Restricting Sleep Duration Alters Resting And Postprandial Respiratory Quotient, But Has Minimal Effects On Overall Energy Expenditure

Introduction: Epidemiological evidence has demonstrated a link between short sleep and obesity. Clinical studies suggest a role of increased energy intake in this relationship, whereas the contributions of energy expenditure (EE) and substrate utilization are less clearly defined. Our aim was to investigate the effects of short sleep on EE and respiratory quotient (RQ) during sleep, basal conditions, and in response to a high-fat meal. Methods: Seven females (age and BMI: 27.4 ± 8.1 years and 26.2 ± 1.6 kg/m2, respectively) participated in a randomized, crossover study lasting 4 days. Participants were studied under two separate conditions: short (4 h/night; time in bed 0100-0500 h) and habitual (8 h/night; time in bed 2300-0700 h) sleep. Meals were served at 0800, 1200, and 1900 h, with a snack at 1600 h. Data included 24-h EE and sleep metabolic rate (SMR) from the metabolic chamber and fasting resting metabolic rate (RMR) and postprandial energy expenditure (PPEE) over a 6 h period after consumption of a high-fat breakfast on day 4. Results are expressed as mean ± SD. Results: Total 24-h EE was 1,907 ± 229 kcal and 1,830 ± 63 kcal for short and habitual sleep, respectively (p=0.084, paired t-test). Mean SMR was 0.967 ± 0.19 kcal/min throughout the 4-h sleep period and 0.895 ± 0.09 kcal/min throughout the 8-h sleep period (p=0.211, paired t-test). When we examined the 8-h period spanning the sleep episode during the habitual sleep phase, there was a significant sleep condition x time interaction for EE (p<0.001). During the short sleep phase, this measurement included 4 h of sleep and 4 h of non-sleep time. Specifically, EE in the short sleep condition was significantly higher than in the habitual sleep condition mostly during non-sleep times: at 0000-0100, 0100-0200, 0500-0600, and 0600-0700 h, resulting in an increase of 0.21 ± 0.19 kcal/min (p=0.009) throughout the full 8-h period. RQ significantly declined across the 2300-0700 time period (p<0.001), but did not differ between conditions. RMR after 3 nights of short vs. habitual sleep did not differ between conditions, whereas fasting RQ was significantly lower (p=0.026) after short vs. habitual sleep. Postprandial RQ and PPEE did not differ between conditions. The postprandial RQ peak was significantly reduced in short vs. habitual sleep (p=0.008, paired t-test). Conclusions: We demonstrate here that short sleep results in increased EE during nocturnal hours spent awake, but does not significantly alter SMR. Over the 24-h period, however, it results in a slight increase in EE, which was not significant with this sample size. These findings imply that the greater prevalence of obesity in individuals with short sleep observed in epidemiological studies is most likely attributable to greater food intake that is not offset by the small increase in EE associated with greater time spent awake.