Increased sympathetic and decreased parasympathetic cardiovascular modulation in normal humans with acute sleep deprivation

Abstract

Cardiovascular autonomic modulation during 36 h of total sleep deprivation (SD) was assessed in 18 normal subjects (16 men, 2 women, 26.0 +/- 4.6 yr old). ECG and continuous blood pressure (BP) from radial artery tonometry were obtained at 2100 on the first study night (baseline) and every subsequent 12 h of SD. Each measurement period included resting supine, seated, and seated performing computerized tasks and measured vigilance and executive function. Subjects were not supine in the periods between measurements. Spectral analysis of heart rate variability (HRV) and BP variability (BPV) was computed for cardiac parasympathetic modulation [high-frequency power (HF)], sympathetic modulation [low-frequency power (LF)], sympathovagal balance (LF/HF power of R-R variability), and BPV sympathetic modulation (at LF). All spectral data were expressed in normalized units [(total power of the components/total power-very LF) x 100]. Spontaneous baroreflex sensitivity (BRS), based on systolic BP and pulse interval powers, was also measured. Supine and sitting, BPV LF was significantly increased from baseline at 12, 24, and 36 h of SD. Sitting, HRV LF was increased at 12 and 24 h of SD, HRV HF was decreased at 12 h SD, and HRV LF/HF power of R-R variability was increased at 12 h of SD. BRS was decreased at 24 h of SD supine and seated. During the simple reaction time task (vigilance testing), the significantly increased sympathetic and decreased parasympathetic cardiac modulation and BRS extended through 36 h of SD. In summary, acute SD was associated with increased sympathetic and decreased parasympathetic cardiovascular modulation and decreased BRS, most consistently in the seated position and during simple reaction-time testing.

Heart rate variability and endothelial function after sleep deprivation and recovery sleep among male shift and non-shift workers

“…The significantly higher SDNN observed following a night of sleep deprivation is in agreement with a study from Viola et al (58). A few studies have reported significantly higher LF/HF and/or normalized LF power (24)(25)(26), a longer NN interval (60), and a lower NN50 (46) during and after total and partial sleep deprivation. Other studies, however, have found no difference in HRV parameters in these conditions (61,62).…”

“…In addition, it is thought that the risk for CVD among shift workers may depend on the extent of circadian misalignment and sleep deprivation (21). Although it is thought that sleep deprivation and the risk for CVD are linked (22,23), only a few studies have reported higher sympathetic activity and decreased vasodilatation during and after (partial) sleep deprivation (24)(25)(26).…”

Improving Human Cognitive Processing by Applying Accessibility Standards for Information and Communication Technology

“…HRV is often combined with other measurement methods like blood pressure, skin temperature etc. to testify certain interpretations in the context of stress measurement (Zhong et al, 2005;Lupien et al, 2006) and emotions (Lupien and Brière, 2000). The consolidation of HRV and EEG data showed that high beta EEG power correlates with increased HRV significantly (Seo and Lee, 2010).…”

The Relationship Between Sleep Duration and Blood Pressure in the Adult Population

“…Mechanismus, jakým nedostatečný spánek přispívá k vysokému tlaku není dosud zcela objasněn. V experimentálních studiích je u spánkově deprimovaných jedinců zřetelné zvýšení sympatické nervové aktivity, zvýšení srdeční frekvence a zvýšení sodíkové retence (Gangwisch et al, 2006, s. 833;Zhong et al, 2005Zhong et al, , s. 2024. Nedostatečná délka spánku je také prokazatelně spojena s poklesem leptinu, se zvýšením ghrelinu a se zvýšením kortizolu, dále se zvýšenou chutí k jídlu a s insulinovou resistencí, které mohou také nepřímo přispívat k hypertenzi (Adámková, 2009, s. 27).…”