Abstract
Acute sleep deprivation (SD) alters cardiovascular autonomic control (CAC) and is associated with an increased risk of cardiovascular disorders. However, the effects of partial SD on CAC are unclear. Thus, we aimed to investigate the effects of partial SD on CAC during sleep. We randomized seventeen healthy subjects to a restriction group (RES, n = 8, subjects slept two‐thirds of normal sleep time based on individual habitual sleep duration for 8 days and 8 nights) or a Control group (CON, n = 9, subjects were allowed to sleep their usual sleep time). Attended polysomnographic (PSG) studies were performed every night; a subset of them was selected for the analysis at baseline (day 3‐D3), the first night after sleep restriction (day 5‐D5), at the end of sleep restriction period (day 11‐D11), and at the end of recovery phase (day 14‐D14). We extracted electrocardiogram (ECG) and respiration from the PSG and divided into wakefulness (W), nonrapid eye movements (REM) sleep (N2 and N3) and REM sleep. CAC was evaluated by means of linear spectral analysis, nonlinear symbolic analysis and complexity indexes. In both RES and CON groups, sympathetic modulation decreased and parasympathetic modulation increased during N2 and N3 compared to W and REM at D3, D5, D11, D14. Complexity analysis revealed a reduction in complexity during REM compared to NREM sleep in both DEP and CON. After 8 days of moderate SD, cardiac autonomic dynamics, characterized by decreased sympathetic, and increased parasympathetic modulation, and higher cardiac complexity during NREM sleep, compared to W and REM, are preserved.
Highlights
Symbolic analysis revealed that 0V, marker of sympathetic modulation, was lower in N2 and N3 compared to W and REM on D3, it decreased in N3 compared to W and REM in D5, in N2 and N3 compared to REM at D11 and in N2 and N3 compared to W
2LV% and 2UV% were higher in N3 compared to W and REM at D3, higher in N3 with respect to REM at D5, higher in N2 and N3 compared to REM at D11 and higher in N2 and N3 compared to REM at D14
Corrected Conditional Entropy (CCE) was higher during N3 compared to W at D3 and higher in N2 and N3 compared to REM at D11
Summary
Acute sleep loss is associated with an increased risk of developing cardiovascular diseases, cerebrovascular disorders, metabolic disorders (Eguchi et al 2008; Cappuccio et al 2010), and infectious diseases (Patel et al 2012).From a pathophysiological point of view, sleep loss is associated with activation of several molecular and integrative regulatory mechanisms, such as disruption of the autonomic nervous system (ANS) (Tasali et al 2008; Tobaldini et al 2013b, 2014), an impaired immune and inflammatory response (Imeri and Opp 2009).The ANS plays a key role in linking sleep deprivation with detrimental clinical consequences of sleep loss. Acute sleep loss is associated with an increased risk of developing cardiovascular diseases, cerebrovascular disorders, metabolic disorders (Eguchi et al 2008; Cappuccio et al 2010), and infectious diseases (Patel et al 2012). From a pathophysiological point of view, sleep loss is associated with activation of several molecular and integrative regulatory mechanisms, such as disruption of the autonomic nervous system (ANS) (Tasali et al 2008; Tobaldini et al 2013b, 2014), an impaired immune and inflammatory response (Imeri and Opp 2009). It has been shown that after 24 h of complete sleep loss, heart rate (HR) and arterial blood pressure (ABP) were higher compared to baseline in healthy subjects (Zhong et al 2005; Sauvet et al 2014; Sunbul et al 2014). An important change in the sympathovagal balance, in terms of increased sympathetic component and reduction in vagal modulation
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