Abstract
Introduction
Stress reactivity and autonomic nervous system (ANS) dysregulation have been suggested to be the pathophysiology of insomnia. Based on the finding PSG-measured short sleep duration was associated with higher morbidity of metabolic and cardiovascular disease. Vgontzas and Fernandez-Mandoza (2013) proposed that objective sleep duration is a biomarker for insomnia phenotypes. The phenotype with short objective sleep duration is associated with increased stress-related physiological hyperarousal. The present study aims to test this hypothesis by comparing the stress-induced cardiovascular reactivity between insomnia patients with short and long objective sleep durations.
Methods
27 insomnia patients (age mean 34.48 ±12.87, Male: Female= 6:21) without comorbidity of psychiatric, medical or sleep disorders participated in this study. They went through one night of 8-hour PSG recording and were divided into two groups by their total sleep time with a cutoff of 6 hours. Nine participants were in short sleep duration group and 18 in longer sleep duration group. Psychophysiological reactivity profile, as recorded with EKG, skin conductance (SC), body temperature (BT), blood volume pulse (BVP), respiration rate (RR), was measured under three conditions: baseline resting state, arithmetic word problems solving, and recovery resting state.
Results
Both groups showed similar stress physiological response with increased heart rate (HR) and SC, nearly equivalent BT and BVP, and decreased RR when solving arithmetic problems, and opposite reaction during recovery resting state. Mann-Whitney U test comparing the changes from baseline resting state on all the psychophysiological measures between two phenotypes of insomnia showed no significant differences: stress-induced heart-rate (U=106, p=.119.) recovery heart-rate (U=44, p=.095), stress-induced skin conductance (U=104.5, p=.132),recovery skin conductance (U=51.5, p=.198), stress-induced body temperature (U=79, p=.897),recovery body temperature (U=60.5, p=.418), stress-induced blood volume pulse amplitude (U=77, p=1.0), and recovery blood volume pulse amplitude (U=69, p=.735), stress-induced respiration rate (U=76, p =.696), and recovery respiration rate (U=85, p=.658).
Conclusion
Our results indicate that the insomnia phenotypes with short and long objective sleep duration are not different in their stress-induced physiological responses. Future studies are needed to confirm these results and to explore other mechanisms for the increased metabolic and cardiovascular disease risk in insomnia patients with short objective sleep duration.
Support (if any):
Comparison of blood volume pulse and skin conductance responses to mental and affective stimuli at different anatomical sites
