Cardiovascular reactivity to acute psychological stress following sleep deprivation.
Cardiovascular reactivity to acute psychological stress following sleep deprivation.
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DOI:
10.1097/psy.0b013e31822ff440
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发表时间:
2011-10
影响因子:
3.3
通讯作者:
Buysse DJ
中科院分区:
文献类型:
--
作者:
Franzen PL;Gianaros PJ;Marsland AL;Hall MH;Siegle GJ;Dahl RE;Buysse DJ
Psychological stress and sleep disturbances are highly prevalent and are both implicated in the etiology of cardiovascular diseases. Given the common co-occurrence of psychological distress and sleep disturbances including short sleep duration, this study examined the combined effects of these two factors on blood pressure reactivity to acute mental challenge tasks following well-rested and sleep deprived experimental conditions. Participants (n=20) were healthy young adults free from current or past sleep, psychiatric, or major medical disorders. Using a within-subjects crossover design, we examined acute stress reactivity under two experimental conditions: following a night of normal sleep in the laboratory and following a night of total sleep deprivation. Two standardized psychological stress tasks were administered, a Stroop color-word naming interference task and a speech task, which were preceded by a pre-stress baseline and followed by a post-stress recovery period. Each period was 10 minutes in duration, and blood pressure recordings were collected every 2.5 minutes throughout each period. Mean blood pressure responses during the stress and recovery periods were examined with a mixed effects analysis of covariance, controlling for baseline blood pressure. There was a significant interaction between sleep deprivation and stress on systolic blood pressure (F2,82.7=4.05, p=0.02). Systolic blood pressure was higher in the sleep deprivation condition compared with the normal sleep condition during the speech task, as well as during two baseline periods. Sleep deprivation amplified systolic blood pressure increases to psychological stress. Sleep loss may increase cardiovascular risk by dysregulating stress physiology.