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Abstract Introduction Both short sleep duration and circadian rhythm misalignment are associated with increased cardiometabolic risk factors. Although experimental research has demonstrated the independent and interactive effects of these two exposures, few studies have examined the interaction between these two factors on outcomes among free-living participants. The goal of this study is to examine how sleep duration and circadian alignment predict cardiometabolic risk factors and extend prior research by examining the mechanisms of insulin resistance. Methods Participants included adults aged 18-60 y with BMI 25-35 kg/m2 who completed body measurements, at least 7 days of actigraphy and an in lab dim light melatonin onset assessment (DLMO). The main measure of circadian misalignment was the phase angle, or duration between DLMO and habitual sleep onset time in the past 7 days. Participants attended an outpatient visit to the clinical research unit to complete a frequently sampled intravenous glucose tolerance test (FSIVGTT) and data were analyzed using Bergman’s minimal model analysis. Multivariable linear regression models evaluated the effects of sleep duration both individually and their interaction in predicting cardiometabolic outcomes in models controlling for age, sex, race and ethnicity. Results Body measurement data were available for n= 92 participants and FSIVGTT were available for 87 participants (age: M= 36 SD=10 years, 47 female). Average sleep duration was 6.9 hours (SD=0.6) and average phase angle was 3.3 hours (SD=1.0). We found there was higher insulin sensitivity among those with shorter phase angle (Si, estimate= -2.58 CI= -4.63, -0.53 (mU/L)-1min-1, p=.02) and a trend among shorter sleep duration (estimate = -3.71, CI= -7.35, -0.07 (mU/L)-1min-1, p=.05). Phase angle and sleep duration were not associated with metabolic measures, BMI, body fat or hip/waist ratio. Conclusion Results demonstrate contrary to our hypotheses, shorter phase angle and sleep were associated with higher insulin sensitivity and unrelated to other cardiometabolic risk markers in our sample of overweight adults without diabetes. Support (if any) The research reported in this publication was supported in part by the National Heart Lung and Blood Institute under Award Number 1R01HL141706-01A1 and the National Center for Advancing Translational Sciences of the National Institutes of Health under Award Number UL1TR002538
Baron et al. (Sat,) studied this question.