Shechter · International journal of obesity (2005) 2014 · randomized crossover trial · n=10

Postprandial thermogenesis and substrate oxidation are unaffected by sleep restriction.

Cited 29 times in the scientific literature.

Level 2 - randomized trial

Randomized crossover trial

PubMed 24352294 · doi:10.1038/ijo.2013.239 · record verified 2026-08-26

What was done

Ten healthy premenopausal females (aged 22–43 years, BMI 23.4–28 kg/m²) completed a randomized crossover study comparing short sleep (4 hours per night) with habitual sleep (8 hours per night). After three nights in each condition, fasting and postprandial resting metabolic rate (RMR) and respiratory quotient (RQ) were measured using whole-room indirect calorimetry. Thermic effect of food (TEF) was evaluated over a 6-hour period after ingestion of a high-fat liquid meal.

What was found

Short versus habitual sleep did not significantly alter RMR (1.01 ± 0.05 vs 0.97 ± 0.04 kcal/min; P = 0.23). Fasting RQ was significantly lower after short sleep (0.84 ± 0.01 vs 0.88 ± 0.01; P = 0.028). Postprandial energy expenditure (1.13 ± 0.04 vs 1.10 ± 0.04 kcal/min; P = 0.09) and postprandial RQ (0.88 ± 0.01 vs 0.88 ± 0.01; P = 0.50) after the high-fat meal did not differ between conditions. TEF was identical between conditions (0.24 ± 0.02 kcal/min in both; P = 0.98), as was the ~6-hour incremental area under the curve (1.16 ± 0.10 vs 1.17 ± 0.09 kcal/min × 356 min; P = 0.92).

Why it matters

This study indicates that acute sleep restriction does not promote obesity through impairments in diet-induced thermogenesis or postprandial fat oxidation, suggesting research should focus on physical activity or energy intake pathways.

Limits

The study was very small (n = 10) and exclusively enrolled healthy premenopausal women, limiting generalizability to males, older populations, or individuals with obesity. Sleep restriction was limited to three nights, and postprandial responses were tested only using a single acute high-fat liquid challenge.

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