Heidi B Iglayreger1, Mark D Peterson1, Dongmei Liu1, Christine A Parker1, Susan J Woolford2, Bethany J Sallinen Gafka3, Fauziya Hassan4, Paul M Gordon5. 1. The Laboratory for Physical Activity and Exercise Intervention Research, Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, MI. 2. Child Health Evaluation and Research Unit, Department of Pediatrics, University of Michigan, Ann Arbor, MI. 3. Division of Child Behavioral Health, Department of Pediatrics, University of Michigan, Ann Arbor, MI. 4. Division of Pediatric Pulmonology, University of Michigan, Ann Arbor, MI; Michael S. Aldrich Sleep Disorders Center, University of Michigan, Ann Arbor, MI. 5. The Laboratory for Physical Activity and Exercise Intervention Research, Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, MI; Department of Health, Human Performance and Recreation, Baylor University, Waco, TX. Electronic address: Paul_M_Gordon@baylor.edu.
Abstract
OBJECTIVE: To examine the independent contributions of objectively measured sleep duration and fragmentation on cardiometabolic risk accumulation in free-living obese adolescents. STUDY DESIGN: Characteristics of metabolic syndrome (waist circumference, mean arterial pressure, fasting high-density lipoprotein cholesterol, triglycerides, glucose) were measured in obese adolescents and standardized residuals (z-scores) were summed (inverse high-density lipoprotein cholesterol) to create a continuous cardiometabolic risk score (cMetScore), adjusted for age, sex, and race. Sleep and physical activity were objectively measured in habitual, free-living conditions for 7 days (SenseWear Pro3, BodyMedia, Pittsburgh, Pennsylvania; n = 37; 54% female, ages 11-17 years). Associations between sleep duration and cMetScore were assessed via multiple linear regression. RESULTS: Body mass index, total sleep time, and sleep session length were each correlated with cMetScore (P < .05 all). Total sleep time was inversely and independently associated with cMetScore (r = -0.535, P = .001) and was the best independent predictor of metabolic risk. CONCLUSIONS: Sleep duration inversely predicts cardiometabolic risk in obese adolescents, even when we controlled for various measures of physical activity, anthropometry, and adiposity. Further research should investigate the biological mechanism of this relationship and the potential treatment effect of sleep intervention in decreasing cardiometabolic risk in this population.
OBJECTIVE: To examine the independent contributions of objectively measured sleep duration and fragmentation on cardiometabolic risk accumulation in free-living obese adolescents. STUDY DESIGN: Characteristics of metabolic syndrome (waist circumference, mean arterial pressure, fasting high-density lipoprotein cholesterol, triglycerides, glucose) were measured in obese adolescents and standardized residuals (z-scores) were summed (inverse high-density lipoprotein cholesterol) to create a continuous cardiometabolic risk score (cMetScore), adjusted for age, sex, and race. Sleep and physical activity were objectively measured in habitual, free-living conditions for 7 days (SenseWear Pro3, BodyMedia, Pittsburgh, Pennsylvania; n = 37; 54% female, ages 11-17 years). Associations between sleep duration and cMetScore were assessed via multiple linear regression. RESULTS: Body mass index, total sleep time, and sleep session length were each correlated with cMetScore (P < .05 all). Total sleep time was inversely and independently associated with cMetScore (r = -0.535, P = .001) and was the best independent predictor of metabolic risk. CONCLUSIONS: Sleep duration inversely predicts cardiometabolic risk in obese adolescents, even when we controlled for various measures of physical activity, anthropometry, and adiposity. Further research should investigate the biological mechanism of this relationship and the potential treatment effect of sleep intervention in decreasing cardiometabolic risk in this population.
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