P6579Effefcts of repeated exposure to insufficient sleep on human microvascular function

Abstract

Background/Introduction: Mechanical environment likely contributes to the atherosclerotic process, activating cytokine production in the endothelial wall, leading to the buildup of plaque, thickening of the vessel wall and narrowing of the artery. Cardiovascular risk factors are increased in association with insufficient or inadequate sleep, but the mechanisms for these associations are unknown. The current investigation tested the role of sleep in vascular contributions to inflammatory and cellular adhesion pathways using microvasculature reactivity of the skin. Purpose: To investigate the effects of repeated exposure to periods (blocks of 3 nights of sleeping 4 hours per night, repeated 4 times), of insufficient sleep on microvascular functioning. Methods: In a 22‐day in‐hospital protocol, 43 healthy participants (22 women, 21 men) were randomly assigned to 4 cycles of repeated sleep restriction (permitted 4h of sleep/night from 0300‐0700 for 3 nights followed by a recovery sleep, repeated 4 times), or a sleep control group (8h/night from 2300‐0700). Endothelium‐dependent vasodilation was measured by applying acetylcholine chloride by iontophoresis, while the use of sodium nitroprusside (SNP) measured the endothelium‐independent vasodilatation to evaluate smooth muscle function. The MIC1 Iontophoresis System Monitor (Moor Instruments Ltd, Millwey, Devon England) and the Laser Doppler Perfusion Imager (Lisca PIM 2.0, Lisca Development AB, Linkoping, Sweden) were used. The coefficient of variation of the baseline measurement before Laser Doppler Flowmetry iontophoresis of acetylcholine was 14.1% and during maximal hyperemic response after the iontophoresis 13.7%. Results: Age, gender, BMI, BP and HR were not different between groups, and both had similar habitual sleep duration (∼7h) and efficiency (∼85%) estimated by actigraph and sleep log before study. Sleep restriction reduced sleep to <4 hours per night, for each 3 day exposure to the short sleep schedule. Resting skin forearm blood flow measured by a laser scanner image was increased (p<0.01). The skin forearm blood flow was further increased after the iontophoresis of acetylcholine and SNP. The increase was apparent during testing following the 2nd, 3rd and 4th bout of 3 days of insufficient sleep for both tests in sleep restriction group compared to sleep control group (all p<0.05). Conclusion: During repeated exposure to insufficient sleep, microvasculature of the forearm shows increased vasodilation during resting conditions. This may be a compensatory mechanism to reduce blood pressure that is elevated during insufficient sleep stress.