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Effect of Repeated Exposure to Sleep Restriction on Interleukin 6 Levels in Humans
Author(s) -
Bhatt Vrushank,
Diolombi Moussa,
Haack Monika,
Mullington Janet
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.615.7
Subject(s) - sleep restriction , sleep (system call) , medicine , morning , endocrinology , sleep deprivation , circadian rhythm , computer science , operating system
Repeated exposures to sleep restriction with short in‐between periods of recovery sleep are increasingly common in society, in particular for individuals with irregular work schedules. Short periods of experimental sleep restriction have been shown to elevate inflammatory markers, such as interleukin 6 (IL‐6) which has been suggested to increase the risk for cardiometabolic diseases. However, the effect of repeated exposure to sleep restriction on IL‐6 is unknown. Forty‐three healthy participants (age 32 + 2 yrs; BMI 24 + 1 kg/m 2 ; 21 men and 22 women) were randomized to a 22‐day study of repeated cycles of sleep restriction (4hr sleep/night for 3 nights followed by one recovery sleep, 4 cycles) or routine sleep (8hr sleep/night). Blood was sampled from fasting recumbent participants in the morning after awakening, during baseline, third day of each sleep restriction or control cycle, and following recovery sleep. Plasma concentrations of IL‐6 were measured using high sensitivity immunosorbent assay (R&D Systems ELISA). The sleep restriction group showed a significant increase in IL‐6 levels during the first sleep restriction cycle, exceeding control levels by 30% (p<0.05). These levels did not return to baseline in the remaining sleep restriction cycles when compared with the control group. IL‐6 levels return to baseline levels after recovery sleep. In conclusion, these findings suggest that repeated patterns of sleep restriction elevate circulating levels of IL‐6 which may contribute to the development of risk for cardiovascular and cardiometabolic diseases. Supported by NIH (HL‐106782).