Sleep Extension Research Articles

Restricted and unrestricted sleep schedules of Asian adolescent, high-level student athletes: effects on sleep durations, marksmanship and cognitive performance

The present study sought to compare the effects of a restricted and unrestricted sleep schedule on shooting, cognitive performance and measures of sleepiness and fatigue of Asian, adolescent high-level student athletes. Twenty-four (12 female; 14.1 ± 1.4 years) athletes performed assessments of shooting and cognitive performance (psychomotor vigilance and working memory) at the start and end of five-day restricted or unrestricted sleep (two conditions). Restricted sleep during a five-day training week resulted in no significant performance changes in cognitive or shooting performance compared with unrestricted sleep during a five-day training week, despite there being moderate-to-strong associations between increases in total sleep time and certain aspects of shooting performance. Daytime fatigue levels during the unrestricted sleep period were significantly lower than during sleep restriction. These findings highlight the relationships between nocturnal sleep extension and shooting performance amongst high-level athletes.

Effect of Sleep Extension on the Subsequent Testosterone, Cortisol and Prolactin Responses to Total Sleep Deprivation and Recovery.

Total sleep deprivation (TSD) in humans is associated with altered hormonal levels, which may have clinical relevance. Less is known about the effect of an extended sleep period before TSD on these hormonal changes. Fourteen subjects participated in two experimental counterbalanced conditions (randomised cross-over design): extended sleep (21.00-07.00h time in bed, EXT) and habitual sleep (22.30-07.00h time in bed, HAB). For each condition, subjects performed two consecutive phases: six nights of either EXT or HAB. These nights were followed by 3days in the sleep laboratory with blood sampling at 07.00 and 17.00h at baseline (B-07.00 and B-17.00), after 24 and 34h of continuous awakening (24h-CA, 34h-CA) and after one night of recovery sleep (R-07.00 and R-17.00) to assess testosterone, cortisol, prolactin and catecholamines concentrations. At 24h of awakening, testosterone, cortisol and prolactin concentrations were significantly lower compared to B-07.00 and recovered basal levels after recovery sleep at R-07.00 (P<0.001 for all). However, no change was observed at 34h of awakening compared to B-17.00. No effect of sleep extension was observed on testosterone, cortisol and catecholamines concentrations at 24 and 34h of awakening. However, prolactin concentration was significantly lower in EXT at B-07.00 and R-07.00 compared to HAB (P<0.05, P<0.001, respectively). In conclusion, 24h of awakening inhibited gonadal and adrenal responses in healthy young subjects and this was not observed at 34h of awakening. Six nights of sleep extension is not sufficient to limit decreased concentrations of testosterone and cortisol at 24h of awakening but may have an impact on prolactin concentration.

Benefits of Sleep Extension on Sustained Attention and Sleep Pressure Before and During Total Sleep Deprivation and Recovery.

To investigate the effects of 6 nights of sleep extension on sustained attention and sleep pressure before and during total sleep deprivation and after a subsequent recovery sleep. Subjects participated in two experimental conditions (randomized cross-over design): extended sleep (EXT, 9.8 ± 0.1 h (mean ± SE) time in bed) and habitual sleep (HAB, 8.2 ± 0.1 h time in bed). In each condition, subjects performed two consecutive phases: (1) 6 nights of either EXT or HAB (2) three days in-laboratory: baseline, total sleep deprivation and after 10 h of recovery sleep. Residential sleep extension and sleep performance laboratory (continuous polysomnographic recording). 14 healthy men (age range: 26-37 years). EXT vs. HAB sleep durations prior to total sleep deprivation. Total sleep time and duration of all sleep stages during the 6 nights were significantly higher in EXT than HAB. EXT improved psychomotor vigilance task performance (PVT, both fewer lapses and faster speed) and reduced sleep pressure as evidenced by longer multiple sleep latencies (MSLT) at baseline compared to HAB. EXT limited PVT lapses and the number of involuntary microsleeps during total sleep deprivation. Differences in PVT lapses and speed and MSLT at baseline were maintained after one night of recovery sleep. Six nights of extended sleep improve sustained attention and reduce sleep pressure. Sleep extension also protects against psychomotor vigilance task lapses and microsleep degradation during total sleep deprivation. These beneficial effects persist after one night of recovery sleep.

Short sleep duration and dietary intake: epidemiologic evidence, mechanisms, and health implications.

Links between short sleep duration and obesity, type 2 diabetes, hypertension, and cardiovascular disease may be mediated through changes in dietary intake. This review provides an overview of recent epidemiologic studies on the relations between habitual short sleep duration and dietary intake in adults from 16 cross-sectional studies. The studies have observed consistent associations between short sleep duration and higher total energy intake and higher total fat intake, and limited evidence for lower fruit intake, and lower quality diets. Evidence also suggests that short sleepers may have irregular eating behavior deviating from the traditional 3 meals/d to fewer main meals and more frequent, smaller, energy-dense, and highly palatable snacks at night. Although the impact of short sleep duration on dietary intake tends to be small, if chronic, it may contribute to an increased risk of obesity and related chronic disease. Mechanisms mediating the associations between sleep duration and dietary intake are likely to be multifactorial and include differences in the appetite-related hormones leptin and ghrelin, hedonic pathways, extended hours for intake, and altered time of intake. Taking into account these epidemiologic relations and the evidence for causal relations between sleep loss and metabolism and cardiovascular function, health promotion strategies should emphasize improved sleep as an additional factor in health and weight management. Moreover, future sleep interventions in controlled studies and sleep extension trials in chronic short sleepers are imperative for establishing whether there is a causal relation between short sleep duration and changes in dietary intake.

Sleep extension improves serving accuracy: A study with college varsity tennis players

ObjectiveThis study investigated the effects of sleep extension on tennis serving accuracy, as well as daytime sleepiness in college varsity tennis players. MethodsTwelve (seven females and five males) healthy students on a college varsity tennis team maintained their habitual sleep–wake schedule for a one-week baseline period followed by a one-week sleep extension period. Participants were requested to sleep at least nine hours, including naps, during the sleep extension period. Serving accuracy was assessed when participants were sleep deprived (prior to the sleep extension period) and after the sleep extension period. Levels of daytime sleepiness were monitored via the Epworth Sleepiness Scale and the Stanford Sleepiness Scale, and caffeine consumption was recorded throughout the study. ResultsParticipants slept significantly more in the second week — the sleep extension week — compared with the first week — the baseline week (8.85 vs. 7.14h; p<0.05). Following the sleep extension period, accuracy of the tennis serves improved significantly (35.7% vs. 41.8%; p<0.05), and the Epworth Sleepiness Scale and Stanford Sleepiness Scale scores declined significantly (12.15 vs. 5.67; p<0.05 and 3.56 vs. 2.67; p<0.05, respectively). ConclusionsThis study demonstrates that an increase in sleep of approximately 2h per night significantly increased athletic performance in college varsity tennis players.

Sleep Hygiene and Recovery Strategies in Elite Soccer Players.

In elite soccer, players are frequently exposed to various situations and conditions that can interfere with sleep (e.g., playing night matches interspersed with 3 days; performing activities demanding high levels of concentration close to bedtime; use of products containing caffeine or alcohol in the period preceding bedtime; regular daytime napping throughout the week; variable wake-up times or bedtime), potentially leading to sleep deprivation. We outline simple, practical, and pharmaceutical-free sleep strategies that are coordinated to the constraints of elite soccer in order to promote sleep. Sleep deprivation is best alleviated by sleep extension; however, sleep hygiene strategies (i.e., consistent sleep pattern, appropriate napping, and active daytime behaviors) can be utilized to promote restorative sleep. Light has a profound impact on sleep, and sleep hygiene strategies that support the natural environmental light-dark cycle (i.e., red-light treatment prior to sleep, dawn-simulation therapy prior to waking) and prevent cycle disruption (i.e., filtering short wavelengths prior to sleep) may be beneficial to elite soccer players. Under conditions of inordinate stress, techniques such as brainwave entrainment and meditation are promising sleep-promoting strategies, but future studies are required to ascertain the applicability of these techniques to elite soccer players. Consuming high-electrolyte fluids such as milk, high-glycemic index carbohydrates, some forms of protein immediately prior to sleep, as well as tart cherry juice concentrate and tryptophan may promote rehydration, substrate stores replenishment, muscle-damage repair and/or restorative sleep. The influence of cold water immersion performed close to bedtime on subsequent sleep is still debated. Conversely, the potential detrimental effects of sleeping medication must be recognized. Sleep initiation is influenced by numerous factors, reinforcing the need for future research to identify such factors. Efficient and individualized sleep hygiene strategies may consequently be proposed.

Ursolic acid enhances pentobarbital-induced sleeping behaviors via GABAergic neurotransmission in mice

Prunella vulgaris is widely used as a herbal medicine for cancers, inflammatory diseases, and other infections. Although it has long been used, few studies have examined its effects on central nervous system function. Here, we first observed that ethanolic extracts of P. vulgaris (EEPV) prolonged pentobarbital-induced sleep duration in mice. It is known that EEPV consists of many active components including triterpenoid (ursolic acid and oleanolic acid), which have many biological activities. Therefore, we evaluated which EEPV components induced sleep extension in pentobarbital-mediated sleeping model in mice. Surprisingly, despite their structural similarity and other common functions such as anti-inflammation, anti-cancer, and tissue protection, only ursolic acid enhanced sleep duration in pentobarbital-treated mice. These results were attenuated by bicuculline treatment, which is a GABAA receptor antagonist. The present results suggest that ursolic acid from P. vulgaris enhances sleep duration through GABAA receptor activation and could be a therapeutic candidate for insomnia treatment.

Sleep and Recovery in Team Sport: Current Sleep-Related Issues Facing Professional Team-Sport Athletes.

While the effects of sleep loss on performance have previously been reviewed, the effects of disturbed sleep on recovery after exercise are less reported. Specifically, the interaction between sleep and physiological and psychological recovery in team-sport athletes is not well understood. Accordingly, the aim of the current review was to examine the current evidence on the potential role sleep may play in postexercise recovery, with a tailored focus on professional team-sport athletes. Recent studies show that team-sport athletes are at high risk of poor sleep during and after competition. Although limited published data are available, these athletes also appear particularly susceptible to reductions in both sleep quality and sleep duration after night competition and periods of heavy training. However, studies examining the relationship between sleep and recovery in such situations are lacking. Indeed, further observational sleep studies in team-sport athletes are required to confirm these concerns. Naps, sleep extension, and sleep-hygiene practices appear advantageous to performance; however, future proof-of-concept studies are now required to determine the efficacy of these interventions on postexercise recovery. Moreover, more research is required to understand how sleep interacts with numerous recovery responses in team-sport environments. This is pertinent given the regularity with which these teams encounter challenging scenarios during the course of a season. Therefore, this review examines the factors that compromise sleep during a season and after competition and discusses strategies that may help improve sleep in team-sport athletes.

Metabolic and hormonal effects of 'catch-up' sleep in men with chronic, repetitive, lifestyle-driven sleep restriction.

SummaryObjectiveAcutely restricting sleep worsens insulin sensitivity in healthy individuals whose usual sleep is normal in duration and pattern. The effect of recovery or weekend ‘catch‐up’ sleep on insulin sensitivity and metabolically active hormones in individuals with chronic sleep restriction who regularly ‘catch‐up’ on sleep at weekends is as yet unstudied.Design19 men (mean ± SEM age 28·6 ± 2·0 years, BMI 26·0 ± 0·8 kg/m2) with at least 6 months’ history (5·1 ± 0·9 years) of lifestyle‐driven, restricted sleep during the working week (373 ± 6·6 min/night) with regular weekend ‘catch‐up’ sleep (weekend sleep extension 37·4 ± 2·3%) completed an in‐laboratory, randomized, crossover study comprising two of three conditions, stratified by age. Conditions were 3 weekend nights of 10 hours, 6 hours or 10 hours time‐in‐bed with slow wave sleep (SWS) suppression using targeted acoustic stimuli.MeasurementsInsulin sensitivity was measured in the morning following the 3rd intervention night by minimal modelling of 19 samples collected during a 2‐h oral glucose tolerance test. Glucose, insulin, c‐peptide, leptin, peptide YY (PYY), ghrelin, cortisol, testosterone and luteinizing hormone (LH) were measured from daily fasting blood samples; HOMA‐IR, HOMA‐β and QUICKI were calculated.ResultsInsulin sensitivity was higher following three nights of sleep extension compared to sustained sleep restriction. Fasting insulin, c‐peptide, HOMA‐IR, HOMA‐β, leptin and PYY decreased with ‘catch‐up’ sleep, QUICKI and testosterone increased, while morning cortisol and LH did not change. Targeted acoustic stimuli reduced SWS by 23%, but did not alter insulin sensitivity.ConclusionsThree nights of ‘catch‐up’ sleep improved insulin sensitivity in men with chronic, repetitive sleep restriction. Methods to improve metabolic health by optimizing sleep are plausible.

Sleep and glycemic control in type 1 diabetes.

Our aim in the present study was to elucidate how type 1 diabetes mellitus (T1DM) and sleep parameters interact, which was rarely evaluated up to the moment. Eighteen T1DM subjects without chronic complications, and 9 control subjects, matched for age and BMI, were studied. The following instruments used to evaluate sleep: the Epworth Sleepiness Scale, sleep diaries, actimeters, and polysomnography in a Sleep Lab. Glycemic control in T1DM individuals was evaluated through: A1C, home fingertip glucometer for 10 days (concomitant with the sleep diary and actimeter), and CGM or concomitant with continuous glucose monitoring (during the polysomnography night). Comparing with the control group, individuals with diabetes presented more pronounced sleep extension from weekdays to weekends than control subjects (p = 0.0303). Among T1DM, glycemic variability (SD) was positively correlated with sleep latency (r = 0.6525, p = 0.0033); full awakening index and arousal index were positively correlated with A1C (r = 0.6544, p = 0.0081; and r = 0.5680, p = 0.0272, respectively); and mean glycemia values were negatively correlated with sleep quality in T1DM individuals with better glycemic control (mean glycemia < 154 mg/dL). Our results support the hypothesis of an interaction between sleep parameters and T1DM, where the glycemic control plays an important role. More studies are needed to unveil the mechanisms behind this interaction, which may allow, in the future, clinicians and educators to consider sleep in the effort of regulating glycemic control.

Recovery from potential sleep debt via sleep extension may improve emotion regulation

Recovery from potential sleep debt via sleep extension may improve emotion regulation

The sleep-wake cycle and Alzheimer's disease: what do we know?

Sleep-wake disturbances are a highly prevalent and often disabling feature of Alzheimer's disease (AD). A cardinal feature of AD includes the formation of amyloid plaques, associated with the extracellular accumulation of the amyloid-β (Aβ) peptide. Evidence from animal and human studies suggests that Aβ pathology may disrupt the sleep-wake cycle, in that as Aβ accumulates, more sleep-wake fragmentation develops. Furthermore, recent research in animal and human studies suggests that the sleep-wake cycle itself may influence Alzheimer's disease onset and progression. Chronic sleep deprivation increases amyloid plaque deposition, and sleep extension results in fewer plaques in experimental models. In this review geared towards the practicing clinician, we discuss possible mechanisms underlying the reciprocal relationship between the sleep-wake cycle and AD pathology and behavior, and present current approaches to therapy for sleep disorders in AD.

Hawthorne effect with transient behavioral and biochemical changes in a randomized controlled sleep extension trial of chronically short-sleeping obese adults: implications for the design and interpretation of clinical studies.

ObjectiveTo evaluate the effects of study participation per se at the beginning of a sleep extension trial between screening, randomization, and the run-in visit.DesignSubjects were screened, returned for randomization (Comparison vs. Intervention) after 81 days (median), and attended run-in visit 121 days later.SettingOutpatient.PatientsObese (N = 125; M/F, 30/95; Blacks/Whites/Other, N = 73/44/8), mean weight 107.6±19.7 kg, <6.5 h sleep/night.InterventionNon-pharmacological sleep extension.MeasurementsSleep duration (diaries and actigraphy watch), sleep quality (Pittsburgh Sleep Quality Index), daily sleepiness (Epworth Sleepiness Scale), fasting glucose, insulin and lipids.ResultsPrior to any intervention, marked improvements occurred between screening and randomization. Sleep duration increased (diaries: 357.4 ±51.2 vs. 388.1±48.6 min/night; mean±SD; P<0.001 screening vs. randomization; actigraphy: 344.3 ±41.9 vs. 358.6±48.2 min/night; P<0.001) sleep quality improved (9.1±3.2 vs. 8.2±3.0 PSQI score; P<0.001), sleepiness tended to improve (8.9±4.6 vs. 8.3±4.5 ESS score; P = 0.06), insulin resistance decreased (0.327±0.038 vs. 0.351±0.045; Quicki index; P<0.001), and lipids improved, except for HDL-C. Abnormal fasting glucose (25% vs. 11%; P = 0.007), and metabolic syndrome (42% vs. 29%; P = 0.007) both decreased. In absence of intervention, the earlier metabolic improvements disappeared at the run-in visit.LimitationsRelatively small sample size.ConclusionsImprovements in biochemical and behavioral parameters between screening and randomization changed the “true” study baseline, thereby potentially affecting outcome. While regression to the mean and placebo effect were considered, these findings are most consistent with the “Hawthorne effect”, according to which behavior measured in the setting of an experimental study changes in response to the attention received from study investigators. This is the first time that biochemical changes were documented with respect to the Hawthorne effect. The findings have implications for the design and conduct of clinical research.Trial RegistrationClinicalTrials.gov NCT00261898.

Tensor Based Singular Spectrum Analysis for Automatic Scoring of Sleep EEG

A new supervised approach for decomposition of single channel signal mixtures is introduced in this paper. The performance of the traditional singular spectrum analysis algorithm is significantly improved by applying tensor decomposition instead of traditional singular value decomposition. As another contribution to this subspace analysis method, the inherent frequency diversity of the data has been effectively exploited to highlight the subspace of interest. As an important application, sleep electroencephalogram has been analyzed and the stages of sleep for the subjects in normal condition, with sleep restriction, and with sleep extension have been accurately estimated and compared with the results of sleep scoring by clinical experts.

Increasing preoperative sleep reduces postoperative pain and analgesic use

Increasing preoperative sleep reduces postoperative pain and analgesic use

A review of evidence for the link between sleep duration and hypertension.

There are lines of evidence from experimental sleep deprivation studies, population-based epidemiological studies, and an interventional study that point to the potential efficacy of adequate quality sleep to prevent and treat hypertension. Experimental sleep restriction has been shown to raise blood pressure and heart rate. Insufficient sleep on a chronic basis can raise average 24-hour blood pressure and lead to structural adaptations that entrain the cardiovascular system to operate at an elevated blood pressure equilibrium and increase the risk for hypertension. Disruptions in the timing and duration of sleep could also disrupt circadian rhythmicity and autonomic balance, which can increase the prevalence of the nondipping pattern, disturb diurnal rhythm of cardiac output, and increase blood pressure variability. Short sleep duration has been found to be associated with higher blood pressure and hypertension in both cross-sectional and longitudinal epidemiological studies. The association appears stronger in middle-aged adults and in women. Experimental sleep extension has been shown to significantly reduce blood pressure in individuals with prehypertension or stage 1 hypertension. The observed association between sleep duration and hypertension raises the hypothesis that interventions to extend sleep and improve sleep quality could serve as effective primary, secondary, and tertiary preventive measures for hypertension.

Effects of extended sleep on female athlete's performance and nutrition (633.2)

The purpose of this study was to investigate the effects of one extra hour of sleep on physical performance and nutrition behaviors on college female track athletes. Eleven females (age 20.6 ± 1.6 yrs) maintained normal sleep habits for a one week. Baseline data was followed by a one week sleep extension period (night time and napping). Anaerobic power and fatigue was measured using the Wingate Test. The ASA 24‐hour food‐recall questionnaire was used to test nutrient intake. Reaction time, perceived stress, and mood were measured using the Psychomotor Vigilance Task (PVT), Cohen's Stress Test, and Profile of Mood States (POMS), respectively. Preliminary data was collected on 11 female subjects. Subjects increased total sleep from baseline (423.5 ± 44.4 minutes, 443.9 ± 55.2 minutes respectively), however this was not significant (z = ‐1.2480, p = 0.2258). No significant differences were seen in maximum power (z = 0.00, p = 1.0000) and fatigue (z = 0.0657, p = 0.9476) following sleep extension. Although not significant, mean PVT reaction time increased (z = ‐0.8213, p = 0.4115) and POMS scores improved (z = 0.7560, p = 0.4496) following more sleep. The athletes showed no significant effects in caloric (z = 0.1313, p = 0.8968) or total fat intake (z = ‐0.2627, p = 0.7928) after sleep extension. Improvements in physical performance and nutritional behaviors were not seen after sleep extension in college female track athletes.Grant Funding Source: WVU Experimental Station Hatch Funding

Sleep Extension Improves Neurocognitive Functions in Chronically Sleep-Deprived Obese Individuals

BackgroundSleep deprivation and obesity, are associated with neurocognitive impairments. Effects of sleep deprivation and obesity on cognition are unknown, and the cognitive long-term effects of improvement of sleep have not been prospectively assessed in short sleeping, obese individuals.ObjectiveTo characterize neurocognitive functions and assess its reversibility.DesignProspective cohort study.SettingTertiary Referral Research Clinical Center.PatientsA cohort of 121 short-sleeping (<6.5 h/night) obese (BMI 30–55 kg/m2) men and pre-menopausal women.InterventionSleep extension (468±88 days) with life-style modifications.MeasurementsNeurocognitive functions, sleep quality and sleep duration.ResultsAt baseline, 44% of the individuals had an impaired global deficit score (t-score 0–39). Impaired global deficit score was associated with worse subjective sleep quality (p = 0.02), and lower urinary dopamine levels (p = 0.001). Memory was impaired in 33%; attention in 35%; motor skills in 42%; and executive function in 51% of individuals. At the final evaluation (N = 74), subjective sleep quality improved by 24% (p<0.001), self-reported sleep duration increased by 11% by questionnaires (p<0.001) and by 4% by diaries (p = 0.04), and daytime sleepiness tended to improve (p = 0.10). Global cognitive function and attention improved by 7% and 10%, respectively (both p = 0.001), and memory and executive functions tended to improve (p = 0.07 and p = 0.06). Serum cortisol increased by 17% (p = 0.02). In a multivariate mixed model, subjective sleep quality and sleep efficiency, urinary free cortisol and dopamine and plasma total ghrelin accounted for 1/5 of the variability in global cognitive function.LimitationsDrop-out rate.ConclusionsChronically sleep-deprived obese individuals exhibit substantial neurocognitive deficits that are partially reversible upon improvement of sleep in a non-pharmacological way. These findings have clinical implications for large segments of the US population.Trail registrationwww.ClinicalTrials.gov NCT00261898. NIDDK protocol 06-DK-0036

Sleep and Alzheimer disease pathology—a bidirectional relationship

Factors other than age and genetics may increase the risk of developing Alzheimer disease (AD). Accumulation of the amyloid-β (Aβ) peptide in the brain seems to initiate a cascade of key events in the pathogenesis of AD. Moreover, evidence is emerging that the sleep-wake cycle directly influences levels of Aβ in the brain. In experimental models, sleep deprivation increases the concentration of soluble Aβ and results in chronic accumulation of Aβ, whereas sleep extension has the opposite effect. Furthermore, once Aβ accumulates, increased wakefulness and altered sleep patterns develop. Individuals with early Aβ deposition who still have normal cognitive function report sleep abnormalities, as do individuals with very mild dementia due to AD. Thus, sleep and neurodegenerative disease may influence each other in many ways that have important implications for the diagnosis and treatment of AD.

Sleep extension improves fasting insulin levels in adults who are habitually sleep restricted

Introduction Laboratory and epidemiological studies have evidenced an association between behavioral sleep restriction and an increased risk for the development of diabetes. The present study investigates the effects of bedtime extensions on fasting glucose and insulin levels in adults who are chronically sleep restricted during weekdays. Materials and methods Participants were sleep restricted as part of their lifestyle choices (self-reported sleep 7 h per weekday with increased bedtimes during WE). Wrist activity monitoring was obtained for 8 weeks, first for 2 weeks while following their regular bedtimes, then for 6 weeks while trying to increase their bedtimes by one hour per day and to adhere to prescribed sleep hygiene guidelines. At the end of the 2 weeks of habitual bedtimes, the participants completed a questionnaire on caloric intake for one day before the fasting blood sample. At the end of the 6 weeks of sleep extension, they were requested to follow exactly the same diet one day before the second fasting blood sample. Glucose and insulin were assayed before and after the sleep intervention. Results Eleven subjects completed the entire study (9 women/2 men, 28.5 ± 6.5 years old, 21.2 ± 2.8 kg/m2). On average, sleep time successfully increased by about 44 min per weekday (p = 0.001) without any significant change in the sleep amount obtained during WE. There was a large inter-individual variability in the increase in sleep time (range 9–95 min) without any change in sleep efficiency. Fasting insulin levels decreased significantly after sleep extension (p = 0.036) without any significant change in fasting glucose levels, indicating a lower diabetes risk with sleep extension. Noteworthy, this decrease in insulin levels correlated with weight changes (Kendall o = −0.50, p 0.05) and with increases in sleep time (Kendall o = 0.48, p 0.05). Conclusion Our findings demonstrate that sleep extension is feasible in adults who are chronically sleep restricted and beneficial in reducing fasting insulin levels, but is highly individual-dependent. Further investigation on sleep extension in pre-diabetics and diabetics who are chronically sleep restricted is needed to explore the possibilities of improving the severity of diabetes by sleep extension protocols. Acknowledgements The study was funded by a “Brains Back to Brussels”, from INNOVIRIS, the Institut Bruxellois pour la Recherche et l’Innovation – Region Bruxelles-Capitale.