One week after the diet switch, there is a strong correlation between body weight change and wake change G and wake to NREM transitions in the dark phase H. DIO, diet-induced obesity; NREM, nonrapid eye movement; RC, regular chow.

We also assessed how absolute wakefulness was affected at Week 9 between these comparisons. These changes to total wake time were again accompanied by concomitant changes in NREM sleep time Figure S2B.

We found large changes to bout architecture 1 w following the diet switch, with acute HFD fragmenting and acute RC consolidating both sleep and wakefulness. We observed similar trends for NREM bout number and length during the dark phase Figure S2C and S2D.

We also analyzed how absolute bout architecture compared at Week 9. One week of HFD trended toward fragmenting wakefulness during the dark phase, but 1 w of RC significantly consolidated wakefulness and NREM sleep during the dark phase Table 2.

Thus, HFD or RC consumption for 1 w can significantly alter sleep and wakefulness. Previous studies have shown that switching mice with DIO back to RC for at least 4 w can rescue sleep behavior and even cognitive ability.

We found sleep architecture was similar between groups of mice that consumed the same diet during the final week, regardless of their chronic diet. We analyzed delta power using two different methods, both of which are commonly used in sleep research.

We performed sleep deprivation during ZT 0—6 by a combination of novel enrichment and gentle handling. Thus, we found no evidence to indicate that sleep homeostasis is affected by either acute or chronic dietary manipulations. NREM sleep delta power 1—4 Hz during undisturbed sleep recordings A,B and following 6-h sleep deprivation C,D.

Total wake E , NREM F , and REM sleep G during the sleep deprivation Zeitgeber time ZT 0—6 and recovery period ZT 6— There are no differences between any dietary condition comparisons, indicating that sleep homeostasis in unaffected by dietary changes or diet-induced obesity.

Additionally, we found no differences in recovery sleep following forced wakefulness, indicating that the changes observed cannot be explained by alterations in sleep homeostasis. Multiple reports, including this present study, have found that wakefulness is decreased in obese animal models.

Both strains of transgenic leptin-deficient mice spent less time in REM sleep compared with wild-type controls. There are a few methodological differences that may explain these disparities.

First, DIO experiments require long periods of social isolation while weight gain manifests, whereas genetically induced obese animals are only isolated directly prior to sleep recordings. Younger animals are more susceptible to depressive-like symptoms following stress, such as isolation.

Future studies could use advanced sleep recording techniques i. Additionally, it is possible that REM sleep is affected by acute diet switch.

Previous studies have consistently found worsened wake and sleep fragmentation in both genetically obese animals and those with DIO. Conversely, DIO mice acutely consuming RC exhibit normalized bout fragmentation during the active phase.

Multiple linear regression analysis revealed that the dietary condition, but not the animals' body weight, was significantly associated with the number of short wake bouts Table 3. Thus, acute diet switch drove significant, bidirectional changes to wake bout stability independent of body weight.

Prior studies found less dramatic changes to bout length and number at earlier time points. Nonetheless, diet-induced effects on fragmentation are consistent between studies, although future work needs to confirm the onset of this phenotype. Genetically obese mice are fed a standard chow diet, but are in a state of perpetual weight gain and obesity.

Last, our linear regression analysis determined that both body weight and dietary condition significantly contribute to modeling wake time. Interestingly, only dietary condition was significantly related to wake fragmentation, specifically the number of short wake bouts during the dark phase.

Nonetheless, future work with different diets e. Increased delta power 1—4 Hz following sleep deprivation indicates the depth and intensity of sleep, and is the current gold standard for testing sleep homeostasis. Chronic HFD increased NREM sleep and decreased wakefulness during the beginning of the dark phase, when the activity of mice peaks.

Further, wake and NREM fragmentation increased during the dark phase. Acute diet switch also affected total wake and NREM time with no effect on REM , but these effects were not localized to a particular time of day.

Taken together, we hypothesize that HFD induces wake bout instability during the active phase, which leads to increased total sleep time across the day. Orexin or hypo-cretin signaling is necessary for wake bout stability, because disruption of this pathway induces narcolepsy.

There are some inherent limitations with this study design. First, we tracked caloric intake throughout the study, but we did not measure energy expenditure and locomotor activity. Without information about both intake and expenditure, energy balance cannot be directly quantified.

One possibility is that caloric intake was overestimated for RC-fed conditions because some mice will shred this diet, making accurate measurements difficult. However, caloric intake may indeed be similar at these time points, suggesting that changes in caloric expenditure drives the energy imbalance and body weight changes.

Future studies need to measure all aspects of energy balance by directly assessing caloric intake, energy expenditure, and locomotor activity. Second, we did not determine if sleep and wakefulness are affected earlier than 1 w after dietary manipulations.

Last, there are important differences between the control RC diet and the HFD. The HFD has a much better taste than the RC, which affects motivated and hedonic food intake. Future studies need to control for the diet content, consistency, and presentation e.

In summary, we have found that short-term changes to diet bidirectionally affect energy balance i. These findings are consistent with obese patients who, after undergoing bariatric surgery, report improvements in sleepiness and vigilance despite still being quite obese.

The authors thank Brendan Keenan for his helpful discussions regarding statistical analysis and his insightful comments and edits to the manuscript. We would also like to thank Matthew Hayes for his technical advice.

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Journal Article. Perron, BS , Isaac J. Perron, BS. Perron, BS, S. Oxford Academic. Allan I. Pack, MBChB, PhD. Sigrid Veasey, MD. Revision received:. PDF Split View Views. Cite Cite Isaac J. Select Format Select format. ris Mendeley, Papers, Zotero.

enw EndNote. bibtex BibTex. txt Medlars, RefWorks Download citation. Permissions Icon Permissions. Abstract Study Objectives:. diet switch , fragmentation , high fat diet , obesity , sleep. Figure 1. Open in new tab Download slide. Figure 2. Table 1 High-fat diet-induced obesity significantly fragments both wakefulness and sleep.

Open in new tab. Figure 3. Figure 4. Figure 6. Table 2 Acute diet switch significantly fragments or consolidates sleep and wakefulness.

Figure 5. Figure 7. Prevalence of childhood and adult obesity in the United States, Google Scholar Crossref. Search ADS. Daytime sleepiness in obesity: mechanisms beyond obstructive sleep apnea--a review.

The effect of CPAP in normalizing daytime sleepiness, quality of life, and neurocognitive function in patients with moderate to severe OSA.

Polysomnography before and after weight loss in obese patients with severe sleep apnea. Waking and sleeping in the rat made obese through a high-fat hypercaloric diet. Daily acclimation handling does not affect hippocampal long-term potentiation or cause chronic sleep deprivation in mice. High-fat diet disrupts behavioral and molecular circadian rhythms in mice.

Google Scholar PubMed. OpenURL Placeholder Text. Western diet increases wheel running in mice selectively bred for high voluntary wheel running. Dietary therapy mitigates persistent wake deficits caused by mild traumatic brain injury.

High-fat diet consumption disrupts memory and primes elevations in hippocampal IL-1beta, an effect that can be prevented with dietary reversal or IL-1 receptor antagonism.

Elevated sleep quality and orexin receptor mRNA in obesity-resistant rats. Social defeat and isolation induce clear signs of a depression-like state, but modest cardiac alterations in wild-type rats. The effects of environmental enrichment on depressive and anxiety-relevant behaviors in socially isolated prairie voles.

Chronic social instability induces anxiety and defective social interactions across generations. Google Scholar OpenURL Placeholder Text. The sleep disorder canine narcolepsy is caused by a mutation in the hypocretin orexin receptor 2 gene. Genetic ablation of orexin neurons in mice results in narcolepsy, hypophagia, and obesity.

Hypothalamic prepro-orexin mRNA level is inversely correlated to the non-rapid eye movement sleep level in high-fat diet-induced obese mice. High fat diet induces specific pathological changes in hypothalamic orexin neurons in mice. Homeostatic and hedonic signals interact in the regulation of food intake.

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For more accurate results please sign in Sign in. Resource sharing is only allowed under specific terms and conditions. See Details. Sleep patterns, diet quality and energy balance. Chaput, Jean-Philippe. Is Part Of. Behavioral psychophysiology. Biological and medical sciences.

digestive, oral, and skin physiology. Eating behavior. Energy Metabolism - physiology. Environmental health. Feeding Behavior - physiology. Feeding Behavior - psychology.

Fundamental and applied biological sciences. Internal medicine. Medical sciences. Metabolic diseases. Obesity - etiology. Obesity - psychology.

Sleep - physiology. Sleep in non-human animals. Short sleep duration, poor sleep quality, and later bedtimes are all associated with increased food intake, poor diet quality, and excess body weight.

Insufficient sleep seems to facilitate the ingestion of calories when exposed to the modern obesogenic environment of readily accessible food. Lack of sleep has been shown to increase snacking, the number of meals consumed per day, and the preference for energy-rich foods.

Proposed mechanisms by which insufficient sleep may increase caloric consumption include: 1 more time and opportunities for eating, 2 psychological distress, 3 greater sensitivity to food reward, 4 disinhibited eating, 5 more energy needed to sustain extended wakefulness, and 6 changes in appetite hormones.

Globally, excess energy intake associated with not getting adequate sleep seems to be preferentially driven by hedonic rather than homeostatic factors. Moreover, the consumption of certain types of foods which impact the availability of tryptophan as well as the synthesis of serotonin and melatonin may aid in promoting sleep.

Electrodes were attached to the scalp Cz, C3, C4, O1, O2, A1, A2, Gnd for electroencephalographic EEG recordings, above, below, and beside the eyes for horizontal and vertical electrooculogram, and on the chin for electromyogram. Recordings were scored offline by one investigator S.

according to standard criteria by Rechtschaffen and Kales, 11 and independently assessed by a second sleep laboratory analyst unaware of the study design and hypothesis.

The following sleep parameters were determined: sleep period time SPT, i. All participants attended a prestudy overnight recording session with PSG to ensure that they had normal sleep architecture.

Plasma glucose, insulin, leptin, serum lipids, TSH, free thyroxin, GH, and cortisol, as well as routine biochemical and hematological assays were performed using standard commercially available assays.

Concentrations of both total ghrelin and plasma orexin A were assessed using commercially available enzyme-linked immunosorbent assay kits for humans EZGRTK; Millipore, Billerica, MA and Uscn Life Science Inc. For overnight pulsatility analysis, we collected serum samples every 10 min from to , via a long line running from the participants to the adjacent room to avoid any interference with their sleep.

Cluster analysis was used for the detection of discrete TSH, GH, and cortisol peaks. For the current analysis a 2 × 1 test cluster configuration was used, two data points for the test nadir and one for the test peak, and a t -statistic of 2. The locations and widths of all significant concentration peaks were identified, the total number of peaks was counted, and the mean peak interval was calculated in minutes as well as peak height, width, and area.

In addition, valley mean and nadir, area under the curve, and total average value were calculated. Blood pressure was measured using a wrist-type blood pressure monitor OMRON Healthcare, Hamburg, Germany. Heart rate was measured continuously using a wireless sensor applied to the chest wall Actiheart, CamNtech Ltd, Cambridge, UK.

This digitalizes the electrocardiogram signal and stores the R-R interval time-series from which heart rate can be calculated.

Heart rate data was exported to a spreadsheet via Actiheart software version 4. Sleep data collected by the PSG device was examined to determine a window of time min between and during which each participant was asleep. Average heart rate while sleeping and on waking was calculated, and the difference between average asleep and average waking heart rate for each participant on each day was recorded.

Using validated questionnaires we collected data on neuroglycopenia and autonomic symptoms, 13 mood, 14 and sleepiness. We measured alertness by reaction times and error rates in a computer-based vigilance performance test during the three study phases. Unless specified otherwise, data are expressed as mean and SEM.

Data were tested for normality using graphical and numerical methods Shapiro-Wilk test. Data were compared by analysis of variance ANOVA with repeated measures to test for within-subjects changes.

The within-subjects P value was adjusted using the Greenhouse-Geisser correction factor for lack of sphericity. Pairwise comparisons of the study phases were performed by two-sided Student t -test when appropriate.

by multiplying the uncorrected P value by the number of comparisons. For analyses of correlation between fasting hormones and sleep parameters, the nonparametric Spearman correlation test was used and repeated in sensitivity analyses excluding outliers.

Data were analyzed using Stata software package version Twelve adult males mean age Blood pressure, body composition, baseline biochemical and hematological parameters, and self-reported quality of sleep scores were within normal ranges Table S1 in the supplemental material.

However, those individuals provided with ad libitum meals for a third day continued to overeat, eating 2, kcal in excess on the third day Figure 1A. Barcharts of changes in the duration of sleep stages at baseline, during caloric restriction, and free feeding; and scatterplots of overnight pulsatile secretion of thyroid-stimulating hormone, growth hormone, and cortisol.

Durations of all sleep stages were analyzed using analysis of variance ANOVA with repeated measures to test for within-subject changes. Pairwise comparisons of the three study phases were performed by two-sided Student t -test when appropriate.

A P value of 0. D—F Pulsatile secretion of thyroid-stimulating hormone D , growth hormone E and cortisol secretion F was measured in blood samples taken every 10 min from midnight until at baseline, after 2 days of caloric restriction and after 2 days of free feeding.

PSG recordings were performed at baseline, after CR and FF, and were visually scored by investigators blinded to the study design. TST and sustained sleep efficiency were not affected by changes in energy balance Table 1.

Disordered sleep has been associated with impaired memory retention. Alertness, as measured by reaction times and error rates in a vigilance performance test, did not change during the study data not shown. Sleep-dependent consolidation of procedural and declarative memory tested by a standard finger tapping task and paired associate word learning task were preserved during all study phases Figure S2 in the supplemental material and not modified by changes in energy balance.

There was a discrete improvement in overall mood score as assessed by the Profile Of Mood States POMS questionnaire immediately upon FF compared to CR, but no significant changes in mood subdomains Table S2 in the supplemental material.

Changes in energy balance can affect the hypothalamic regulation of pituitary hormone synthesis and secretion, which may in turn influence sleep architecture. We measured serum TSH, GH, and cortisol release a marker of hypothalamopituitary adrenal axis activation every 10 min for 6 h overnight when participants were asleep as confirmed by PSG recordings.

Mean hormone concentrations and parameters of pulsatile secretion were analyzed at baseline, after CR and FF using the pulse detection cluster algorithm Table 2 ; Table S3 in the supplemental material.

There were no differences in the number of pulses and pulse width. There was no change in the pulsatile secretion of GH from baseline to CR, whereas FF was associated with a decrease in mean GH concentrations and integrated total AUC compared to baseline and CR values Figure 1E ; Table 2.

In conjunction, the interval between peaks was longer during FF compared to baseline. No differences in cortisol secretion were seen as result of changes in energy balance Figure 1F ; Table S3 in the supplemental material. Analysis of pulsatile thyroid-stimulating hormone and growth hormone secretion.

To examine activation of the autonomic nervous system, we measured heart rate continuously throughout the study. The mean sleeping heart rate predominantly influenced by para-sympathetic tone was unchanged after CR but increased by 5. The increase in heart rate on waking sleeping-to-waking heart rate increment; predominantly due to sympathetic nervous system activation increased from 5.

Autonomic symptoms predominantly adrenergic were more prominent upon CR and decreased in FF Table S4 in the supplemental material.

Barcharts of changes in heart rate at baseline, during caloric restriction, and free feeding. Mean sleeping heart rate A and the sleeping-to-waking heart rate increment B were measured every night in all 12 participants at baseline, during caloric restriction and free feeding.

Vertical bars represent the standard error of the mean. Measurements were compared using analysis of variance ANOVA with repeated measures to test for within-subject changes.

Fasting plasma glucose decreased by 1. Plasma ghrelin levels exhibit diurnal variation, act as a short-term hunger signal peaking before meal initiation, and are affected by sleep restriction.

Barcharts of changes in peripheral hormones and orexin at baseline, during caloric restriction, and free feeding. Hormone levels were compared using analysis of variance ANOVA with repeated measures to test for within-subject changes.

We hypothesized that changes in peripheral hormones or in orexin might mediate the change in duration of stage 4 sleep seen with CR. Although there was no correlation between fasting leptin, insulin, or total ghrelin and the duration of stage 4 sleep in CR data not shown , plasma orexin levels correlated with specific sleep parameters after 48 h of CR Figure 4A.

Scatterplots of correlation of plasma orexin A levels with sleep parameters after 48 h of caloric restriction CR among nine participants. The duration of stage 4 sleep correlated positively with orexin level in CR A , as well as orexin decline from baseline to CR B.

There was no correlation between the number of awakenings and the absolute level of orexin in CR C. The number of awakenings in CR correlated negatively with orexin decline from baseline to CR D.

In this study we found that acute CR for 2 days significantly increased the duration of the deepest stage of sleep, stage 4 sleep. The effect of CR on stage 4 sleep was normalized with FF, which restored energy balance.

Our findings align with a study from the s that observed an increased duration of SWS stages 3 and 4 together and reduced REM sleep in males studied before and after four days of complete starvation associated with weight loss, with reversal of these changes in refeeding characterized by weight regain.

One possibility is that increasing the time spent in the deepest stage of sleep may allow for the conservation of energy resources in response to acute CR. To date, very little is known about sleep architecture in rare severely obese patients with congenital leptin deficiency, a disorder that is often complicated by marked central and obstructive sleep apneas own observations.

We found that the decline in plasma orexin from baseline to CR was positively correlated with the duration of stage 4 sleep in CR and inversely correlated with the number of awakenings.

This finding is intriguing but will require further investigation. We do not know whether, or how far, plasma orexin levels reflect orexin-mediated signaling in the brain. However, Strawn et al.

These observations in healthy volunteers are entirely consistent with studies in patients with genetic disruption of leptin signaling 34 , 35 and in individuals with obesity following weight loss 36 a state of partial leptin deficiency.

These physiological changes were predominantly mediated by falling leptin concentrations and could be reversed by concomitant leptin administration in previous studies. However, intriguingly, we found that these parameters exceeded baseline values after 2 days of FF.

The explanation for these findings is unclear. Such changes could contribute to an exaggerated compensatory response to CR, for example, by overeating. Some participants were studied during a third day of FF as we hypothesized that their food intake would return to baseline levels.

These findings warrant further investigation and, if replicated, may shed light on the physiological response to weight loss and the mechanisms that promote weight regain. In this study, we did not observe a significant change in GH pulses with CR in contrast to some, but not all, previous studies.

Notably, we found that mean GH concentrations and integrated total AUC were significantly reduced during FF compared to baseline and CR. The pulsatile secretion of GH is predominantly the product of stimulatory GH-releasing hormone GHRH -expressing neurons and inhibitory somatostatin-expressing neurons in the hypothalamus.

Leptin treatment of rats food deprived for 48 h increases somatostatin messenger RNA levels, 38 which would result in suppression of pulsatile GH secretion as seen in this study.

It is recognized that pulsatile GH secretion is suppressed in obesity, but it is striking that we observed comparable levels of GH suppression after 2 days of FF when participants were consuming excess calories but had restored energy balance.

Variations in pulsatile release define the physiological actions of GH, which is a critical mediator of insulin action and glucose homeostasis. We postulate that the suppression of GH secretion as seen in this study may reflect the physiological response to maintain glucose homeostasis in light of excess caloric consumption.

This hypothesis requires further testing in experimental studies. These studies provide a mechanistic framework for investigating the well-recognized associations between obesity and sleep disorders and between sleep debt and obesity risk.

The authors thank the volunteers who took part in the study, as well as Dr. Keith Burling and Dr. Peter Barker who performed the biochemical assays NIHR Cambridge Biomedical Research Centre Core Biochemical Assay Laboratory.

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Journal Article. Tinh-Hai Collet, MD , Tinh-Hai Collet, MD. Oxford Academic. Agatha A. van der Klaauw, MD. Elana Henning, BSocSc. Julia M.

Keogh, BSc. Diane Suddaby, BSc. Sekesai V. Dachi, BSc. Síle Dunbar, BSc. Sarah Kelway, BSc. Suzanne L. Dickson, PhD. Sadaf Farooqi, MD. Sebastian M. Schmid, MD Sebastian M. Effects of sleep restriction on body weight and food intake in healthy adults. Appetite ; 59 : e51 abstract. Effects of two five-day bouts of chronic sleep restriction on caloric intake in healthy adults.

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Effects of acute changes in scheduled sleep duration on eating behavior. Obesity ; 19 : S abstract. Kubota C, Hibi M, Mizuno T, Mitsui Y, Uchida S. Effect of sleep restriction on physical functions—a respiratory chamber study. LeCheminant JD, Romney L, Clark T, Bailey BW, Larson M, Tucker LA.

The relationship between sleep deprivation and the energy balance pathways of diet and physical activity. Med Sci Sports Exerc ; 45 : abstract. Tasali E, Broussard J, Day A, Kilkus J, Van Cauter E. Sleep curtailement in healthy young adults is associated with increased ad lib food intake.

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Partial sleep deprivation and energy balance in adults: an emerging issue for consideration by dietetics practitioners. J Acad Nutr Diet ; : — Download references.

GP and JD had primary responsibility for final content. All authors were substantially involved in the writing process. All authors read and approved the final manuscript.

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nature european journal of clinical nutrition original article article. Subjects Lifestyle modification Nutrition Risk factors. Conclusions: The pooled effects of the studies with extractable data indicated that PSD resulted in increased EI with no effect on EE, leading to a net positive energy balance, which in the long term may contribute to weight gain.

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An automated gas analysis system CPX Ultima CardiO2; Medical Graphics Corp, St Paul, MN was used to record breath-by-breath gas exchange measurements. These fat oxidation values were plotted against the relative-exercise intensity, expressed as the percentage of maximum oxygen uptake VO2max ; a third-degree polynomial curve was built to determine MFO and FATmax MFO was also expressed as MFO LM in order to relativize it to the lean mass.

Maximal carbohydrate oxidation was not included in the analyses since it is not a key factor of energy metabolism during exercise Indeed, our recent systematic review has analyzed a total of studies which included data about fuel oxidation during exercise None of those studies reported maximal carbohydrate oxidation during exercise.

The incremental protocol started at a speed of 5. We used the same indirect calorimetry and software as in the MFO assessment. Diet was assessed using three hour recalls carried out on 3 separate days 2 weekdays and 1 weekend day by a qualified and trained research dietitian.

Dietary recalls were done on different days than the MFO and VO 2 assessments. In the face-to-face interviews, the participants were asked to recall all food consumed during the previous day.

These data were introduced by two independent qualified and trained dietitians in the EvalFINUT® software. Energy and weight data of daily food and beverages were obtained from the hours recalls.

The traditional Mediterranean diet is associated with a lower prevalence of chronic diseases i. obesity, metabolic syndrome, cardiovascular diseases, cancer and mortality The adherence to the traditional Mediterranean Diet MedDiet was estimated by using the point questionnaire of adherence to the MedDiet used and validated in the PREDIMED trial The PREDIMED questionnaire includes 12 questions related to frequency intake of key foods and 2 questions related to specific dietary habits of the MedDiet.

Each question scores 0 or 1 point. The global score ranges from 0 to 14, being 0 points null adherence and 14 points complete adherence to the MedDiet. The PREDIMED questionnaire proved to be very useful in a large Spanish cohort for a quick adherence estimation to the traditional MedDiet The sample size and power calculations were made based on the data of a pilot study of the FIT-AGEING study This study aimed to compare the influence of different exercise programs on BMR, BFox and MFO in sedentary middle-aged adults.

We based the sample size calculations on a minimum predicted change in MFO of 0. The present study is based on a secondary analysis using baseline data from the FIT-AGEING study, and therefore a specific sample size calculation was not conducted.

We used the Shapiro—Wilk test, visual check of histograms, Q-Q and box plots to verify all variable distributions. The descriptive parameters were reported as mean and standard deviation. Given that we did not observe a sex interaction, we conducted the analysis including men and women together.

Simple linear regressions were performed to examine the association between sleep time and quality PSQI global score, total sleep time, sleep efficiency and wake after sleep onset with BMR, BMR LM , BFox, BCHox, MFO, MFO LM and FATmax. We also conducted multiple linear regression models to test these associations after adjusting for sex Model 1 , sex and age Model 2 and sex, age and FMI Model 3.

Pearson correlation was performed to assess the association between sleep parameters and dietary outcomes. To quantify the mediating role of dietary intake i. energy, macronutrient, fiber, ethanol and lipid profile intake, and PREDIMED total score in the relationship between sleep parameters and BMR and fuel oxidation, we conducted mediation analyses We used the PROCESS macro version 3.

Bootstrapping is a nonparametric resampling procedure that does not require the assumption of normality of the sampling distribution 46 The mediation was estimated using the indirect effect, which indicates the change in the effect of the independent variable on the outcome that can be endorsed to the proposed mediator.

All analyses were conducted using the Statistical Package for Social Sciences SPSS, v. Graphical presentations were prepared using GraphPad Prism 8 GraphPad Software, San Diego, CA, USA.

Ethical approval for the study was given by the Ethics Committee on Human Research at the University of Granada and Servicio Andaluz de Salud CEI-Granada N Written informed consent was obtained from all subjects.

This study was in accordance with the last revised ethical guidelines of the Declaration of Helsinki. The characteristics of the study sample are shown in Table 1. We repeated all previous associations controlling for menopausal status pre- or post-menopausal in order to avoid the possible cofounder of female hormones, and the results did not change data not shown.

We observed only a negative association of fiber intake and PSQI global score and cholesterol intake negatively and positively associated with total sleep time and wake after sleep onset respectively Table S5.

However, we observed a modification effect of different dietary factors i. fiber and ethanol intake; Table S5. S1 — S4. The main finding of the present study is that a poor subjective sleep quality was associated with lower BFox independently of sex, age and body composition outcomes.

No consistent association was observed between any sleep quality and time parameters with BMR, MFO and FATmax. Moreover, our results indicated that the association of PSQI global score with BFox was not mediated by dietary intake and MedDiet adherence.

We observed an inverse association between total sleep time and BMR which disappeared after controlling for confounders. The energy expenditure is lowest during sleep, therefore a high total sleep time is related with a prolonged period of the lowest energy expenditure Sleep deprivation could increase energy expenditure since energy expenditure is reduced during sleep Sharma et al.

proposed that these reduction in energy expenditure could be influenced by circadian rhythm, body temperature and muscle temperature However, the results should be interpreted with caution because this association disappeared after controlling for sex, age and FMI. Several physiological mechanisms could explain the relationship between sleep quality and BFox.

Sleep restriction is associated with insulin resistance characterized by a decreased insulin-mediated glucose uptake 49 , which could develop metabolic inflexibility characterized by an impaired BFox Short sleep duration and sleep fragmentation arealso related to low leptin levels or leptin resistance 51 which are associated with an impaired fatty acid oxidation Sleep disruption discontinuity of sleep can lead to the disruption of circadian rhythms 13 , which orchestrate crucial physiological and behavioral functions, being one of these the regulation of carbohydrate and fatty acid metabolism Higher sleep duration and quality are associated with a healthier gut microbiome 53 , which could suppress insulin signaling, increase β-oxidation and inhibit fat oxidation derived from the production of short-chain fatty acids Furthermore, sleep disruption discontinuity of sleep could decrease melatonin production 13 , which has important metabolic functions, such as lipolysis, regulating the energy flow An increase in the production of pro-inflammatory cytokines and reactive oxygen species is observed in impaired sleep patterns Both inflammation and oxidative stress could modulate metabolic flexibility, specifically fat oxidation 56 , Therefore, based on the above-mentioned mechanisms, a healthy sleep pattern could improve metabolic health via the increment of BFox and viceversa.

In addition, an impaired sleep pattern, determined by a low sleep duration could increase energy intake through several potential mechanisms: increment of time and opportunities for eating, psychological distress, sensitivity to food reward, energy needed to sustain wakefulness, hunger hormones and decrease dietary restraint A lack of sleep or low sleep quality could increase the intake of high energy-dense foods, high fat and sugary snacks, which are low in fiber In this sense, although we did not find any association between energy and macronutrient intake, we observed that fiber intake was negatively associated with PSQI global score.

Fiber intake could have different metabolic effects i. insulin sensitivity and glycemia improvement 58 , that could have a potential role in the regulation of fat oxidation. However, we did not find any mediating role of dietary intake i. fiber intake between the association of PSQI with BFox.

The lack of a mediating role may be due to specific issues: i since dietary outcomes were assessed in a specific time point, it could be that the dietary intake was insufficiently maintained over time to modify BFox; ii the possible lower and upper threshold for when dietary intake i.

fat intake could modify fat oxidation 59 ; iii the inter-individual variability, body composition and metabolic status influence on fat oxidation 8 ; iv a sleep patterns insufficiently maintained over time.

The lack of association between any sleep outcomes with BMR and MFO could be explained by different factors. Sleep is a complex phenomenon influenced by behavioral and physiological mechanisms i.

These factors could influence the relationship between sleep parameters and BMR and MFO. We also observed an inverse association between total sleep time with MFO.

A previous study of Konishi et al. observed that a night of sleep deprivation did not affect MFO in healthy young men It has been reported several detrimental effects of long sleep for optimal health In addition, long sleep could increase fatigue, physiological deprivation, which could influence insulin resistance and hormonal imbalance Although the mechanisms are not clear, the above-mentioned mechanisms could have influenced this relationship.

Surprisingly, different results were observed when the association between sleep quality and energy metabolism was performed considering subjective instead of objective measures of sleep quality. It has been previously reported that PSQI and accelerometer records measure different attributes of sleep, highlighting the bias of accelerometry to register wakefulness, thus lying in bed awake but motionless is likely to be coded as sleep Therefore, it is recommended to use both methods to obtain complementary information additionally to the body movements These differences in measurement of sleep attributes could explain the different results of the associations between sleep quality and energy metabolism.

Despite accelerometer records and subjective measurements are a valid and extensively used measure of sleep quality 26 , 65 they cannot differentiate between rapid eye movement sleep REM and non-rapid eye movement sleep NREM , restricting the detailed assessment of the real biologic process of sleep.

REM and NREM phases are metabolically different In REM sleep glucose uptake is increased, leading to anaerobic glucose metabolism 67 , 68 , therefore sleep quality in each phase could be differently associated with energy metabolism.

Future studies that examine the relationship between REM and NREM sleep using polysomnography records with BMR and fuel oxidation in basal conditions and during exercise are needed. The present study should be interpreted with caution; the study has a cross-sectional design that does not allow to establish causal relationship.

sleep deprivation under well-controlled lab conditions in order to establish causal relationship. Furthermore, sleep and dietary parameters were assessed only in a specific timepoint, which do not allow us to extrapolate our results to chronic sleep or dietary patterns.

The difficulty of an accurate dietary evaluation with possible underreporting or misclassification should be considered, as in all cross-sectional studies. Lastly, the narrow PSQI global score range should be taken into account when interpreting our results. In conclusion, our study showed that a subjective poor sleep quality was associated with lower BFox.

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Pineal Res. Sala, C. Sleep patterns, diet quality and energy balance. Chaput, Jean-Philippe. Is Part Of. Behavioral psychophysiology. Biological and medical sciences. digestive, oral, and skin physiology. Eating behavior. Energy Metabolism - physiology.

Environmental health. Feeding Behavior - physiology. Feeding Behavior - psychology. Fundamental and applied biological sciences. Internal medicine. Medical sciences. Metabolic diseases. Obesity - etiology.

Obesity - psychology. Sleep - physiology. Sleep in non-human animals. Short sleep duration, poor sleep quality, and later bedtimes are all associated with increased food intake, poor diet quality, and excess body weight. Insufficient sleep seems to facilitate the ingestion of calories when exposed to the modern obesogenic environment of readily accessible food.

Lack of sleep has been shown to increase snacking, the number of meals consumed per day, and the preference for energy-rich foods.

Proposed mechanisms by which insufficient sleep may increase caloric consumption include: 1 more time and opportunities for eating, 2 psychological distress, 3 greater sensitivity to food reward, 4 disinhibited eating, 5 more energy needed to sustain extended wakefulness, and 6 changes in appetite hormones.

Globally, excess energy intake associated with not getting adequate sleep seems to be preferentially driven by hedonic rather than homeostatic factors. Moreover, the consumption of certain types of foods which impact the availability of tryptophan as well as the synthesis of serotonin and melatonin may aid in promoting sleep.

In summary, multiple connections exist between sleep patterns, eating behavior and energy balance. Sleep should not be overlooked in obesity research and should be included as part of the lifestyle package that traditionally has focused on diet and physical activity. Abstract There is increasing evidence showing that sleep has an influence on eating behaviors.