0074 INVESTIGATING THE EFFECT OF ACUTE SLEEP DEPRIVATION ON HYPOTHALAMIC-PITUITARY-ADRENAL-AXIS RESPONSE TO A PSYCHOSOCIAL STRESSOR

作者
Iván Vargas,A Gencarelli,W Khader,A DiGuiseppe,J Boyle,Alexandria Muench,Nestor L. Lopez‐Duran
出处
期刊:Sleep [Oxford University Press]
卷期号:40 (suppl_1): A28-A28 被引量:1
标识
DOI:10.1093/sleepj/zsx050.073
摘要

The hypothalamic-pituitary-adrenal (HPA) axis has been previously identified as one potential mechanism that may explain the link between sleep deprivation and negative health outcomes. However, few studies have examined the direct impact of sleep deprivation on HPA-axis functioning, particularly in the context of stress. Therefore, the aim of the current study was to investigate the relationship between acute sleep deprivation and HPA-axis reactivity to a psychosocial stressor. Participants included 40 healthy, young adults between the ages of 18 - 29. The current protocol included spending two nights in the laboratory. After an adaptation night, participants were randomized into either a sleep deprivation condition (n = 20; 29 consecutive hours awake) or a control condition (n = 20; 8-hour sleep opportunity). Following the experimental night, all participants completed the Trier Social Stress Test (TSST). Salivary cortisol was collected before, during, and after the TSST. We used random effects growth curve models to examine the impact of experimental condition on cortisol stress trajectories - i.e., the effect of condition on pre-stress, baseline cortisol (intercept) and cortisol reactivity (non-linear slope) from baseline. Compared to participants in the control condition, participants in the sleep deprivation condition had greater baseline (i.e., pre-stress) cortisol [b = .727, p = .03], yet a blunted cortisol response to the TSST [b = -.026, p < .01]. These effects remained significant while controlling for known covariates (e.g., gender, mood, caffeine use). Taken together, a combination of elevated baseline cortisol (and its subsequent impact on HPA-axis regulatory processes) and a relative ‘ceiling’ on the amount of cortisol a laboratory stressor can produce may explain why participants in the sleep deprivation condition demonstrated blunted cortisol responses. The current findings suggest that future research investigating the relationship between health outcomes and HPA-axis stress reactivity should account for variability in sleep during the night prior to exposing participants to stress. Funding for this research was provided by the University of Michigan Department of Psychology and Rackham Graduate School, Blue Cross Blue Shield of Michigan Foundation, and the American Psychological Association of Graduate Students.
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