Total sleep deprivation alters cardiovascular reactivity to acute stressors in humans.
Total sleep deprivation alters cardiovascular reactivity to acute stressors in humans.
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DOI：
10.1152/japplphysiol.00561.2012
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发表时间：
2012-09
影响因子：
3.3
通讯作者：
Huan Yang;John J Durocher;Robert A. Larson;Joseph P Dellavalla;J. Carter
中科院分区：
文献类型：
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作者：
Huan Yang;John J Durocher;Robert A. Larson;Joseph P Dellavalla;J. Carter
心血管对精神压力（MS）和冷加压试验（CPT）的反应性增强与心血管疾病风险增加有关。最近的流行病学研究表明睡眠剥夺是高血压的一个重要危险因素，但睡眠剥夺与心血管反应性之间的关系仍不明确。我们假设24小时完全睡眠剥夺（TSD）将增加心血管反应MS和CPT和钝MS诱导的前臂血管舒张。由于TSD和高血压之间的关联在女性中似乎更强，因此次要目的是探索性别差异。28名年轻健康受试者（14名男性和14名女性）在正常睡眠（NS）和24小时TSD（随机，交叉设计）后，记录MS和CPT期间的平均动脉压（MAP）、心率（HR）和肌肉交感神经活动（MSNA）。NS组和TSD组的MAP、FVC和MSNA（n = 10）对MS的反应无显著性差异（条件×时间，P > 0.05）。NS组和TSD组MAP和MSNA（n = 6）对CPT的反应无显著性差异（条件×时间，P > 0.05）。相比之下，MS和CPT期间的HR增加在TSD后增强（条件×时间，P ≤ 0.05），并且这些增强的HR反应在两次恢复期间持续存在。在分析性别差异时，对MS和CPT的心血管反应性在性别之间没有差异（条件×时间×性别，P > 0.05）。我们的结论是，TSD不显着改变MAP，MSNA，或前臂血管反应MS和CPT。在急性应激源期间和之后的增强的心动过速反应提供了关于睡眠剥夺、应激和心血管风险之间的新兴联系的新见解。
Exaggerated cardiovascular reactivity to mental stress (MS) and cold pressor test (CPT) has been linked to increased risk of cardiovascular disease. Recent epidemiological studies identify sleep deprivation as an important risk factor for hypertension, yet the relations between sleep deprivation and cardiovascular reactivity remain equivocal. We hypothesized that 24-h total sleep deprivation (TSD) would augment cardiovascular reactivity to MS and CPT and blunt the MS-induced forearm vasodilation. Because the associations between TSD and hypertension appear to be stronger in women, a secondary aim was to probe for sex differences. Mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity (MSNA) were recorded during MS and CPT in 28 young, healthy subjects (14 men and 14 women) after normal sleep (NS) and 24-h TSD (randomized, crossover design). Forearm vascular conductance (FVC) was recorded during MS. MAP, FVC, and MSNA (n = 10) responses to MS were not different between NS and TSD (condition × time, P > 0.05). Likewise, MAP and MSNA (n = 6) responses to CPT were not different between NS and TSD (condition × time, P > 0.05). In contrast, increases in HR during both MS and CPT were augmented after TSD (condition × time, P ≤ 0.05), and these augmented HR responses persisted during both recoveries. When analyzed for sex differences, cardiovascular reactivity to MS and CPT was not different between sexes (condition × time × sex, P > 0.05). We conclude that TSD does not significantly alter MAP, MSNA, or forearm vascular responses to MS and CPT. The augmented tachycardia responses during and after both acute stressors provide new insight regarding the emerging links among sleep deprivation, stress, and cardiovascular risk.