Sleep Extension in Short Sleepers: An Evaluation of Feasibility and Effectiveness for Weight Management and Cardiometabolic Disease Prevention.

Sleep duration has become increasingly recognized as an important influencer of health. Epidemiologic and observational studies have shown associations between short sleep duration and increased risk for chronic cardiometabolic disorders, including obesity, type 2 diabetes, and cardiovascular disease. These associations have led to investigations into the potential causal pathways through which short sleep may increase risk for these disorders. Clinical intervention studies have demonstrated that restricting sleep in normal sleepers has adverse health effects, including insulin resistance, and increased blood pressure. The totality of evidence points to negative health effects of short sleep and the recognition of sleep as a lifestyle behavior that may be targeted for disease prevention. It is well established that consistent, adequate sleep is associated with the lowest risk of obesity and cardiometabolic disorders. Yet, it is unclear whether increasing sleep in short sleepers can improve health. In today's society, it is common for individuals to deprive themselves of sleep during the work week, with the intent to sleep longer during the weekend, or have "catch-up sleep." Studies that have examined the health effects of extended sleep, post-sleep restriction, revealed some improvements in health outcomes. However, it is uncertain whether the improvements observed with catch-up sleep are sufficient to reverse the negative health effects of constant sleep restriction. Few intervention studies have been undertaken to determine whether extending sleep, long-term, in short sleepers is feasible and whether it can reduce the disease risk burden associated with short sleep duration. The purpose of this review is to highlight these studies and evaluate information related to the impact of sleep extension on risk factors for chronic cardiometabolic disorders. We discuss limitations of current research, including variability in participant characteristics and the extent to which sleep behaviors are modified and monitored. Although the evidence-base for benefits of sleep extension is still in the early stages, studies to date indicate that prolonging sleep, in short sleepers, may improve cardiometabolic risk. Finally, our review calls attention to areas that require further study and for larger scale studies of behavior modification to establish the health effects of sleep extension in short sleepers.

Effects of CPAP on energy expenditure in obese obstructive sleep apnoea patients: A pilot study.

We conducted a placebo-controlled crossover pilot study investigating the effects of 2 mo of active and sham continuous positive airway pressure (CPAP) on energy expenditure (EE) via whole-room indirect calorimetry in three obese obstructive sleep apnoea (OSA) patients. Total 24-h (active: 2970 ± 254 kcal/d, sham: 2705 ± 217 kcal/d; p = 0.015) and mean sleeping (active: 1.60 ± 0.20 kcal/min; sham: 1.47 ± 0.17 kcal/min; p = 0.038) EE were significantly increased after active vs. sham CPAP. Findings suggest that CPAP may correct a hypoxia-related adaptive decrease in thermogenesis.

Sleep disturbances, body fat distribution, food intake and/or energy expenditure: pathophysiological aspects.

Data from cross-sectional and longitudinal studies have illustrated a relationship between short sleep duration (SSD) and weight gain. Individuals with SSD are heavier and gain more weight over time than normal-duration sleepers. This sleep-obesity relationship may have consequences for obesity treatments, as it appears that short sleepers have reduced ability to lose weight. Laboratory-based clinical studies found that experimental sleep restriction affects energy expenditure and intake, possibly providing a mechanistic explanation for the weight gain observed in chronic short sleepers. Specifically, compared to normal sleep duration, sleep restriction increases food intake beyond the energetic costs of increased time spent awake. Reasons for this increased energy intake after sleep restriction are unclear but may include disrupted appetite-regulating hormones, altered brain mechanisms involved in the hedonic aspects of appetite, and/or changes in sleep quality and architecture. Obstructive sleep apnea (OSA) is a disorder at the intersection of sleep and obesity, and the characteristics of the disorder illustrate many of the effects of sleep disturbances on body weight and vice versa. Specifically, while obesity is among the main risk factors for OSA, the disorder itself and its associated disturbances in sleep quality and architecture seem to alter energy balance parameters and may induce further weight gain. Several intervention trials have shown that weight loss is associated with reduced OSA severity. Thus, weight loss may improve sleep, and these improvements may promote further weight loss. Future studies should establish whether increasing sleep duration/improving sleep quality can induce weight loss.

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.

The role of sleep duration in the regulation of energy balance: effects on energy intakes and expenditure.

Short sleep duration and obesity are common occurrence in today's society. An extensive literature from cross-sectional and longitudinal epidemiological studies shows a relationship between short sleep and prevalence of obesity and weight gain. However, causality cannot be inferred from such studies. Clinical intervention studies have examined whether reducing sleep in normal sleepers, typically sleeping 7-9 h/night, can affect energy intake, energy expenditure, and endocrine regulators of energy balance. The aim of this review is to evaluate studies that have assessed food intake, energy expenditure, and leptin and ghrelin levels after periods of restricted and normal sleep. Most studies support the notion that restricting sleep increases food intake, but the effects on energy expenditure are mixed. Differences in methodology and component of energy expenditure analyzed may account for the discrepancies. Studies examining the effects of sleep on leptin and ghrelin have provided conflicting results with increased, reduced, or unchanged leptin and ghrelin levels after restricted sleep compared to normal sleep. Energy balance of study participants and potential sex differences may account for the varied results. Studies should strive for constant energy balance and feeding schedules when assessing the role of sleep on hormonal profile. Although studies suggest that restricting sleep may lead to weight gain via increased food intake, research is needed to examine the impact on energy expenditure and endocrine controls. Also, studies have been of short duration, and there is little knowledge on the reverse question: does increasing sleep duration in short sleepers lead to negative energy balance?

Short sleep duration increases energy intakes but does not change energy expenditure in normal-weight individuals.

BACKGROUND: Evidence suggests a relation between short sleep duration and obesity. OBJECTIVE: We assessed energy balance during periods of short and habitual sleep in normal-weight men and women. DESIGN: Fifteen men and 15 women aged 30-49 y with a body mass index (in kg/m(2)) of 22-26, who regularly slept 7-9 h/night, were recruited to participate in this crossover inpatient study. All participants were studied under short (4 h/night) and habitual (9 h/night) sleep conditions, in random order, for 5 nights each. Food intake was measured on day 5, and energy expenditure was measured with the doubly labeled water method over each period. RESULTS: Participants consumed more energy on day 5 during short sleep (2813.6 ± 593.0 kcal) than during habitual sleep (2517.7 ± 593.0 kcal; P = 0.023). This effect was mostly due to increased consumption of fat (20.7 ± 37.4 g; P = 0.01), notably saturated fat (8.7 ± 20.4 g; P = 0.038), during short sleep. Resting metabolic rate (short sleep: 1455.4 ± 129.0 kcal/d; habitual sleep: 1486.5 ± 129.5 kcal/d; P = 0.136) and total energy expenditure (short sleep: 2589.2 ± 526.5 kcal/d; habitual sleep: 2611.1 ± 529.0 kcal/d; P = 0.832) did not differ significantly between sleep phases. CONCLUSIONS: Our data show that a reduction in sleep increases energy and fat intakes, which may explain the associations observed between sleep and obesity. If sustained, as observed, and not compensated by increased energy expenditure, the dietary intakes of individuals undergoing short sleep predispose to obesity. This trial is registered at clinicaltrials.gov as NCT00935402.

Greater resting energy expenditure and lower respiratory quotient after 1 week of supplementation with milk relative to supplementation with a sugar-only beverage in children.

Previous studies have linked overweight to lower milk and calcium consumption and have proposed a role of milk consumption on energy expenditure (EE). The goal of this study was to compare EE and food intake after a meal of either mixed-nutrient or single-nutrient beverage and examine whether supplementation with that beverage for 1 week will impact EE. This was a randomized, controlled crossover study testing the effect of 2 beverages, milk or fruit-flavored beverage, before and after a supplementation period of 1 week on EE. Food intake at a meal after a snack intake of each beverage was assessed at the end of each measurement period. Ten children, aged 9 to 10 years, participated in all of the testing sessions in the study. There was a significant beverage by testing day interaction on daily EE and thermic effect of food (TEF), whereby EE was greater with milk consumption relative to the fruit-flavored beverage on day 8 (P = .0014) and with fruit-flavored beverage consumption on day 1 vs day 8 (P = .01). Similarly, the TEF was greater with milk compared with fruit-flavored beverage consumption on day 8 (P = .0007) and with fruit-flavored beverage consumption on day 1 relative to day 8 (P = .0097). The TEF declined more rapidly during 6 hours after a fruit-flavored beverage than a milk meal (P = .0018). Food intake did not differ after snack consumption of each beverage before and after milk and fruit-flavored beverage supplementation periods. Over the longer term, consumption of milk beverages may have more favorable effects on energy balance in children than consumption of fruit-flavored beverages.

A new hand-held indirect calorimeter to measure postprandial energy expenditure.

OBJECTIVE: To verify the accuracy of a new hand-held metabolic rate measuring device (MedGem) in quantifying postprandial energy expenditure (PP EE). MedGem measurements were compared to measurements obtained with a conventional indirect calorimeter (Delta-Trac). RESEARCH METHODS AND PROCEDURES: The resting metabolic rate of 15 healthy subjects was measured for 20 minutes using Delta-Trac followed by a 10-minute measurement period using MedGem. EE was again measured for 7 hours after consumption of a 2510-kJ breakfast. Measurements were read from the Delta-Trac for the initial 50 minutes of each hour followed by a single reading from the MedGem after 5 to 10 minutes of measurement. Measured EE was calculated as the average of the total measurement period for Delta-Trac and for eight readings using MedGem; PP EE was calculated as the average of all measurements obtained after breakfast consumption. RESULTS: There was no difference in resting metabolic rate between the two methods (6455.1 +/- 417.6 vs. 6468.5 +/- 337.2 kJ/d for Delta-Trac and MedGem, respectively). Measured EE and PP EE values with Delta-Trac (7019.1 +/- 400.8 and 7099.8 +/- 399.2 kJ/d, respectively) and MedGem (6775.6 +/- 372.0 and 6819.5 +/- 379.9 kJ/d, respectively) were not significantly different. There was no bias detected in any of the measurements made with MedGem compared with those of Delta-Trac. DISCUSSION: The new hand-held EE measuring device can accurately track PP EE relative to a conventional indirect calorimetry system and, therefore, provides a new opportunity to assess PP EE in research settings and large-scale trials.

Medium-chain triglycerides increase energy expenditure and decrease adiposity in overweight men.

OBJECTIVE: The objectives of this study were to compare the effects of diets rich in medium-chain triglycerides (MCTs) or long-chain triglycerides (LCTs) on body composition, energy expenditure, substrate oxidation, subjective appetite, and ad libitum energy intake in overweight men. RESEARCH METHODS AND PROCEDURES: Twenty-four healthy, overweight men with body mass indexes between 25 and 31 kg/m(2) consumed diets rich in MCT or LCT for 28 days each in a crossover randomized controlled trial. At baseline and after 4 weeks of each dietary intervention, energy expenditure was measured using indirect calorimetry, and body composition was analyzed using magnetic resonance imaging. RESULTS: Upper body adipose tissue (AT) decreased to a greater extent (p < 0.05) with functional oil (FctO) compared with olive oil (OL) consumption (-0.67 +/- 0.26 kg and -0.02 +/- 0.19 kg, respectively). There was a trend toward greater loss of whole-body subcutaneous AT volume (p = 0.087) with FctO compared with OL consumption. Average energy expenditure was 0.04 +/- 0.02 kcal/min greater (p < 0.05) on day 2 and 0.03 +/- 0.02 kcal/min (not significant) on day 28 with FctO compared with OL consumption. Similarly, average fat oxidation was greater (p = 0.052) with FctO compared with OL intake on day 2 but not day 28. DISCUSSION: Consumption of a diet rich in MCTs results in greater loss of AT compared with LCTs, perhaps due to increased energy expenditure and fat oxidation observed with MCT intake. Thus, MCTs may be considered as agents that aid in the prevention of obesity or potentially stimulate weight loss.