Postprandial thermogenesis and substrate oxidation are unaffected by sleep restriction

Abstract

Background/ObjectivesThe extent to which alterations in energy expenditure (EE) in response to sleep restriction contribute to the short sleep-obesity relationship is not clearly defined. Short sleep may induce changes in resting metabolic rate (RMR), thermic effect of food (TEF), and postprandial substrate oxidation.Subjects/MethodsTen females (age and BMI: 22-43 y and 23.4-28 kg/m2) completed a randomized, crossover study assessing the effects of short (4 h/night) and habitual (8 h/night) sleep duration on fasting and postprandial RMR and respiratory quotient (RQ). Measurements were taken after 3 nights using whole-room indirect calorimetry. The TEF was assessed over a 6-h period following consumption of a high-fat liquid meal.ResultsShort vs. habitual sleep did not affect RMR (1.01 ± 0.05 and 0.97 ± 0.04 kcal/min; p=0.23). Fasting RQ was significantly lower after short vs. habitual sleep (0.84 ± 0.01 and 0.88 ± 0.01; p=0.028). Postprandial EE (short: 1.13 ± 0.04 and habitual: 1.10 ± 0.04, p=0.09) and RQ (short: 0.88 ± 0.01 and habitual: 0.88 ± 0.01, p=0.50) after the high-fat meal were not different between conditions. TEF was similar between conditions (0.24 ± 0.02 kcal/min in both; p=0.98), as was the ~6-h incremental area under the curve (1.16 ± 0.10 and 1.17 ± 0.09 kcal/min x 356 min after short and habitual sleep, respectively; p=0.92).ConclusionsCurrent findings observed in non-obese healthy premenopausal women do not support the hypothesis that alterations in TEF and postprandial substrate oxidation are major contributors to the higher rate of obesity observed in short sleepers. In exploring a role of sleep duration on EE, research should focus on potential alterations in physical activity to explain the increased obesity risk in short sleepers.