Ari Shechter1, Marie-Pierre St-Onge2. 1. New York Obesity Research Center, Columbia University, New York, NY, USA. 2. New York Obesity Research Center, Columbia University, New York, NY, USA. Electronic address: ms2554@columbia.edu.
Abstract
OBJECTIVE AND BACKGROUND: We and others have reported that experimentally induced short sleep does not affect resting metabolic rate and leads to increased laboratory-measured 24-h energy expenditure. Here, we aimed to determine if sleep timing and/or quality are related to physical activity (PA) levels. METHODS: Measures of PA via waist actigraphy, sleep diary, and sleep quality questionnaires were collected over a 7-18-day period in 22 adults (mean age ± standard deviation (SD): 35.8 ± 4.6 years, and mean body mass index ± SD: 23.8 ± 1.1 kg/m(2)) who were on their habitual sleep-wake and activity schedules. RESULTS: During the recording period, mean (±SD) bedtime and wake times were 00:17 ± 1:07 h (range: 22:02-02:07 h) and 08:20 ± 1:14 h (range: 06:30-10:11 h), respectively. After controlling for sleep duration, later bedtime, wake time, and midpoint of sleep were associated with less time spent in moderate-to-vigorous PA (p = 0.013, p = 0.005, and p = 0.007, respectively), and increased time in sedentary PA (p = 0.016, p = 0.013, and p = 0.013, respectively). CONCLUSIONS: Current results suggest that even relatively small alterations in sleep timing may influence PA. However, causality cannot be inferred from this cross-sectional study. Clinical intervention studies should be conducted to assess the relationship between sleep timing and energy balance.
OBJECTIVE AND BACKGROUND: We and others have reported that experimentally induced short sleep does not affect resting metabolic rate and leads to increased laboratory-measured 24-h energy expenditure. Here, we aimed to determine if sleep timing and/or quality are related to physical activity (PA) levels. METHODS: Measures of PA via waist actigraphy, sleep diary, and sleep quality questionnaires were collected over a 7-18-day period in 22 adults (mean age ± standard deviation (SD): 35.8 ± 4.6 years, and mean body mass index ± SD: 23.8 ± 1.1 kg/m(2)) who were on their habitual sleep-wake and activity schedules. RESULTS: During the recording period, mean (±SD) bedtime and wake times were 00:17 ± 1:07 h (range: 22:02-02:07 h) and 08:20 ± 1:14 h (range: 06:30-10:11 h), respectively. After controlling for sleep duration, later bedtime, wake time, and midpoint of sleep were associated with less time spent in moderate-to-vigorous PA (p = 0.013, p = 0.005, and p = 0.007, respectively), and increased time in sedentary PA (p = 0.016, p = 0.013, and p = 0.013, respectively). CONCLUSIONS: Current results suggest that even relatively small alterations in sleep timing may influence PA. However, causality cannot be inferred from this cross-sectional study. Clinical intervention studies should be conducted to assess the relationship between sleep timing and energy balance.
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