Sleep deprivation is associated with dysregulation of the autonomic nervous system, adverse cardiovascular events, cognitive and complex motor performance impairment. Less is known about the effects of acute total sleep deprivation (ATSD) on physiological coupling. We aimed to determine the effects of 24-h ATSD on the physiological coupling between complex subsystems by evaluating the cardiorespiratory, cardiovascular and cortico-cardiac interactions. This study enrolled 38 young healthy participants aged 23.2 ± 2.4 years. Multiple synchronous physiological signals including electrocardiography, photoplethysmography, bio-electrical impedance, electroencephalography, and continuous hemodynamic data, were performed over a baseline night after regular sleep and after a night with 24-h ATSD in the supine position. The magnitude squared coherence, phase synchronization index, and heartbeat evoked potential amplitudes, were obtained from 10-min synchronous physiological recordings to estimate the coupling strength between two time series. Parameters of hemodynamic characteristics and heart rate variability were also calculated to quantify autonomic regulation. Results indicated that the magnitude squared coherence (0.38 ± 0.17 vs. 0.29 ± 0.12, p = 0.015) between respiration and heart rate variability along with the magnitude squared coherence (0.36 ± 0.18 vs. 0.27 ± 0.13, p = 0.012) between respiration and pulse transit time were significantly decreased after 24-h ATSD. There were no significant differences (all p > 0.05) in phase synchronization indices, heartbeat evoked potential amplitudes as well as other analyzed measurements between baseline and 24-h ATSD states. We conclude that exposure to 24-h ATSD appears to weaken the cardiorespiratory and respiratory-cardiovascular coupling strength of young healthy adults. These findings suggest that physiological coupling analysis may serve as a complementary approach for characterizing and understanding the complex effects of sleep deprivation.

Introduction: Accumulating evidence suggests that enhanced external counterpulsation (EECP) influences cardiac functions, hemodynamic characteristics and cerebral blood flow. However, little is known about whether or how the EECP affects the brain-heart coupling to produce these physiological and functional changes. We aimed to determine if the brain-heart coupling is altered during or after EECP intervention by assessing the heartbeat evoked potential (HEP) in healthy adults.Methods: Based on a random sham-controlled design, simultaneous electroencephalography and electrocardiography signals as well as blood pressure and flow status data were recorded before, during and after two consecutive 30-min EECP in 40 healthy adults (female/male: 17/23; age: 23.1 ± 2.3 years). HEP amplitude, frequency domain heart rate variability, electroencephalographic power and hemodynamic measurements of 21 subjects (female/male: 10/11; age: 22.7 ± 2.1 years) receiving active EECP were calculated and compared with those of 19 sham control subjects (female/male: 7/12; age: 23.6 ± 2.5 years).Results: EECP intervention caused immediate obvious fluctuations of HEP from 100 to 400 ms after T-peak and increased HEP amplitudes in the (155–169) ms, (354–389) ms and (367–387) ms time windows after T-peak in the region of the frontal pole lobe. The modifications in HEP amplitude were not associated with changes in the analyzed significant physiological measurements and hemodynamic variables.Discussion: Our study provides evidence that the HEP is modulated by immediate EECP stimuli. We speculate that the increased HEP induced by EECP may be a marker of enhanced brain-heart coupling. HEP may serve as a candidate biomarker for the effects and responsiveness to EECP.

IntroductionEnhanced external counterpulsation (EECP) is a non-invasive assisted circulation technique for its clinical application in the rehabilitation and management of ischemic cardiovascular and cerebrovascular diseases, which has complex physiological and hemodynamic effects. However, the effects of EECP on the coupling of physiological systems are still unclear. We aimed to investigate the immediate effects of EECP on the coupling between integrated physiological systems such as cardiorespiratory and cardiovascular systems.MethodsBased on a random sham-controlled design, simultaneous electrocardiography, photoplethysmography, bio-electrical impedance, and continuous hemodynamic data were recorded before, during and after two consecutive 30 min EECP in 41 healthy adults. Physiological coupling strength quantified by phase synchronization indexes (PSI), hemodynamic measurements and heart rate variability indices of 22 subjects (female/male: 10/12; age: 22.6 ± 2.1 years) receiving active EECP were calculated and compared with those of 19 sham control subjects (female/male: 7/12; age: 23.6 ± 2.5 years).ResultsImmediately after the two consecutive EECP interventions, the physiological coupling between respiratory and cardiovascular systems PSIRES–PTT (0.34 ± 0.14 vs. 0.49 ± 0.17, P = 0.002), the physiological coupling between cardiac and cardiovascular systems PSIIBI–PTT (0.41 ± 0.14 vs. 0.52 ± 0.16, P = 0.006) and the total physiological coupling PSItotal (1.21 ± 0.35 vs. 1.57 ± 0.49, P = 0.005) in the EECP group were significantly lower than those before the EECP intervention, while the physiological coupling indexes in the control group did not change significantly (P > 0.05).ConclusionOur study provides evidence that the PSI is altered by immediate EECP intervention. We speculate that the reduced PSI induced by EECP may be a marker of disturbed physiological coupling. This study provides a new method for exploring the mechanism of EECP action and may help to further optimize the EECP technique.