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  • Original Article
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Clinical Studies and Practice

Postprandial thermogenesis and substrate oxidation are unaffected by sleep restriction

International Journal of Obesity volume 38, pages 1153–1158 (2014)Cite this article

Subjects

Abstract

Background/objectives:

The 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/methods:

Ten females (age and body mass index: 22–43 years and 23.4–28 kg m−2) completed a randomized, crossover study assessing the effects of short (4 h per night) and habitual (8 h per night) sleep duration on fasting and postprandial RMR and respiratory quotient (RQ). Measurements were taken after three nights using whole-room indirect calorimetry. The TEF was assessed over a 6-h period following consumption of a high-fat liquid meal.

Results:

Short versus habitual sleep did not affect RMR (1.01±0.05 and 0.97±0.04 kcal min−1; P=0.23). Fasting RQ was significantly lower after short versus 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−1 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−1 × 356 min after short and habitual sleep, respectively; P=0.92).

Conclusions:

Current 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.

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Acknowledgements

We thank Majella O’Keeffe PhD and also the staff of the Bionutrition Unit at the Irving Institute for Clinical and Translational Research for their help in conducting the study, and also our research participants. This study was supported by the National Institutes of Health grants R01 HL091352 (M-P St-O), T32 DK007559 (AS) and P30 DK26687 (New York Obesity Nutrition Research Center), and St Luke’s/Roosevelt Pilot and Feasibility grant (M-P St-O). This publication was supported by the National Center for Advancing Translational Sciences, National Institutes of Health, through grant number UL1 TR000040, formerly the National Center for Research Resources, grant number UL1 RR024156. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

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Authors and Affiliations

  1. New York Obesity Nutrition Research Center, St Luke’s-Roosevelt Hospital, New York, NY, USA

    A Shechter, R Rising, S Wolfe, J B Albu & M-P St-Onge

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  1. A Shechter
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  3. S Wolfe
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Correspondence to M-P St-Onge.

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MPSO designed the research; AS, RR and SW conducted the research; AS, RR, SW, JBA and MPSO collected the data; AS, RR and MPSO analyzed the data; AS and MPSO wrote the manuscript. MPSO had primary responsibility for final content; all authors read and approved the final manuscript.

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Shechter, A., Rising, R., Wolfe, S. et al. Postprandial thermogenesis and substrate oxidation are unaffected by sleep restriction. Int J Obes 38, 1153–1158 (2014). https://doi.org/10.1038/ijo.2013.239

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