Background
Sleep deprivation (SD) and acute social stress are common, often unavoidable, and frequently co-occurring stressors in high-risk professions. Both stressors are known to acutely induce inflammatory responses and an increasing body of literature suggests this may lead to cognitive impairment. This study examined the combined effects of total SD and acute social stress on cognitive performance and took a comprehensive approach to explore their (shared) underlying mechanism leading to cognitive decline. Method: We recorded cognitive performance on a response inhibition task and a multitask and monitored a range of inflammatory, psychophysiological and self-reported markers in 101 participants, both before and after one night of either sleep (control group: N = 48) or SD (N = 53), and both before and after a social stressor (Trier Social Stress Test).
Discussion
SD generally decreased cognitive performance and increased required mental effort. By contrast, the isolated effects of a social stressor were not generic, showing a positive effect on cognitive performance when sleep deprived. Our study is the first that studied combined effects of sleep deprivation and acute social stress on cognitive performance and inflammatory markers. It provides a comprehensive overview of effects of these stressors on a range of variables. We did not show unequivocal evidence of an underlying physiological mechanism explaining changes in performance due to (the combination of) sleep deprivation and social stress, but consider IL-22 as a possible cytokine involved in this mechanism and certainly worth following up on in future research.
Results
SD decreased cognitive performance. The social stress test also results in cognitive performance decline in the control group on the response inhibition task, but improved rather than decreased performance of sleep deprived participants on both tasks. The subjective ratings of mental effort also reflect this antagonistic interaction, indicating that the social stressor when sleep-deprived also reduced mental effort. In the inflammatory and physiological measures, this pattern was only reflected by IL-22 in blood. SD reduced blood IL-22 concentrations, and the social stress reduced IL-22 in the control group as well, but not in sleep-deprived participants. There were no interactive effects of SD and social stress on any other inflammatory or psychophysiological measures. The effects of the social stress test on autonomic measures and subjective results suggest that increased arousal may have benefited sleep-deprived participants' cognitive performance.