Two nights of recovery sleep restores the dynamic lipemic response, but not the reduction of insulin sensitivity, induced by five nights of sleep restriction

Author:

Ness Kelly M.123ORCID,Strayer Stephen M.12,Nahmod Nicole G.2,Chang Anne-Marie2,Buxton Orfeu M.12456,Shearer Gregory C.13

Affiliation:

1. The Huck Institutes of the Life Sciences, Pennsylvania State University, University Park, Pennsylvania

2. Department of Biobehavioral Health, Pennsylvania State University, University Park, Pennsylvania

3. Department of Nutritional Sciences, Pennsylvania State University, University Park, Pennsylvania

4. Division of Sleep and Circadian Disorders, Harvard Medical School, University Park, Pennsylvania

5. Department of Social and Behavioral Sciences, Harvard Chan School of Public Health, Boston, Massachusetts

6. Sleep Health Institute, Departments of Medicine and Neurology, Brigham and Women’s Hospital, Boston, Massachusetts

Abstract

Chronic inadequate sleep is associated with increased risk of cardiometabolic diseases. The mechanisms involved are poorly understood but involve changes in insulin sensitivity, including within adipose tissue. The aim of this study was to assess the effects of sleep restriction on nonesterified fatty acid (NEFA) suppression profiles in response to an intravenous glucose tolerance test (IVGTT) and to assess whether 2 nights of recovery sleep (a “weekend”) is sufficient to restore metabolic health. We hypothesized that sleep restriction impairs both glucose and lipid metabolism, specifically adipocyte insulin sensitivity, and the dynamic lipemic response of adipocyte NEFA release during an IVGTT. Fifteen healthy men completed an inpatient study of 3 baseline nights (10 h of time in bed/night), followed by 5 nights of 5 h of time in bed/night and 2 recovery nights (10 h of time in bed/night). IVGTTs were performed on the final day of each condition. Reductions in insulin sensitivity without a compensatory change in acute insulin response to glucose were consistent with prior studies (insulin sensitivity P = 0.002; acute insulin response to glucose P = 0.23). The disposition index was suppressed by sleep restriction and did not recover after recovery sleep ( P < 0.0001 and P = 0.01, respectively). Fasting NEFAs were not different from baseline in either the restriction or recovery conditions. NEFA rebound was significantly suppressed by sleep restriction ( P = 0.01) but returned to baseline values after recovery sleep. Our study indicates that sleep restriction impacts NEFA metabolism and demonstrates that 2 nights of recovery sleep may not be adequate to restore glycemic health.

Funder

HHS | NIH | National Center for Advancing Translational Sciences (NCATS)

HHS | NIH | National Institute of General Medical Sciences (NIGMS)

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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