Exploring the Influence of Acid-Base Status on Athletic Performance during Simulated Three-Day 400 m Race.

This study aimed to investigate the ability of highly trained athletes to consistently perform at their highest level during a simulated three-day 400 m race and to examine the impact of an alkaline diet associated with chronic consumption of bicarbonate-rich water or placebo on their blood metabolic responses before and after the three races. Twenty-two highly trained athletes, divided into two groups-one with an alkalizing diet and placebo water (PLA) and the other with an alkalizing diet and bicarbonate-rich water (BIC)-performed a 400 m race for three consecutive days. Performance metrics, urine and blood samples assessing acid-base balance, and indirect markers of neuro-muscular fatigue were measured before and after each 400 m race. The evolution of the Potential Renal Acid Load (PRAL) index and urinary pH highlights the combination of an alkalizing diet and bicarbonate-rich hydration, modifying the acid-base state (p < 0.05). Athletes in the PLA group replicated the same level of performance during three consecutive daily races without an increase in fatigue-associated markers. Athletes experienced similar levels of metabolic perturbations during the three 400 m races, with improved lactate clearance 20 min after the third race compared to the first two (p < 0.05). This optimization of the buffering capacity through ecological alkaline nutrition and hydration allowed athletes in the BIC group to improve their performance during the third 400 m race (p < 0.01). This study highlights athletes' ability to replicate high-level performances over three consecutive days with the same extreme level of metabolic disturbances, and an alkaline diet combined with bicarbonate-rich water consumption appears to enhance performance in a 400 m race.

24-h passive heat and cold exposures did not modify energy intake and appetite but strongly modify food reward.

Effects of acute thermal exposures on appetite appear hypothetical in reason of very heterogeneous methodologies. The aim of this study was therefore to clearly define the effects of passive 24-h cold (16°C) and heat (32°C) exposures on appetitive responses compared to a thermo neutral condition (24°C). Twenty-three healthy, young, and active male participants realised three sessions (from 1 pm) in a laboratory conceived like an apartment dressed with the same outfit (Clo=1). Three meals composed of three or four cold or warm dishes were served ad libitum to assess energy intake (EI). Leeds Food Preference Questionnaires were used before each meal to assess food reward. Subjective appetite was regularly assessed and levels of appetitive hormones (acylated ghrelin, GLP-1, leptin, and PYY) were assessed before and after the last meal (lunch). Contrary to the literature, total EI was not modified by cold or heat exposure (p=0.120). Accordingly, hunger scores (p=0.554) were not altered. Levels of acylated ghrelin and leptin were marginally higher during the 16 (p=0.032) and 32°C (p<0.023) sessions, respectively. Interestingly, implicit wanting for cold and low-fat foods at 32°C and for warm and high-fat foods at 16°C were increased during the whole exposure (p < 0.024). Moreover, cold entrées were more consumed at 32 °C (p<0.062) and warm main dishes more consumed at 16°C (p<0.025). Thus, passive cold and hot exposures had limited effects on appetite and it seems that offering some choice based on food temperature may help individuals to express their specific food preferences and maintain EI.

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 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.

Impact of the Rapid Normalization of Chronic Hyperglycemia on the Receptor Activator of Nuclear Factor-Kappa B Ligand and the Osteoprotegerin System in Patients Living with Type 2 Diabetes: RANKL-GLYC Study.

The RANKL-GLYC study aims to explore the impact of the rapid correction of chronic hyperglycemia on the receptor activator of nuclear factor-kappa B ligand (RANKL) and its antagonist osteoprotegerin (OPG). RANKL and OPG are considered the main factors in the pathophysiology of Charcot neuroarthropathy, a devastating complication of the joints that remains poorly understood. The study began recruiting patients in September 2021 and ends in June 2022; the final study results are scheduled for January 2023.

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.

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.

Genetic Determinants of Neurobehavioral Responses to Caffeine Administration during Sleep Deprivation: A Randomized, Cross Over Study (NCT03859882).

This study investigated whether four single nucleotide polymorphisms (SNPs) moderated caffeine effects on vigilance and performance in a double-blind and crossover total sleep deprivation (TSD) protocol in 37 subjects. In caffeine (2 × 2.5 mg/kg/24 h) or placebo-controlled condition, subjects performed a psychomotor vigilance test (PVT) and reported sleepiness every six hours (Karolinska sleepiness scale (KSS)) during TSD. EEG was also analyzed during the 09:15 PVT. Carriers of the TNF-α SNP A allele appear to be more sensitive than homozygote G/G genotype to an attenuating effect of caffeine on PVT lapses during sleep deprivation only because they seem more degraded, but they do not perform better as a result. The A allele carriers of COMT were also more degraded and sensitive to caffeine than G/G genotype after 20 h of sleep deprivation, but not after 26 and 32 h. Regarding PVT reaction time, ADORA2A influences the TSD effect but not caffeine, and PER3 modulates only the caffeine effect. Higher EEG theta activity related to sleep deprivation was observed in mutated TNF-α, PER3, and COMT carriers, in the placebo condition particularly. In conclusion, there are genetic influences on neurobehavioral impairments related to TSD that appear to be attenuated by caffeine administration. (NCT03859882).

Genotyping on blood and buccal cells using loop-mediated isothermal amplification in healthy humans.

Genetic variations contribute to phenotypic individual vulnerabilities to sleep debt, particularly for five single nucleotide polymorphisms (SNPs). Loop-mediated isothermal amplification and melting curve analysis (LAMP-MC) is a recently developed method to characterize SNPs. The aim of present study was to evaluate the LAMP-MC method on blood and buccal cells for detection of five SNPs of interest in healthy humans. We first analyzed signals obtained from LAMP-MC method on 42 samples. Then we compared the results with those of referent TaqMan method. The LAMP-MC method produced specific melting curves for the five SNPs. A high concordance of genotyping results was observed between the two methods for rs5751876_ADORA2A, rs1800629_TNF-α, rs73598374_ADA and rs228697_PER3 in blood and saliva (Cohen's kappa coefficient >0.80). A good agreement ( = 0.61) was observed for rs4680_COMT in blood only. LAMP-MC is a simple and reliable method to study genetic influences on health, sleep debt-related performance impairments and countermeasures.

Beneficial effects of exercise training on cognitive performances during total sleep deprivation in healthy subjects.

OBJECTIVE: Exercise training has been shown to improve learning and memory, and to protect against the negative impact of sleep deprivation. The aim of this study was to investigate the effects of seven weeks of moderate- and high-intensity interval exercise training on vigilance/sustained attention, inhibition processes and working memory during 40-h total sleep deprivation (TSD) in 16 healthy young men. METHODS: The subjects were evaluated before (Baseline, BAS) and during TSD, and the day after a night of recovery sleep (Recovery, REC). RESULTS: Exercise training significantly decreased errors and increased speed assessed by the psychomotor vigilance task (PVT) during TSD and REC while no difference was found in executive inhibition (Go-noGo task) and working memory (2-Back task) performances. The multiple sleep latency test results were higher during BAS and REC at Post-exercise training, and no difference occurred in subjective sleepiness and daytime microsleeps over the 40-h TSD. The PVT speed was positively correlated with maximal oxygen consumption and maximal aerobic power measured before entry in the in-laboratory TSD protocol, and stage 3 sleep duration measured during the first night in the in-laboratory TSD protocol (N-1). Exercise training effects on sleep were found during the night recovery with lower stage-3 sleep and higher rapid eye movement (REM) sleep durations. An exercise training effect was also found on free insulin-like growth factor I levels with lower levels during TSD at Post-exercise training. CONCLUSIONS: In healthy young men, exercise training reduced sleep pressure at baseline and protected against sustained attention deficits induced by TSD with persistent effect after one night of recovery sleep. Nevertheless, exercise training was not effective in reducing deficits in executive inhibition and working memory induced by TSD.

The Impact of Genetic Variations in ADORA2A in the Association between Caffeine Consumption and Sleep.

ADORA2A has been shown to be responsible for the wakefulness-promoting effect of caffeine and the 1976T>C genotype (SNP rs5751876, formerly 1083T>C) to contribute to individual sensitivity to caffeine effects on sleep. We investigate the association between six single nucleotide polymorphisms (SNP) from ADORA2A and self-reported sleep characteristics and caffeine consumption in 1023 active workers of European ancestry aged 18-60 years. Three groups of caffeine consumers were delineated: low (0-50 mg/day, less than one expresso per day), moderate (51-300 mg/day), and high (>300 mg/day). We found that at caffeine levels higher than 300 mg/day, total sleep time (TST) decreased (F = 13.9, p < 0.01), with an increase of insomnia (ORa [95%CI] = 1.5 [1.1-1.9]) and sleep complaints (ORa [95%CI] = 1.9 [1.1-3.3]), whatever the ADORA2A polymorphism. Odds ratios were adjusted (ORa) for sex, age, and tobacco. However, in low caffeine consumers, lower TST was observed in the T allele compared to homozygote rs5751876 and rs3761422 C carriers. Conversely, higher TST was observed in rs2298383 T allele compared to C and in rs4822492G allele compared to the homozygote C (p < 0.05). These 4 SNPs are in strong linkage disequilibrium. Haplotype analysis confirmed the influence of multiple ADORA2a SNPs on TST. In addition, the rs2298383 T and rs4822492 G alleles were associated with higher risk of sleep complaints (Ora = 1.9 [1.2-3.1] and Ora = 1.5 [1.1-2.1]) and insomnia (Ora = 1.5 [1.3-2.5] and Ora = 1.9 [1.3-3.2). The rs5751876 T allele was associated with a decreased risk of sleep complaints (Ora = 0.7 [0.3-0.9]) and insomnia (Ora = 0.5 [0.3-0.9]). Our results identified ADORA2A polymorphism influences in the less-than-300-mg-per-day caffeine consumers. This opens perspectives on the diagnosis and pharmacology of sleep complaints and caffeine chronic consumption.

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.

Limited Benefit of Sleep Extension on Cognitive Deficits During Total Sleep Deprivation: Illustration With Two Executive Processes.

Introduction: Sleep extension has been associated with better alertness and sustained attention capacities before, during and after sleep loss. However, less is known about such beneficial effect on executive functions (EFs). Our aim was to investigate such effects on two EFs (i.e., inhibition and working memory) for subjects submitted to total sleep deprivation and one-night of recovery. Methods: Fourteen healthy men (26-37 years old) participated in an experimental cross-over design with two conditions: extended sleep (EXT, 9.8 ± 0.1 h of Time In Bed, TIB) and habitual sleep (HAB, 8.2 ± 0.1 h TIB). During these two conditions subjects underwent two consecutive phases: Six nights of either EXT or HAB followed by 3 days in-laboratory: baseline (BASE), TSD (38 h) and after recovery (REC). EFs capacities were assessed through Go-NoGo (inhibition) and 2N-Back (working memory) tasks. Both EFs capacities were measured at different time (BASE/TSD/REC: 09:30, 13:00, 16:00; TSD: 21:00, 00:00, 03:00, 06:30). Results: In both conditions (HAB and EXT), TSD was associated with deficits in inhibition (higher errors and mean reaction time from TSD 09:30 until the end; p < 0.05) and working memory (lower corrects responses from TSD 06:30 or 09:30; p < 0.05). We observed no significant differences between HAB and EXT conditions on EFs capacities during BASE, TSD, and REC periods. Conclusion: Six nights of sleep extension is neither efficient to reduce core EFs deficits related to TSD nor to improve such capacities after a recovery night. These results highlight that sleep extension (six nights of 10 h of TIB) is not effective to limit EFs deficits related to TSD suggesting a disconnection inside cognition between executive and sustained attention processes. Clinical Trials: NCT02352272.

Using relaxation techniques to improve sleep during naps.

Insufficient sleep is a common occurrence in occupational settings (e.g. doctors, drivers, soldiers). The resulting sleep debt can lead to daytime sleepiness, fatigue, mood disorder, and cognitive deficits as well as altered vascular, immune and inflammatory responses. Short daytime naps have been shown to be effective at counteracting negative outcomes related to sleep debt with positive effects on daytime sleepiness and performance after a normal or restricted night of sleep in laboratory settings. However, the environmental settings in the workplace and the emotional state of workers are generally not conducive to beneficial effects. Here, we tested whether relaxation techniques (RT) involving hypnosis might increase total sleep time (TST) and/or deepen sleep. In this study, eleven volunteers (aged 37-52) took six early-afternoon naps (30 min) in their occupational workplace, under two different conditions: control 'Naps' or 'Naps + RT' with a within-subjects design. Our results demonstrate that adding RT to naps changes sleep architecture, with a significant increase in the TST, mostly due to N2 sleep stage (and N3, to a lesser extent). Therefore, the deepening of short naps with RT involving hypnosis might be a successful non-pharmacological way to extend sleep duration and to deepen sleep in occupational settings.

Sleep Extension before Sleep Loss: Effects on Performance and Neuromuscular Function.

PURPOSE: This study aimed to investigate the effects of six nights of sleep extension on motor performance and associated neuromuscular function before and after one night of total sleep deprivation (TSD). METHODS: Twelve healthy men participated in two experimental conditions (randomized crossover design): extended sleep (EXT, 9.8 ± 0.1 h time in bed) and habitual sleep (HAB, 8.2 ± 0.1 h time in bed). In each condition, subjects performed six nights of either EXT or HAB at home followed by an assessment of motor performance and neuromuscular function at baseline (D0) and after one night of TSD, i.e., 34-37 h of continuous wakefulness (D1). Maximal voluntary contractions with superimposed femoral nerve electrical and transcranial magnetic stimulations and stimulations on relaxed muscles were investigated before and after submaximal isometric knee extensor exercises performed until task failure. RESULTS: Time to exhaustion was longer in EXT compared with HAB (+3.9% ± 7.7% and +8.1% ± 12.3% at D0 and D1, respectively). Performance at D1 decreased from D0 similarly between conditions (-7.2% ± 5.6% and -3.7% ± 7.3% in HAB and EXT, respectively). At D1, the RPE during exercise was lower in EXT compared with HAB (-7.2% ± 7.5%) with no difference at D0. No difference was observed in voluntary activation between the two conditions. CONCLUSIONS: Six nights of sleep extension improved sustained contraction time to exhaustion, and this result cannot be explained by smaller reductions in voluntary activation, measured by both nerve and transcranial magnetic stimulation. The beneficial effect on motor performance in the EXT condition was likely due to reduced RPE after TSD.