Experimental sleep curtailment causes wake-dependent increases in 24-h energy expenditure as measured by whole-room indirect calorimetry.

BACKGROUND: Epidemiologic evidence has shown a link between short sleep and obesity. Clinical studies suggest a role of increased energy intake in this relation, whereas the contributions of energy expenditure (EE) and substrate utilization are less clearly defined. OBJECTIVE: Our aim was to investigate the effects of sleep curtailment on 24-h EE and respiratory quotient (RQ) by using whole-room indirect calorimetry under fixed-meal conditions. DESIGN: Ten females aged 22-43 y with a BMI (in kg/m²) of 23.4-27.5 completed a randomized, crossover study. Participants were studied under short- (4 h/night) and habitual- (8 h/night) sleep conditions for 3 d, with a 4-wk washout period between visits. Standardized weight-maintenance meals were served at 0800, 1200, and 1900 with a snack at 1600. Measures included EE and RQ during the sleep episode on day 2 and continuously over 23 h on day 3. RESULTS: Short compared with habitual sleep resulted in significantly higher (± SEM) 24-h EE (1914.0 ± 62.4 compared with 1822.1 ± 43.8 kcal; P = 0.012). EE during the scheduled sleep episode (0100-0500 and 2300-0700 in short- and habitual-sleep conditions, respectively) and across the waking episode (0800-2300) were unaffected by sleep restriction. RQ was unaffected by sleep restriction. CONCLUSIONS: Short compared with habitual sleep is associated with an increased 24-h EE of ~92 kcal (~5%)--lower than the increased energy intake observed in prior sleep-curtailment studies. This finding supports the hypothesis that short sleep may predispose to weight gain as a result of an increase in energy intake that is beyond the modest energy costs associated with prolonged nocturnal wakefulness.

Metabolic consequences of chronic sleep restriction in rats: changes in body weight regulation and energy expenditure.

Epidemiological studies have shown an association between short or disrupted sleep and an increased risk to develop obesity. In animal studies, however, sleep restriction leads to an attenuation of weight gain that cannot be explained by changes in energy intake. In the present study, we assessed whether the attenuated weight gain under conditions of restricted sleep is a consequence of an overall increase in energy expenditure. Adult male rats were subjected to a schedule of chronic sleep restriction (SR) for 8 days with a 4h window of unrestricted rest per day. Electroencephalogram and electromyogram recordings were performed to quantify the effect of the sleep restriction schedule on sleep-wake patterns. In a separate experiment, we measured sleep restriction-induced changes in body weight, food intake, and regulatory hormones such as glucose, insulin, leptin and corticosterone. To investigate whether a change in energy expenditure underlies the attenuation of weight gain, energy expenditure was measured by the doubly labeled water method from day 5 until day 8 of the SR protocol. Results show a clear attenuation of weight gain during sleep restriction but no change in food intake. Baseline plasma glucose, insulin and leptin levels are decreased after sleep restriction which presumably reflects the nutritional status of the rats. The daily energy expenditure during SR was significantly increased compared to control rats. Together, we conclude that the attenuation of body weight gain in sleep restricted rats is explained by an overall increase in energy expenditure together with an unaltered energy intake.

Effects of sleep fragmentation in healthy men on energy expenditure, substrate oxidation, physical activity, and exhaustion measured over 48 h in a respiratory chamber.

BACKGROUND: Epidemiologic studies show an inverse or U-shaped relation between sleep duration and BMI. Decreases in total energy expenditure (TEE) and physical activity have been suggested to be contributing factors. OBJECTIVE: The objective was to assess the effect of sleep fragmentation on energy metabolism and energy balance in healthy men. DESIGN: Fifteen healthy male subjects [mean ± SD BMI (in kg/m(2)): 24.1 ± 1.9; age: 23.7 ± 3.5 y] were included in a randomized crossover study in which energy expenditure, substrate oxidation, and physical activity (by radar) were measured twice for 48 h in a respiration chamber while subjects were monitored by electroencephalography to determine slow-wave sleep (SWS), rapid eye movement (REM) sleep, and total sleeping time (TST). During 2 nights, sleep (2330-0730 h) was either fragmented or nonfragmented. RESULTS: Fragmented sleep led to reductions in TST, SWS, and REM sleep (P < 0.001). TEE did not differ (9.96 ± 0.17 compared with 9.83 ± 0.13 MJ/d, NS) between the sleep groups, nor did the components of energy expenditure, with the exception of activity-induced energy expenditure (AEE; 1.63 ± 0.15 compared with 1.42 ± 0.13 MJ/d for fragmented and nonfragmented sleep, respectively; P < 0.05). Physical activity, exhaustion, sleepiness, respiratory quotient (RQ), and carbohydrate oxidation were elevated in comparison with nonfragmented sleep [physical activity counts: 2371 ± 118 compared with 2204 ± 124 counts/d, P < 0.02; exhaustion: 40.1 ± 3.8 compared with 21.8 ± 2.4 mm (by using a visual analog scale; VAS), P < 0.001; sleepiness: 47.4 ± 4.2 compared with 33.9 ± 4.6 mm (VAS), P < 0.001; RQ: 0.94 ± 0.04 compared with 0.91 ± 0.03, P < 0.05; and carbohydrate oxidation: 346.3 ± 23.8 compared with 323.7 ± 22.5 g/d, P < 0.05], whereas fat oxidation was reduced (29.1 ± 9.1 compared with 61.0 ± 6.6 g/d, P < 0.01). CONCLUSIONS: Fragmented compared with nonfragmented sleep induced reductions in the most important sleep phases, which coincided with elevated AEE, physical activity, exhaustion, and sleepiness. RQ and carbohydrate oxidation increased and fat oxidation decreased, which may predispose to overweight. This trial is registered at www.who.int/ictrp and www.trialregister.nl as NTR1919.

Energy expenditure during sleep, sleep deprivation and sleep following sleep deprivation in adult humans.

Sleep has been proposed to be a physiological adaptation to conserve energy, but little research has examined this proposed function of sleep in humans. We quantified effects of sleep, sleep deprivation and recovery sleep on whole-body total daily energy expenditure (EE) and on EE during the habitual day and nighttime. We also determined effects of sleep stage during baseline and recovery sleep on EE. Seven healthy participants aged 22 ± 5 years (mean ± s.d.) maintained ∼8 h per night sleep schedules for 1 week before the study and consumed a weight-maintenance diet for 3 days prior to and during the laboratory protocol. Following a habituation night, subjects lived in a whole-room indirect calorimeter for 3 days. The first 24 h served as baseline ­ 16 h wakefulness, 8 h scheduled sleep ­ and this was followed by 40 h sleep deprivation and 8 h scheduled recovery sleep. Findings show that, compared to baseline, 24 h EE was significantly increased by ∼7% during the first 24 h of sleep deprivation and was significantly decreased by ∼5% during recovery, which included hours awake 25-40 and 8 h recovery sleep. During the night time, EE was significantly increased by ∼32% on the sleep deprivation night and significantly decreased by ∼4% during recovery sleep compared to baseline. Small differences in EE were observed among sleep stages, but wakefulness during the sleep episode was associated with increased energy expenditure. These findings provide support for the hypothesis that sleep conserves energy and that sleep deprivation increases total daily EE in humans.

Energy expenditure is affected by rate of accumulation of sleep deficit in rats.

STUDY OBJECTIVES: Short sleep is a putative risk factor for obesity. However, prolonged total sleep deprivation (TSD) leads to negative energy balance and weight loss in rodents, whereas sleep-restricted humans tend to gain weight. We hypothesized that energy expenditure (VO2) is influenced by the rate of accumulation of sleep deficit in rats. DESIGN AND INTERVENTION: Six Sprague-Dawley rats underwent chronic sleep-restriction (CSR, 6-h sleep opportunity at ZT0-6 for 10 days) and stimulus-control protocols (CON, 12-h sleep opportunity for 10 days, matched number of stimuli) in a balanced cross-over design. Four additional rats underwent TSD (4 days). Sleep was manipulated using a motor-driven walking wheel. MEASUREMENTS AND RESULTS: Electroencephalography, electromyography, and body temperature were measured by telemetry, and VO2, by respirometry. Total sleep deficits of 55.1 +/- 6.4 hours, 31.8 +/- 6.8 hours, and 38.2 +/- 2.3 hours accumulated over the CSR, CON, and TSD protocols, respectively. Responses to TSD confirmed previous reports of elevated VO2 and body temperature. These responses were attenuated in CSR, despite a greater cumulative sleep deficit. Rate of rise of VO2 was strongly correlated with rate of accumulation of sleep deficit, above a threshold deficit of 3.6 h x day(-1). CONCLUSION: The change in VO2 is affected by rate of accumulation of sleep deficit and not the total sleep loss accrued. Negative energy balance, observed during TSD, is strongly attenuated when brief daily sleep opportunities are available to rats (CSR), despite greater accumulated sleep deficit.

Diurnal salivary cortisol levels in postpartum mothers as a function of infant feeding choice and parity.

Daily stress and sleep deprivation can influence the diurnal pattern of cortisol, which normally consists of high morning levels and a gradual decline throughout the day. While most individuals have consistent declining cortisol concentrations over days, others display either flat or inconsistent profiles. Postpartum mothers experience considerable home demands and sleep deprivation, yet, breastfeeding mothers perceive lower stress and reduced negative mood states compared to bottlefeeders. On the other hand, multiparity (having more than one child) is associated with reduced steepness in diurnal cortisol decline. Interestingly, no study to date has investigated the diurnal cortisol pattern and its stability across days in postpartum women as a function of their choice of infant feeding and parity. In this study, we measured salivary cortisol at four different time points during the day, on two non-consecutive days in first-time (primiparous) and second-time (multiparous) mothers at 5-20 weeks postpartum who were exclusively breastfeeding or bottlefeeding, and in non-postpartum mothers of young children (1-6 years). Among multiparous mothers, we found that cortisol levels in those who were bottlefeeding were higher than in breastfeeding mothers at both awakening and 1600 h. This effect remained significant after controlling for individual differences related to infant feeding choice, such as estradiol levels, education and income. No effect of infant feeding choice on cortisol concentrations was observed in primiparous mothers. While a consistent decline across days was common, some mothers presented a flat or inconsistent profile, a profile that was not associated with infant feeding choice or parity. Importantly, mothers with consistent declining profiles had the highest household income. Our findings suggest that although breastfeeding might promote a tighter regulation of diurnal basal cortisol secretion, in particular for multiparous mothers who are likely to be exposed to greater home demands and maternal responsibilities, some aspects of socioeconomic status such as income can also play a significant role in the stability of diurnal cortisol secretion across days.

Sleep as a mediator of the relationship between socioeconomic status and health: a hypothesis.

This article discusses the hypothesis that the adverse impact of low socioeconomic status (SES) on health may be partly mediated by decrements in sleep duration and quality. Low SES is frequently associated with a diminished opportunity to obtain sufficient sleep or with environmental conditions that compromise sleep quality. In a recent study, we examined carbohydrate metabolism, endocrine function, and sympatho-vagal balance in young, healthy adults studied after restricting sleep to four hours per night for six nights as compared to a fully rested condition obtained by extending the bed-time period to 12 hours per night for six nights. The state of sleep debt was associated with decreased glucose tolerance, elevated evening cortisol levels, and increased sympathetic activity. The alterations in glucose tolerance and hypothalamo-pituitary-adrenal function were qualitatively and quantitatively similar to those observed in normal aging. These results indicate that sleep loss can increase the "allostatic load" and facilitate the development of chronic conditions, such as obesity, diabetes, and hypertension, which have an increased prevalence in low SES groups.