Respiratory Sinus Arrhythmia Mechanisms in Young Obese Subjects.

Michal Javorka,Radovan Wiszt,Jana Krohova,Luca Faes,Miriam Ciljakova,Alessandro Busacca,Zuzana Turianikova,Riccardo Pernice,Dana Cernochova,Barbora Czippelova,Nikoleta Mazgutova

doi:10.3389/fnins.2020.00204

Abstract

Autonomic nervous system (ANS) activity and imbalance between its sympathetic and parasympathetic components are important factors contributing to the initiation and progression of many cardiovascular disorders related to obesity. The results on respiratory sinus arrhythmia (RSA) magnitude changes as a parasympathetic index were not straightforward in previous studies on young obese subjects. Considering the potentially unbalanced ANS regulation with impaired parasympathetic control in obese patients, the aim of this study was to compare the relative contribution of baroreflex and non-baroreflex (central) mechanisms to the origin of RSA in obese vs. control subjects. To this end, we applied a recently proposed information-theoretic methodology – partial information decomposition (PID) – to the time series of heart rate variability (HRV, computed from RR intervals in the ECG), systolic blood pressure (SBP) variability, and respiration (RESP) pattern measured in 29 obese and 29 age- and gender-matched non-obese adolescents and young adults monitored in the resting supine position and during postural and cognitive stress evoked by head-up tilt and mental arithmetic. PID was used to quantify the so-called unique information transferred from RESP to HRV and from SBP to HRV, reflecting, respectively, non-baroreflex and RESP-unrelated baroreflex HRV mechanisms, and the redundant information transferred from (RESP, SBP) to HRV, reflecting RESP-related baroreflex RSA mechanisms. Our results suggest that obesity is associated: (i) with blunted involvement of non-baroreflex RSA mechanisms, documented by the lower unique information transferred from RESP to HRV at rest; and (ii) with a reduced response to postural stress (but not to mental stress), documented by the lack of changes in the unique information transferred from RESP and SBP to HRV in obese subjects moving from supine to upright, and by a decreased redundant information transfer in obese compared to controls in the upright position. These findings were observed in the presence of an unchanged RSA magnitude measured as the high frequency (HF) power of HRV, thus suggesting that the changes in ANS imbalance related to obesity in adolescents and young adults are subtle and can be revealed by dissecting RSA mechanisms into its components during various challenges.

Highlights

Obesity is a complex, multifactorial chronic disease associated with many adverse health consequences (Laederach-Hofmann et al, 2000; De Lorenzo et al, 2019)
Both head-up tilt (HUT) and mental arithmetics (MA) were accompanied by a significant decrease in the high frequency (HF) power of heart rate variability (HRV) (P < 0.001 for HUT and MA in O and C groups, effect size: 0.524–1)
The distribution across subjects of the three considered PID measures computed on the raw data during the four phases of the protocol are shown in Figure 2 for both obese and control groups (O and C, respectively)

Summary

Introduction

Multifactorial chronic disease associated with many adverse health consequences (Laederach-Hofmann et al, 2000; De Lorenzo et al, 2019). In the European Union, over 20% of school-age children (around 12 million children) suffer from overweight or obesity (Bagchi and Preuss, 2012). This results in an increasing occurrence of obesity-related complications (dyslipidemia, atherosclerotic changes, hypertension, impaired glucose tolerance, type 2 diabetes mellitus, etc.) even in childhood and adolescence (Vanderlei et al, 2010; Juonala et al, 2011; Cote et al, 2013; McCrindle, 2015; Ortega et al, 2016; Urbina et al, 2019). Autonomic nervous system (ANS) activity and imbalance between its two main components (parasympathetic and sympathetic nervous control) are important factors contributing to the initiation and progression of many cardiovascular disorders related to obesity (Ito et al, 2001; Cote et al, 2013; McCrindle, 2015; Ortega et al, 2016; Urbina et al, 2019)

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