Aimee M Caron1, Richard Stephenson. 1. Department of Cell & Systems Biology, University of Toronto, Toronto, Ontario, Canada.
Abstract
STUDY OBJECTIVES: Short sleep is a putative risk factor for obesity. However, prolonged total sleep deprivation (TSD) leads to negative energy balance and weight loss in rodents, whereas sleep-restricted humans tend to gain weight. We hypothesized that energy expenditure (VO2) is influenced by the rate of accumulation of sleep deficit in rats. DESIGN AND INTERVENTION: Six Sprague-Dawley rats underwent chronic sleep-restriction (CSR, 6-h sleep opportunity at ZT0-6 for 10 days) and stimulus-control protocols (CON, 12-h sleep opportunity for 10 days, matched number of stimuli) in a balanced cross-over design. Four additional rats underwent TSD (4 days). Sleep was manipulated using a motor-driven walking wheel. MEASUREMENTS AND RESULTS: Electroencephalography, electromyography, and body temperature were measured by telemetry, and VO2, by respirometry. Total sleep deficits of 55.1 +/- 6.4 hours, 31.8 +/- 6.8 hours, and 38.2 +/- 2.3 hours accumulated over the CSR, CON, and TSD protocols, respectively. Responses to TSD confirmed previous reports of elevated VO2 and body temperature. These responses were attenuated in CSR, despite a greater cumulative sleep deficit. Rate of rise of VO2 was strongly correlated with rate of accumulation of sleep deficit, above a threshold deficit of 3.6 h x day(-1). CONCLUSION: The change in VO2 is affected by rate of accumulation of sleep deficit and not the total sleep loss accrued. Negative energy balance, observed during TSD, is strongly attenuated when brief daily sleep opportunities are available to rats (CSR), despite greater accumulated sleep deficit.
STUDY OBJECTIVES: Short sleep is a putative risk factor for obesity. However, prolonged total sleep deprivation (TSD) leads to negative energy balance and weight loss in rodents, whereas sleep-restricted humans tend to gain weight. We hypothesized that energy expenditure (VO2) is influenced by the rate of accumulation of sleep deficit in rats. DESIGN AND INTERVENTION: Six Sprague-Dawley rats underwent chronic sleep-restriction (CSR, 6-h sleep opportunity at ZT0-6 for 10 days) and stimulus-control protocols (CON, 12-h sleep opportunity for 10 days, matched number of stimuli) in a balanced cross-over design. Four additional rats underwent TSD (4 days). Sleep was manipulated using a motor-driven walking wheel. MEASUREMENTS AND RESULTS: Electroencephalography, electromyography, and body temperature were measured by telemetry, and VO2, by respirometry. Total sleep deficits of 55.1 +/- 6.4 hours, 31.8 +/- 6.8 hours, and 38.2 +/- 2.3 hours accumulated over the CSR, CON, and TSD protocols, respectively. Responses to TSD confirmed previous reports of elevated VO2 and body temperature. These responses were attenuated in CSR, despite a greater cumulative sleep deficit. Rate of rise of VO2 was strongly correlated with rate of accumulation of sleep deficit, above a threshold deficit of 3.6 h x day(-1). CONCLUSION: The change in VO2 is affected by rate of accumulation of sleep deficit and not the total sleep loss accrued. Negative energy balance, observed during TSD, is strongly attenuated when brief daily sleep opportunities are available to rats (CSR), despite greater accumulated sleep deficit.
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