and +2.06°C ± 0.12°C, p = 0.02, respectively). Before TSD, acute caffeine intake significantly increased (vs. placebo) mean temperatures during CWI (p = 0.03) and reduced pain from the onset (p = 0.03) to the end of CWI (p = 0.02) and the first 2 min of rewarming (p = 0.04). There was also a significant main effect of habitual daily caffeine consumption on minimal finger temperatures during CWI, which decreased significantly between 0 and 600 mg consumption (R2 = -0.43, p = 0.01), independently of the effects of day (before and after TSD) and treatment (caffeine and placebo conditions). These findings suggest that acute caffeine intake could be a protective countermeasure to local cold tolerance, particularly during TSD. However, habitual daily caffeine consumption is a factor of individual variability that should be recorded during CWI protocols. Clinical trial NCT03859882.

Environmental high temperatures can strongly affect sleep. Our aim was to assess the protective effect of a High Heat Conductivity Mattress topper (HHCM) on sleep duration and quality during one night's exposure to heat. HHCM efficacy was studied in a randomised double-blind crossover design in fifteen healthy young active subjects by overnight polysomnography in a temperature-controlled sleep laboratory, during 4 nights: 2 nights at 22°C (HHCM and Control Mattress, CM) and 2 nights at 32°C (HHCM and CM). Core body temperature (CBT), skin, room and mattress toppers surface temperatures were continuously recorded. We observed interactions between temperature and mattress conditions. At 22°C, we did not show any beneficial effect of HHCM compared to CM on sleep duration, but a longer N3 sleep stage duration (p = 0.03) and higher slow oscillation spectral density (p = 0.03). Heat night exposure (32°C) induced a decrease in total sleep time (TST) (-24.8 ± 7.1 min, p = 0.02), rapid eye movement (REM) duration (p = 0.03), sleep efficiency (p = 0.04), delta power spectral density (p = 0.03) and an increase of wake after sleep onset (p = 0.03) and transition between stages rate (p = 0.02). At 32°C, in comparison to CM, HHCM induced higher TST (+21.4 ± 16.1 min, p = 0.04), sleep efficiency (p = 0.04), REM duration (p = 0.03), and lower awakening duration (p = 0.03). These effects were associated with lower skin temperature and CBT. In conclusion, HHCM improves sleep quality and has a protective effect on CBT and sleep patterns during heat exposure in active healthy subjects. It could be a countermeasure for promoting sleep in particular during heat waves.

Background: Exercise duration at maximum oxygen uptake ((V) over dotO(2)max) appears to be influenced not only by metabolic factors but also by the interplay between brain dynamics and ventilatory regulation. This study examined how cortical activity, assessed via electroencephalography (EEG), relates to performance and acute fatigue regulation during a constant-load cycling test. We hypothesized that oscillatory activity in the theta, alpha, and beta bands would be associated with ventilatory coordination and endurance capacity. Methods: Thirty trained participants performed a cycling test to exhaustion at 90% maximal aerobic power. EEG and gas exchange were continuously recorded; ratings of perceived exertion were assessed immediately after exhaustion. Results: Beta power was negatively correlated with time spent at (V) over dotO(2)max (r = -0.542, p = 0.002). Theta and Alpha power alone showed no direct associations with endurance, but EEG-metabolic ratios revealed significant correlations. Specifically, the time to reach (V) over dotO(2)max correlated with Alpha/(V) over dotO(2) (p < 0.001), Alpha/(V) over dotCO(2) (p < 0.001), and Beta/(V) over dotCO(2) (p = 0.002). The time spent at (V) over dotO(2)max correlated with Theta/(V) over dotO(2) (p = 0.002) and Theta/(V) over dotCO(2) (p < 0.001). The time-to-exhaustion was correlated with Theta/(V) over dotCO(2) (p < 0.001) and Alpha/(V) over dotCO(2) (p < 0.001). Conclusions: These findings indicate that cortical oscillations were associated with different aspects of acute fatigue regulation. Beta activity was associated with fatigue-related neural strain, whereas Theta and Alpha bands, when normalized to metabolic load, were consistent with a role in ventilatory coordination and motor control. EEG-metabolic ratios may provide exploratory indicators of brain-metabolism interplay during high-intensity exercise and could help guide future brain-body interactions in endurance performance.

Objectif La dette de sommeil est fréquemment rencontrée en milieu militaire, où les opportunités de récupération sont rares et limitées en durée. Notre objectif est d’identifier des paramètres de la structure du sommeil associés aux différents profils de la récupération attentionnelle à l’issue d’une brève opportunité de récupération, en commençant par l’analyse macrostructurelle. Méthodes Trente-neuf sujets sains ont pris part à une séquence expérimentale de 4 jours. Le jour 1 (j1) correspondait à une journée après une nuit de sommeil de base (BS, 8h de temps au lit), j2 à une journée après une privation totale de sommeil, j3 à une journée après une opportunité limitée de sommeil (R1, 3h de temps au lit) et j4 à une journée après une opportunité de sommeil plus importante (R2, 8h de temps au lit). Les sujets réalisaient une Psychomotor Vigilance Task de 10min toutes les 3 heures entre 08h00 et 21h00. La différence du nombre de lapses (réponses>500ms) entre j3 et j1 a été choisie comme index de récupération. Les sujets étaient séparés en trois terciles sur la base de cet index (résilient vs intermédiaire vs vulnérable). Le sommeil était enregistré par polysomnographie durant chacune des nuits afin d’obtenir les paramètres de la macrostructure (TST, WASO, N1, N2, N3, REM, latence d’endormissement, efficacité du sommeil). Ces paramètres ont été comparés entre les trois groupes. Résultats Les trois groupes étaient comparables pour l’âge, le poids, la taille, le sex-ratio, le temps de sommeil avant l’étude et les paramètres du sommeil pour BS. Un effet jour a été observé sur les performances au PVT (nombre moyen de lapses et vitesse au PVT). Aucun effet groupe n’a été observé pour l’ensemble des paramètres du sommeil pour R1, mais aussi pour R2 (p>0,2 pour tous). Conclusion Ces résultats soulignent le fait que les paramètres de la macrostructure ne permettent pas d’identifier le profil de récupération d’un sujet à l’issue d’une opportunité de sommeil. Une analyse plus précise de la méso- et de la microstructure du sommeil sera ainsi nécessaire pour identifier des marqueurs de la qualité du sommeil au regard de la récupération attentionnelle.

Background: Exercise duration at maximum oxygen uptake (V̇˙O2max) appears to be influenced not only by metabolic factors but also by the interplay between brain dynamics and ventilatory regulation. This study examined how cortical activity, assessed via electroencephalography (EEG), relates to performance and acute fatigue regulation during a constant-load cycling test. We hypothesized that oscillatory activity in the theta, alpha, and beta bands would be associated with ventilatory coordination and endurance capacity. Methods: Thirty trained participants performed a cycling test to exhaustion at 90% maximal aerobic power. EEG and gas exchange were continuously recorded; ratings of perceived exertion were assessed immediately after exhaustion. Results: Beta power was negatively correlated with time spent at V̇˙O2max (r = −0.542, p = 0.002). Theta and Alpha power alone showed no direct associations with endurance, but EEG–metabolic ratios revealed significant correlations. Specifically, the time to reach V̇˙O2max correlated with Alpha/V̇˙O2 (p < 0.001), Alpha/V̇˙CO2 (p < 0.001), and Beta/V̇˙CO2 (p = 0.002). The time spent at V̇˙O2max correlated with Theta/V̇˙O2 (p = 0.002) and Theta/V̇˙CO2 (p < 0.001). The time-to-exhaustion was correlated with Theta/V̇˙CO2 (p < 0.001) and Alpha/V̇˙CO2 (p < 0.001). Conclusions: These findings indicate that cortical oscillations were associated with different aspects of acute fatigue regulation. Beta activity was associated with fatigue-related neural strain, whereas Theta and Alpha bands, when normalized to metabolic load, were consistent with a role in ventilatory coordination and motor control. EEG–metabolic ratios may provide exploratory indicators of brain–metabolism interplay during high-intensity exercise and could help guide future brain-body interactions in endurance performance.

Hypoxia (HY) and sleep deprivation have opposite effects on appetite. As HY may alter sleep, it may be informative to assess the accumulative effects of these two stressors on hunger, energy intake (EI), and food reward. Seventeen young, active, healthy males completed four 5-hr sessions in normoxia (NO) or normobaric HY (FIO2 = 13.6%, similar to 3,500 m) after a night of habitual sleep (HS; total sleep time >6 hr) or sleep restriction (SR; total sleep time <3 hr). Subjective appetite was assessed regularly using visual analogic scales and EI during an ad libitum lunch after 3.5 hr of exposure. Food reward was assessed using the Leeds Food Preference Questionnaire just before the lunch. As expected, EI was lower for the HY-HS (4.32 +/- 0.71 MJ; p = .048) and HY-SR (4.16 +/- 0.68 MJ, p = .013) sessions than the NO-HS (4.90 +/- 0.84 MJ) session without acute mountain sickness-related gastrointestinal symptoms. No significant effect of SR alone was observed (NO-SR: 4.40 +/- 0.68 MJ). Subjective appetite was not affected. Explicit liking for high-fat foods was higher with SR than HS (main effect: p = .002) and implicit wanting for high-fat foods was higher for the NO-SR, HY-HS, and HY-SR sessions than the NO-HS session (p < .006). Thus, acute SR did not modify subjective appetite or EI despite the increasing food reward for high-fat foods and did not alter the HY-induced changes of appetite or food reward.

V̇O2max is recognized as a key measure in exercise physiology and sports medicine. However, only 20–50% of maximal incremental exercise tests (IET) result in a plateau of V̇O2 (V̇O2pl). To our knowledge, no study has yet examined the possible difference in brain activity during an IET, in V̇O2pl and non-plateau athletes with the same V̇O2max and age. This study aimed to shed light on the central governor hypothesis, namely that the inability to reach a V̇O2pl may be dictated by the brain rather than by a peripheral physical limit. This hypothesis can now be explored using electroencephalography (EEG) during IET, measuring concomitant power in specific frequency bands. Forty-two athletes were divided into two groups: those who practiced endurance sports and those who did not, and were asked to perform an IET. EEG signals and gas exchange were recorded. A V̇O2pl was observed in twenty-two subjects (52%). EEG power increased in all subjects during IET, except in the alpha band, which showed variability, but not significantly (64% increase, 34% decrease, p = 0.07). No differences were found between endurance athletes and non-endurance athletes, except for V̇O2max (60.10 ± 6.16 vs. 51.77 ± 6.41, p < 0.001). However, the baseline-corrected ratio of EEG power to V̇O2 was found to decrease in all subjects during IET, in the alpha, beta and theta bands. In conclusion, the presence or absence of a V̇O2pl is not related to the type of EEG response during an IET. Nevertheless, the decline in brain and V̇O2 powers/ratios in all frequency bands suggests that aerobic power may be constrained by brain mobilization.

Aircraft pilots face a high mental workload (MW) under environmental constraints induced by high altitude and sometimes sleep restriction (SR). Our aim was to assess the combined effects of hypoxia and sleep restriction on cognitive and physiological responses to different MW levels using the Multi-Attribute Test Battery (MATB)-II with an additional auditory Oddball-like task. Seventeen healthy subjects were subjected in random order to three 12-min periods of increased MW level (low, medium, and high): sleep restriction (SR, <3 h of total sleep time (TST)) vs. habitual sleep (HS, >6 h TST), hypoxia (HY, 2 h, FIO2 = 13.6%, ~3500 m vs. normoxia, NO, FIO2 = 21%). Following each MW level, participants completed the NASA-TLX subjective MW scale. Increasing MW decreases performance on the MATB-II Tracking task (p = 0.001, MW difficulty main effect) and increases NASA-TLX (p = 0.001). In the combined HY/SR condition, MATB-II performance was lower, and the NASA-TLX score was higher compared with the NO/HS condition, while no effect of hypoxia alone was observed. In the accuracy of the auditory task, there is a significant interaction between hypoxia and MW difficulty (F(2–176) = 3.14, p = 0.04), with lower values at high MW under hypoxic conditions. Breathing rate, pupil size, and amplitude of pupil dilation response (PDR) to auditory stimuli are associated with increased MW. These parameters are the best predictors of increased MW, independently of physiological constraints. Adding ECG, SpO2, or electrodermal conductance does not improve model performance. In conclusion, hypoxia and sleep restriction have an additive effect on MW. Physiological and electrophysiological responses must be taken into account when designing a MW predictive model and cross-validation.

Background: Caffeine is a well-known psychostimulant reputed to alleviate the deleterious effects of sleep deprivation. Nevertheless, caffeine can alter sleep duration and quality, particularly during recovery sleep. We evaluated the effects of acute caffeine intake on the duration and quality of recovery sleep following total sleep deprivation (TSD), taking into account daily caffeine consumption. Methods: Forty-one participants performed a double-blind, crossover TSD protocol (38 h of continuous wakefulness) with acute caffeine or placebo. Caffeine (2.5 mg/kg) or placebo was administered twice during continuous wakefulness (last treatment 6.5 h before bedtime for the recovery night). Polysomnographic measurements were recorded using a connected headband. Results: TSD was associated with a rebound in total sleep time (TST) on the recovery night (+110.2 ± 23.2 min, p < 0.001). Caffeine intake decreased this recovery TST (−30.2 ± 8.2 min p = 0.02) and the N3 sleep stage duration (−35.6 ± 23.2 min, p < 0.01). Caffeine intake altered recovery sleep continuity (increased number of long awakenings), stability (higher stage transition frequency), and organization (less time spent in complete sleep cycle) and decreased the delta power spectral density during NREM sleep. On the recovery night, habitual daily caffeine consumption was negatively correlated with TST in caffeine and placebo conditions and positively correlated with wake after sleep onset (WASO) duration and with the frequency of long (>2 min) awakenings in the caffeine condition only. Conclusions: Acute caffeine intake during TSD affects nighttime recovery sleep, with an interaction with daily consumption. These results may influence advice on caffeine intake for night-shift workers. (NCT03859882).

Introduction: Exposure to moderate levels of simulated hypoxia has subtle cognitive effects relative to ground level, in healthy individuals. However, there are few data on the cognitive consequences of the combination of hypoxia and partial sleep deprivation, which is a classic military or civilian operational context. In this study, we tested the hypothesis that exposure to moderate hypoxia while sleep-restricted impairs several domains of cognition, and we also assessed physiological parameters and salivary concentrations of cortisol and alpha-amylase. Method: Seventeen healthy males completed two sessions of cognitive tests (sustained attention using the PVT psychomotor vigilance task and executive functions using the Go-NoGo inhibition task and N-Back working memory task) after 30 min (T + 30 ') and 4 h (T + 240 ') of exposure in a normobaric hypoxic tent (FIO2 = 13.6 %, similar or equal to 3,500 m) (HY). This was completed after one night of sleep restriction (3 a.m. to 6 a.m. bedtime, SRHY) and one night of habitual sleep (10 p.m. to 6 a.m. bedtime, HSHY) (with cross-over randomization). The two nights sleep architecture and physiological parameters (oxygen saturation (SpO(2)) and heart rate (HR) during T + 30 ' and T + 240 ' sessions were analyzed. Salivary cortisol and alpha-amylase (sAA) concentrations were analyzed before hypoxia, after the T + 30 ' and T + 240 ' cognitive sessions, and after leaving the hypoxic tent. Results: Sustained attention (RT and number of lapses in the PVT) and executive functions (Go-NoGo and 1-Back and 2-Back parameters, as inhibition and working memory signatures) were impaired in the SRHY condition compared to HSHY. SpO(2) and HR were higher after 4 h compared with 30 min of hypoxia in the HSHY condition, while only HR was statistically higher in the SRHY condition. In SRHY, salivary AA concentration was lower and cortisol was higher than in HSHY. A significant increase in sAA concentration is observed after the cognitive session at 4 h of hypoxia exposure compared to that at 30 min, only in the SRHY condition. There are significant positive correlations between reaction time and the corresponding heart rate (a non-invasive marker of physiological stress) for the executive tasks in the two sleep conditions. This was not observed for salivary levels of sAA and cortisol, respective reliable indicators of the sympathoadrenomedullary system and the hypothalamic-pituitary adrenocortical system. Conclusion: Exposure to moderate normobaric hypoxia (similar or equal to 3500 m / similar or equal to 11,500 ft simulated) after a single night of 3-hour sleep impairs cognitive performance after 30 min and 4 h of exposure. The key determinants and/or mechanism(s) responsible for cognitive impairment when exposed to moderate hypoxia with sleep restriction, particularly on the executive function, have yet to be elucidated.

(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.

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 degrees C leads to reduced EI compared to a control session (22 degrees 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 degrees C sessions, respectively; p = 0.955). While thirst scores were higher in the 32 than the 22 degrees 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 degrees 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.

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.

Malgré la connaissance d’un fonctionnement cognitif et socio-émotionnel altéré par une privation totale de sommeil (PTS), les mécanismes par lesquels la PTS altère les décisions dans des contextes sociaux sont peu rapportés. Nous voulons ici : – caractériser, pour des sujets en PTS, les décisions de contacts sociaux avec des individus menaçants ; – regarder l’influence du changement d’humeur. Trente-quatre participants, reposé ou après une PTS (27 heures d’éveil), doivent spontanément choisir d’éviter (s’asseoir à côté) ou d’approcher (s’asseoir à l’apposé) d’individus menaçants (peur ou colère). Le changement d’humeur (PANAS) et les capacités d’attention soutenue (PVT) ont aussi été évalués. Bien reposé, les participants évitent les individus menaçants (plus fortement la colère que la peur). Après une PTS, les mêmes sujets continuent d’éviter les individus en colère mais ne font plus de choix clairs d’évitement pour les individus apeurés. Les modèles de décision (Drift-diffusion) révèlent que la PTS ralentirait l’accumulation de preuves (peur) qui aident à la décision. La réduction l’humeur positive (et pas négative) suite à la PTS est positivement corrélée à la réduction de l’évitement des individus apeurés sans aucun lien avec les déficits attentionnels. Tous ces résultats soutiennent l’hypothèse, sous-estimée, d’une altération des choix d’évitement d’individus présentant des manifestations socio-émotionnelles (peur) qui deviennent ambiguës avec la PTS et qui passerait par une diminution de l’humeur positive des sujets.