Effect of long-term sleep restriction on energy balance

Columbia University Health Sciences, New York NY

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Abstract

Epidemiological and longitudinal studies show that short sleep duration (<7h/night) is associated with obesity and weight gain. Clinical studies have provided some clues into the role of sleep in the promotion of obesity. These studies have shown that short sleep leads to increased appetite and food intake, especially for high fat, high carbohydrate snacks, during periods of short (4 h/night) relative to habitual sleep (>7.5 h/night). In our previous R01, we have shown that individuals eat more after a period of short sleep relative to habitual sleep and that neuronal signals in brain reward centers were activated to a greater extent by foods after short compared to habitual sleep. However, there has been no study to date to assess the effects of sleep restriction on energy balance and body composition when sleep restriction is less severe and maintained for a prolonged period of time, as is the case in a natural setting. We therefore propose to test the effects of milder, prolonged sleep restriction (SR: -1.5 hours/night relative to habitual sleep [HS] for 6 wk) on body composition and cardio-metabolic risk. We expect that SR will lead to a positive energy balance and increased adiposity relative to HS. Adult men and women (age 20-40 y and body mass index 25-29.9 kg/m2) will be studied under 2 different conditions: HS (regular bedtime routines, sleep ?7 h/night) and SR (delay bedtimes by 1.5 h, regular wake time, sleep HS-1.5 h/night) for 6 wk each. Sleep periods will occur in random order, at least 1 mo apart. Energy balance will be thoroughly assessed using a multi- component approach: structural MRI to assess changes in adiposity, doubly-labeled water to assess 24-h energy expenditure, actigraphy to assess physical activity level; 3-d food records to assess food intake, functional magnetic resonance imaging (fMRI) to assess neuronal responses to food stimuli. We will also assess cardio-metabolic risk factors from fasting blood samples at baseline and endpoint of each phase. Our working hypothesis is that SR will stimulate the orexin system, which will stimulate appetite and increase food intake. Physical activity level will be reduced, leading to an overall positive energy balance and weight gain (increased adiposity). Cardio-metabolic risk factors will be adversely affected by SR relative to HS, in part as a result of positive energy balance and weight gain. This study will improve our knowledge of the role of sleep, within the context of an ecologically valid model, on the control of food intake and energy expenditure. As a result, it will provide additional evidence for a causal role of short sleep duration in the etiology of obesity and cardio-metabolic risk.