Short-term Sleep Restriction Research Articles

0227 Impact of 5-night sleep restriction on actigraphy-estimated sleep in young adolescents: preliminary associations with ADHD traits

Abstract Introduction Prior research suggests that children with attention-deficit/hyperactivity-disorder (ADHD) may experience disrupted sleep. In typically developing children, short-term sleep restriction increases sleep pressure and efficiency; however, whether a similar homeostatic response occurs in children with ADHD is unknown. Here we explore the effects of 5 nights of experimental sleep restriction on actigraphy-estimated sleep of children with and without high ADHD characteristics. Methods Nineteen young adolescents (Mage=12.24yr, range 10.17-13.88yr; 10F/9M) participated in an at-home crossover protocol. After ≥5 nights of stabilization (10hr time-in-bed[TIB] set to habitual risetimes), participants had five nights of sleep optimization (SO; same stabilization schedule) or restriction (SR; 7.5hr TIB, sleep opportunity reduced by delaying bedtime and advancing risetime equally), a 2-3 night restabilization, and then the reverse schedule. Sleep was assessed via wrist-worn actigraphy (AMI Micro Motionlogger), sleep diaries, and twice-daily phone calls ensuring schedule adherence. Primary sleep variables included: total sleep time (TST; min), sleep period time (SPT; min), and sleep efficiency (TST/SPT*100). Children were grouped by parent-rated Conners 3 ADHD-Probability-Index: < 50% (low-ADHD; n=10, 8F) or >=50% (high-ADHD; n=9, 2F). Results Mixed-effects ANOVAs evaluating condition (SO vs. SR) and group (low- vs. high-ADHD) on schedule adherence indicated significant effects of condition; that is, SR reduced both SPT (M±SD SO=9.08[0.54]hr, SR=7.10[0.57]hr; F(1,17)=479.75, p<.001, ηp2=.97) and TST (M±SD SO=7.92[0.97]hr, SR=6.38[0.86]hr; F(1,17)=302.13, p<.001, ηp2=.95). No group or group-by-condition effects were significant (all ps>.21). For sleep efficiency, a group-x-condition interaction (F(1,17)=8.29, p=.01, ηp2=.33) revealed that SR significantly increased sleep efficiency in low-ADHD children (M±SD SO=85.08[9.95]%, SR=89.74[7.66]%, Bonferroni-p<.001) but not in high-ADHD children (M±SD SO=90.67[3.74]%, SR=91.21[3.19]%, Bonferroni-p=.61). Other between-group effects were not significant (all ps>.12). Conclusion These preliminary data indicate that our sleep restriction protocol successfully reduces sleep opportunity and sleep duration in peripubertal children, including those with high ADHD traits. Notably, sleep restriction improved sleep efficiency in low-ADHD children, whereas sleep efficiency was high and unchanging in our high-ADHD group. It is possible that high-ADHD children maintained higher sleep pressure even after stabilization. While data collection (matching groups on sex and age) continues, we are examining waking EEG markers to explore this possibility. Support (if any) R01HD103655, P20GM139743

Severe, short-term sleep restriction reduces gut microbiota community richness but does not alter intestinal permeability in healthy young men

Sleep restriction alters gut microbiota composition and intestinal barrier function in rodents, but whether similar effects occur in humans is unclear. This study aimed to determine the effects of severe, short-term sleep restriction on gut microbiota composition and intestinal permeability in healthy adults. Fecal microbiota composition, measured by 16S rRNA sequencing, and intestinal permeability were measured in 19 healthy men (mean ± SD; BMI 24.4 ± 2.3 kg/m2, 20 ± 2 years) undergoing three consecutive nights of adequate sleep (AS; 7–9 h sleep/night) and restricted sleep (SR; 2 h sleep/night) in random order with controlled diet and physical activity. α-diversity measured by amplicon sequencing variant (ASV) richness was 21% lower during SR compared to AS (P = 0.03), but α-diversity measured by Shannon and Simpson indexes did not differ between conditions. Relative abundance of a single ASV within the family Ruminococcaceae was the only differentially abundant taxon (q = 0.20). No between-condition differences in intestinal permeability or β-diversity were observed. Findings indicated that severe, short-term sleep restriction reduced richness of the gut microbiota but otherwise minimally impacted community composition and did not affect intestinal permeability in healthy young men.

The emerging importance of tackling sleep-diet interactions in lifestyle interventions for weight management.

Sleep habits are directly related to risk of obesity, and this relationship may be partly mediated through food choices and eating behaviour. Short sleep duration, impaired sleep quality and suboptimal sleep timing are all implicated in weight gain and adverse cardiometabolic health, at least partly mediated through their associations with diet quality. Short-term sleep restriction leads to increased energy intake, and habitually short sleepers report dietary intakes that indicate a less healthy diet compared with adequate sleepers. Evidence is emerging that sleep extension interventions in short sleepers may reduce intake of sugars and overall energy intake. Poor sleep quality, night shift work patterns and social jetlag are also associated with lower diet quality and consumption of energy-dense foods. Incorporating sleep advice into weight management interventions may be more effective than energy-restricted diets and exercise advice alone. However, there are a lack of intervention studies that aim to lengthen sleep, improve sleep quality or adjust irregular sleep timing to investigate the impact on dietary intakes and eating behaviour in participants aiming to lose weight or maintain weight loss. Finally, future research should take account of individual characteristics such as age, sex, life stage and changing working practices when designing combined lifestyle interventions including sleep behaviour change for health and well-being.

Effects of sleep deprivation on sarcopenia and obesity: A narrative review of randomized controlled and crossover trials.

Shortened and fragmented sleeping patterns occupying modern industrialized societies may promote metabolic disturbances accompanied by increased risk of weight gain and skeletal muscle degradation. Short-term sleep restriction may alter energy homeostasis by modifying dopamine brain receptor signaling, leading to hyperpalatable food consumption and risk of increased adiposity. Concomitantly, the metabolic damage caused by lower testosterone and higher cortisol levels may stimulate systemic inflammation, insulin resistance, and suppress pathways involved in muscle protein synthesis. These changes may lead to dysregulated energy balance and skeletal muscle metabolism, increasing the risk of sarcopenic obesity, an additional public health burden. Future trials controlling for food intake and exploring further the influence of sleep deprivation on anabolic and catabolic signaling, and gut peptide interaction with energy balance are warranted.

Severe sleep restriction suppresses appetite independent of effects on appetite regulating hormones in healthy young men without obesity

ObjectiveSeveral nights of moderate (4–5 hr/night) sleep restriction increases appetite and energy intake, and may alter circulating concentrations of appetite regulating hormones. Whether more severe sleep restriction has similar effects is unclear. This study aimed to determine the effects of severe, short-term sleep restriction on appetite, ad libitum energy intake during a single meal, appetite regulating hormones, and food preferences. MethodsRandomized, crossover study in which 18 healthy men (mean ± SD: BMI 24.4 ± 2.3 kg/m2, 20 ± 2 yr) were assigned to three consecutive nights of sleep restriction (SR; 2 hr sleep opportunity/night) or adequate sleep (AS; 7–9 hr sleep opportunity/night) with controlled feeding and activity designed to maintain energy balance throughout the 3-day period. On day 4, participants consumed a standardized breakfast. Appetite, assessed by visual analogue scales, and circulating ghrelin, peptide-YY (PYY), glucagon-like peptide (GLP-1), insulin, and glucose concentrations were measured before and every 20–60 min for 4hr after the meal. Ad libitum energy and macronutrient intakes were then measured at a provided buffet lunch. Food preferences were measured by Leeds Food Preference Questionnaire (LFPQ) administered before and after the lunch. ResultsArea under the curve (AUC) of postprandial hunger (-23%), desire to eat (-23%), and prospective consumption (-18%) ratings were all lower, and postprandial fullness AUC (25%) was higher after SR relative to after AS (p ≤ 0.02). Ad libitum energy intake at the lunch meal was 332 kcal [95% CI: -479, -185] (p<0.001) lower after SR relative to after AS, but relative macronutrient intakes and LFPQ scores did not differ. Postprandial glucose, insulin, PYY, GLP-1, and ghrelin AUCs did not differ between phases. However, mean concentrations of PYY (-11%) and GLP-1 (-4%) over the 4-hr testing period were lower, and glucose concentrations were 6% higher, after SR relative to after AS (p ≤ 0.01). ConclusionIn contrast with reported effects of moderate sleep restriction, severe sleep restriction reduced appetite and energy intake, had no impact food preferences, and had little impact on appetite regulating hormones. Findings suggest that severe sleep restriction may suppress appetite and food intake, at least at a single meal, by a mechanism independent of changes in food preference or appetite regulating hormones.

The spleen mediates chronic sleep restriction-mediated enhancement of LPS-induced neuroinflammation, cognitive deficits, and anxiety-like behavior.

Chronic sleep restriction promotes neuroinflammation and cognitive deficits in neurodegenerative and neurobehavioral diseases. The spleens of mice exposed to chronic and repeated psychological stress serve as a reservoir of inflammatory myeloid cells that are released into the blood and brain following secondary acute stress. Here, we tested whether chronic and repeated short-term sleep restriction (CRSR) would exacerbate lipopolysaccharide (LPS)-induced neuroinflammation, cognitive deficits, and anxiety-like behavior in a spleen-dependent manner. LPS was administered to aged mice 14 days after exposure to CRSR consisting of three cycles of 7 days of sleep restriction with 7-day intervals in between. CRSR increased plasma proinflammatory cytokine levels, blood-brain barrier permeability, hippocampal proinflammatory cytokine levels, and transition of microglia to the M1 phenotype 24 h after LPS treatment. This in turn led to cognitive deficits and anxiety-like behavior. Interestingly, removal of the spleen 14 days prior to CRSR abrogated the enhancement of LPS-induced increases in systemic inflammation, neuroinflammation, cognitive deficits, and anxiety-like behavior. These data indicate that the spleen was essential for CRSR-induced exacerbation of LPS-induced brain damage.

Severe Sleep Restriction Suppresses Appetite Independent of Effects on Food Intake-Regulating Hormones

Abstract Objectives Several nights of moderate (4–5 hr/night) sleep restriction increases appetite and energy intake, and may alter circulating concentrations of food intake-regulating hormones. Whether more severe sleep restriction has similar effects is undetermined. This study aimed to determine the effects of severe, short-term sleep restriction on appetite and food intake-regulating hormones. Methods Randomized, crossover study in which 18 healthy men (mean ± SD: BMI 24.4 ± 2.3 kg/m2, 20 ± 2 yr) were assigned to three consecutive nights of sleep restriction (SR; 2 hr sleep/night) or adequate sleep (AS; 7–9 hr sleep/night) with controlled feeding and activity throughout the 3-day period. On day 4, participants consumed a standardized breakfast. Appetite ratings, and circulating ghrelin, peptide-YY (PYY), glucagon-like peptide (GLP-1), insulin, and glucose concentrations were measured before and for 4hr after the meal. Ad libitum energy and macronutrient intakes were then measured at a provided buffet lunch. Results Median PYY (–21%) and GLP-1 (–14%) concentrations were lower, and median glucose (3%) concentrations were higher after SR relative to after AS (main effect of condition, P &amp;lt; 0.05; condition-by-time interaction, P = NS). Ghrelin and insulin did not differ between conditions. Mean hunger (–23%), desire to eat (–23%), and prospective consumption (–18%) ratings were all lower, and mean fullness (27%) ratings were higher after SR relative to after AS (main effect of condition, P &amp;lt; 0.05; condition-by-time interaction, P = NS). Ad libitum energy intake at the lunch meal was 14% lower after SR relative to after AS (–332 kcal [95% CI: −479, −185] P &amp;lt; 0.001), but macronutrient composition did not differ. Conclusions In contrast with reported effects of moderate sleep restriction, severe sleep restriction reduced appetite and energy intake. Appetite suppression was likely not due to the observed differences in food intake-regulating hormones as sleep-restriction induced reductions in PYY and GLP-1 concentrations would be expected to increase appetite. Funding Sources US Army MRDC. Authors’ views do not reflect official DoD or Army policy.

Effects of sleep restriction on subjective and physiological variables in middle-aged Korean adults: an intervention study

BackgroundAdequate sleep is crucial for normal functioning. However, most people, including middle-aged adults of reproductive age, show a marked reduction in their sleep duration. Thus, sleep is a major issue that should be addressed in health management. We investigated the effects of short-term sleep restriction on subjective parameters (sleepiness, stress, fatigue) and physiological parameters (cortisol, thyrotropin [TSH], thyroxine [T4], triiodothyronine [T3], C-reactive protein [CRP]) in middle-aged adults, the recovery of these parameters after rest, and the associations between parameters. MethodsA total of 118 healthy adults (59 men, 59 women), aged 35–44 years, and without sleep problems, were enrolled. Participants underwent a 4-h sleep restriction per day for 3 day at a hospital, and then returned to their daily lives to take four days of rest. A questionnaire and blood test were administered before and after sleep restriction, and after the recovery period, to assess subjective and physiological parameters. ResultsAfter sleep restriction, sleepiness, fatigue, and stress significantly increased compared to baseline. Cortisol and TSH were elevated after sleep restriction, while T4, T3, and CRP were reduced compared to baseline. After the recovery phase, all parameters were restored to levels similar to baseline levels. Changes in each parameter were mutually associated; fatigue and sleepiness had the strongest association. ConclusionOur results suggest that even a short period of sleep restriction can have an adverse impact on psychological and physiological stress parameters in middle-aged adults, and that adequate rest and sleep are needed to restore them to normal levels.

A study of skin characteristics with long-term sleep restriction in Korean women in their 40s.

Previous studies have demonstrated increased pore size and darkening skin color with total sleep deprivation. There are many studies of skin characteristics with short-term sleep restriction, but there are few studies on skin characteristics when sleep is restricted more than three consecutive days. This study evaluated skin changes with sleep limited to 4hours per night for six nights. The study included 32 Korean women in their 40s. Skin hydration, desquamation, barrier recovery, texture, gloss, transparency, elasticity, crow's feet, frown lines, and color were measured. Individual sleep time was monitored by smartwatches. Subjects slept 8hours per night for six nights in week one and 4hours per night for six nights in week two. Skin hydration was significantly reduced after 1day of sleep deprivation, and it continued to decrease. Skin gloss, desquamation, transparency, elasticity, and wrinkles were significantly aggravated after 1day of sleep deprivation. Skin texture was significantly aggravated on the fourth day of sleep restriction. Elasticity was most affected by reduced sleep, with a standardized coefficient of -.320, indicating a significant decrease over time as compared to other characteristics. Skin hydration was gradually decreased with sleep restriction. Skin texture did not change after only 1day of sleep restriction. It is a new finding that elasticity decreases more than other skin characteristics with prolonged sleep restriction.

Bone turnover is altered during 72 h of sleep restriction: a controlled laboratory study.

The objective of the study was to evaluate how controlled, short-term sleep restriction (SR; 72 h) alters markers of bone formation and resorption and urinary calcium (Ca) output. Ten healthy, sleep-adequate, male soldiers were housed in the research facility one day prior to and for the duration of SR. Diet was controlled to provide adequate energy balance and macronutrient distribution, meeting the recommended dietary allowance (RDA) for Ca. Subjects engaged in light activities to maintain wakefulness and were allowed 2 h of sleep per night (0430-0630 hours). Blood samples were collected each morning at 0 h (baseline) and 24, 48, and 72 h of SR. Serum was assayed for parathyroid hormone (PTH), bone alkaline phosphatase (BAP), tartrate-resistant acid phosphatase (TRAP), and C-terminal telopeptide of type I collagen (CTX). Urine was collected in 24 h increments during SR for measurement of Ca and creatinine (Cr). BAP was reduced at 24 h (P= 0.015) and resorption markers TRAP and CTX were increased after 48 and 72 h of SR compared to baseline (P < 0.05). The ratio of BAP:TRAP was significantly lower (P= 0.017) at 48 and 72 h of SR. In contrast, total 24 h urinary Ca and Ca/Cr excretion were unchanged. Markers of bone formation and resorption are uncoupled in response to as little as 48 h of SR even when Ca intake is at the RDA. Sleep deprivation may be a risk factor for reduced bone health due to perturbations in bone turnover.

Five Nights of Sleep Restriction Attenuates Microvascular Endothelial Function

Adequate sleep is requisite for optimal physiological function, including microvascular endothelial function. Short‐term sleep restriction (5 hours/night) negatively alters glucose metabolism and may also impair microvascular endothelial function via increased sympathetic nervous system activity and inflammatory pathways. The cutaneous microvasculature represents an accessible, well‐described vascular bed to non‐invasively assess the effects of sleep restriction on microvascular function. Our objective was to evaluate cutaneous microvascular endothelial function during baseline sleep replete conditions (10 hours/night time in bed), after 5 nights of sleep restriction (5 hours/night), and again after 2 nights of recovery sleep repletion. This was part of the Sleep Restriction Study (PI: Chang), an 11‐day inpatient study that took place in the Penn State University Clinical Research Center, during which diet and physical activity were controlled. Eight young, healthy men (23.3 ± 3.4 years) participated in the study. Cutaneous microvascular function was measured utilizing a standardized local skin heating protocol to induce endothelial nitric oxide‐synthase‐dependent vasodilation during all three study phases (baseline, sleep restricted, recovery). Red cell flux (laser Doppler flowmetry) was continuously measured on the ventral forearm at thermoneutral temperature (33 °C) and throughout local heating 0.5°C·5 s−1 to 42 °C until a stable (20 min) plateau had been reached. Red cell flux was normalized to cutaneous vascular conductance (CVC: flux·MAP−1) and expressed as a percentage of maximum CVC (43°C: %CVCmax). Compared to the baseline sleep replete state, the response to local heating was attenuated by 10% after 5 nights of sleep restriction (baseline: 89.2 ± 2.0, restricted: 80.4 ± 3.0 %CVCmax; p=0.045) and fully recovered after 2 nights of recovery sleep (88.7 ± 1.8 %CVCmax; p=0.99 compared to baseline). Maximum CVC was not affected by sleep restriction (all p&gt;0.05). These results suggest that 5 nights of sleep restriction impairs microvascular endothelial function, likely through attenuated nitric oxide‐dependent vasodilation, but that 2 nights of recovery sleep restores microvascular endothelial function in young, healthy men.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Does one night of partial sleep deprivation affect the evening performance during intermittent exercise in Taekwondo players?

Athletes and coaches believe that adequate sleep is essential for peak performance. There is ample scientific evidence which support the conclusion that sleep loss seems to stress many physiological functions in humans. The aim of this study was to determine the effect of one night’s sleep deprivation on intermittent exercise performance in the evening of the following day. Ten male Taekwondo players performed the Yo-Yo intermittent recovery test (YYIRT) in three sleep conditions (reference sleep night [RN], partial sleep deprivation at the beginning of night [PSDBN], partial sleep deprivation at the end of night [PSDEN]) in a counterbalanced order, allowing a recovery period ≥36 hr in between them. Heart rate peak (HRpeak), plasma lactate concentrations (Lac) and rating of perceived exertion (RPE) were measured during the test. A significant effect of sleep restriction was observed on the total distance covered in YYIRT (P<0.0005) and Lac (P<0.01) in comparison with the RN. In addition, performance more decreased after PSDEN (P<0.0005) than PSDBN (P<0.05). Also, Lac decreased significantly only after PS-DEN (P<0.05) compared with RN. However, there were no significant changes in HRpeak and RPE after the two types of partial sleep deprivation compared to RN. The present study indicates that short-term sleep restriction affect the intermittent performance, as well as the Lac levels of the Taekwondo players in the evening of the following day, without alteration of HRpeak and RPE.

Inter-Individual Differences in Neurobehavioural Impairment following Sleep Restriction Are Associated with Circadian Rhythm Phase.

Although sleep restriction is associated with decrements in daytime alertness and neurobehavioural performance, there are considerable inter-individual differences in the degree of impairment. This study examined the effects of short-term sleep restriction on neurobehavioural performance and sleepiness, and the associations between individual differences in impairments and circadian rhythm phase. Healthy adults (n = 43; 22 M) aged 22.5 ± 3.1 (mean ± SD) years maintained a regular 8:16 h sleep:wake routine for at least three weeks prior to laboratory admission. Sleep opportunity was restricted to 5 hours time-in-bed at home the night before admission and 3 hours time-in-bed in the laboratory, aligned by wake time. Hourly saliva samples were collected from 5.5 h before until 5 h after the pre-laboratory scheduled bedtime to assess dim light melatonin onset (DLMO) as a marker of circadian phase. Participants completed a 10-min auditory Psychomotor Vigilance Task (PVT), the Karolinska Sleepiness Scale (KSS) and had slow eye movements (SEM) measured by electrooculography two hours after waking. We observed substantial inter-individual variability in neurobehavioural performance, particularly in the number of PVT lapses. Increased PVT lapses (r = -0.468, p < 0.01), greater sleepiness (r = 0.510, p < 0.0001), and more slow eye movements (r = 0.375, p = 0.022) were significantly associated with later DLMO, consistent with participants waking at an earlier circadian phase. When the difference between DLMO and sleep onset was less than 2 hours, individuals were significantly more likely to have at least three attentional lapses the following morning. This study demonstrates that the phase of an individual’s circadian system is an important variable in predicting the degree of neurobehavioural performance impairment in the hours after waking following sleep restriction, and confirms that other factors influencing performance decrements require further investigation.

Short Duration of Sleep Is Associated with Hyperleptinemia in Taiwanese Adults

Higher plasma levels of leptin have been associated with increased cardiometabolic risk. The aim of this study was to investigate the association between short duration of sleep and hyperleptinemia in Taiwanese adults. We examined the association between duration of sleep and hyperleptinemia in 254 men and women recruited from the physical examination center at a regional hospital in southern Taiwan. Hyperleptinemia was defined as a plasma leptin level of 8.13 ng/mL and above. Short sleep duration was defined as < 6.5 h/day. Multiple logistic regression analysis was used to assess the association between short duration of sleep and hyperleptinemia. In females, short duration of sleep (< 6.5 h/day; OR = 2.15, 95% CI = 0.99-4.78), greater hip circumference (OR = 3.00, CI = 1.13-8.78), higher percent body fat (OR = 1.75, CI = 1.07-2.95), and higher white blood cell counts (OR = 1.67, CI = 1.26-2.28) were associated with an increased risk of hyperleptinemia. In males, greater body weight was significantly associated with an increased risk of hyperleptinemia (OR = 3.55, 95% CI = 1.46-10.23). There was also a trend of association (p = 0.096) between short duration of sleep and an increased risk of hyperleptinemia (OR = 4.98, 95% CI = 0.80-42.40). In this study of healthy Taiwanese adults, short duration of sleep was significantly associated with hyperleptinemia in women, and the association was independent of adiposity.

No effects of short‐term sleep restriction, in a controlled feeding setting, on lipid profiles in normal‐weight adults

Short sleep has been associated with cardiovascular risk. The aim of this study was to determine the impact of short-term sleep restriction on lipid profiles and resting blood pressure factors in young, normal-weight individuals (14 men, 13 women). Participants were randomized to five nights of either habitual (9h) or short (4h) sleep in a cross-over design separated by a 3-week washout period. There was no sleep×day interaction on lipid profile and blood pressure. Short-term sleep restriction does not alter lipid profiles and resting blood pressure in healthy, normal-weight individuals. The association between short sleep and increased cardiovascular risk reported in the epidemiological literature may be the result of long-term sleep restriction and poor lifestyle choices.

Sleep restriction is not associated with a positive energy balance in adolescent boys

A short sleep (SS) duration has been linked to obesity in observational studies. However, experimental evidence of the potential mechanisms of sleep restriction on energy balance is conflicting and, to our knowledge, nonexistent in adolescents. We investigated the effects of 3 consecutive nights of partial sleep deprivation on components of energy balance. In a randomized, crossover design, 21 healthy, normal-weight male adolescents (mean ± SD age: 16.8 ± 1.3 y) completed the following 2 experimental conditions, each for 3 consecutive nights: an SS (4 h/night) and a long sleep (LS; 9 h/night) duration. Endpoints were 24-h energy expenditure (EE), spontaneous physical activity (SPA), postintervention diet-induced thermogenesis (DIT), appetite sensations, ad libitum energy intake (EI), and profiles of plasma ghrelin and leptin. The 24-h EE on day 3 was 370 ± 496 kJ higher in the SS condition than in the LS condition (P = 0.003). This difference in EE was explained by prolonged wakefulness in the SS condition and a 19% higher SPA (P = 0.003). In a postintervention breakfast-meal challenge, there was a 0.19-kJ/min smaller incremental AUC in DIT over 4 h in the SS condition than in the LS condition (P = 0.012) with no time × condition effect (P = 0.29). Subjects consumed 13% less energy in the ad libitum meal in the SS condition (P = 0.031), with a concomitant decreased motivation to eat. Concentrations of ghrelin and leptin remained unchanged with sleep restriction. Short-term sleep restriction in male adolescents is associated with a small negative energy balance driven by increased EE from prolonged wakefulness and a concomitant decreased EI and motivation to eat. This trial was registered at clinicaltrials.gov as NCT01198431.

Does inadequate sleep play a role in vulnerability to obesity?

The prevalence of obesity is increasing rapidly worldwide, which is cause for concern because obesity increases the risk of cardiovascular disease and diabetes, reduces life expectancy, and impairs quality of life. A better understanding of the risk factors for obesity is therefore a critical global health concern, and human biologists can play an important role in identifying these risk factors in various populations. The objective of this review is to present the evidence that inadequate sleep may be a novel risk factor associated with increased vulnerability to obesity and associated cardiometabolic disease. Experimental studies have found that short-term sleep restriction is associated with impaired glucose metabolism, dysregulation of appetite, and increased blood pressure. Observational studies have observed cross-sectional associations between short sleep duration (generally <6 h per night) and increased body mass index or obesity, prevalent diabetes, and prevalent hypertension. Some studies also reported an association between self-reported long sleep duration (generally >8 h per night) and cardiometabolic disease. A few prospective studies have found a significant increased risk of weight gain, incident diabetes, and incident hypertension associated with inadequate sleep. Given the potential link between inadequate sleep and obesity, a critical next step is to identify the social, cultural, and environmental determinants of sleep, which would help to identify vulnerable populations. Future human biology research should consider variation in sleep characteristics among different populations and determine whether the associations between sleep and obesity observed in Western populations persist elsewhere.

Short Sleep Duration Promoting Overconsumption of Food: A Reward-Driven Eating Behavior?

Short Sleep Duration Promoting Overconsumption of Food: A Reward-Driven Eating Behavior?

CNS arousal and neurobehavioral performance in a short‐term sleep restriction paradigm

Few studies have investigated waking electrophysiological measures of arousal during sleep restriction. This study examined electroencephalogram (EEG) activity and performance during a 96-hour laboratory protocol where participants slept a baseline night (8 h), were randomly assigned to 3-, 5-, or 8-hour sleep groups for the next two nights sleep restriction (SR1, SR2), and then slept a recovery night (8 h). There were dose-dependent deficits on measures of mood, sleepiness, and reaction time that were apparent during this short-term bout of sleep restriction. The ratio of alpha to theta EEG recorded at rest indicated dose-dependent changes in CNS arousal. At 9:00 hours, both the 3- and 5-hour groups showed EEG slowing (sleepiness) during restriction, with the 3-hour group exhibiting greater deficits. Later in the day at 13:00 hours, the 5-hour group no longer exhibited EEG slowing, but the extent of slowing was more widespread across the scalp for the 3-hour group. High-frequency EEG, a measure of effort, was greater on the mornings following sleep restriction. The 5-hour group had increased beta EEG at central-parietal sites following both nights of restriction, whereas the 3-hour group had increased beta and gamma EEG at occipital regions following the first night only. Short-term sleep restriction leads to deficits in performance as well as EEG slowing that correspond to the amount and duration of sleep loss. High-frequency EEG may be a marker of effort or compensation.

Sleep restriction increases white blood cells, mainly neutrophil count, in young healthy men: A pilot study

This study examines the effects of sleep restricted to four hours for three consecutive nights on blood parameters, known to be associated with cardiovascular risk, in young healthy men. Eight young healthy men (age 24.5 +/- 3.3 years) were studied in the sleep restricted group. Nine young healthy men (age 24 +/- 2 years) were included in the control group and spent the days and nights in the sleep lab, while sleeping eight hours/night. One baseline night was followed by three nights of sleep restriction to four hours and by one recovery night of eight hours. Blood samplings were performed after the baseline night and after the third night of sleep restriction or without restriction for the control group. A significant increase in white blood cells (WBC) (5.79 +/- 1.05 vs. 6.89 +/- 1.31 10(3) cell/microl, p = 0.03), and neutrophils (3.17 +/- 0.69 vs 4.24 +/- 0.97 10(3) cell/microl, p = 0.01) was observed after the third night of sleep restriction. Other blood parameters were not affected. No significant variation was observed in the control group. Sleep restriction affected WBC count, mainly neutrophils, considered as risk factor for cardiovascular disease. Stress induced by the short term sleep restriction could be involved in this observation.