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Introduction The autonomic nervous system (ANS) relies on two essential feedback loops: respiratory sinus arrythmia (RSA) and arterial baroreflex which are both regulated by a complex interplay of sympathetic and parasympathetic activations. The amplitude of RSA is modified by the respiratory frequency, i.e. an increase in respiratory frequency leads to a progressive decline in RSA as vagal effectors become less able to follow variations at higher frequencies. On the contrary, a reduction in the respiratory frequency can increase RSA. Slow Paced Breathing (SPB) is usually associated with deep changes in thoracic volume which increases the parasympathetic tone, and which has numerous expected beneficial effects on health. However, some studies report little or no effects. The goal of this study was to test a personalized SPB training vs. placebo to help disentangle the effects of SPB from those solely linked to breathing awareness or distraction. Methods Twenty-four young healthy volunteers participated in this study. They performed a four-week protocol of personalized SPB exercises (SPB group, n = 12) or control condition (spontaneous breathing, CON group, n = 12). Before and after the interventional period, they performed baroreflex sensitivity (BRS) and heart rate variability (HRV) assessments in our laboratory (labPRE and labPOST). During these four weeks, they performed three times per week an orthostatic test (OT) at home immediately before (hPRE) and after (hPOST) a SPB or CON exercise. The OT consisted of five minutes supine (sup) immediately followed by five minutes standing (stand). Personalized SPB was determined as the breathing frequency that elicited the greatest possible RSA, i.e., the best synchronization between breathing and heart rate. The HRV assessments included measures of heart rate (HR), root mean square of the successive differences (RMSSD), power spectrum in the low- and high-frequency bands (LF and HF). Results HFsup increased only in the SPB group (1062±686 vs 1469±905 ms2) from labPRE to labPOST. In addition, both RMSSDsup (54±29 vs. 62±19 ms) and HFsup (1369±1211 vs. 1469±905 ms2) were greater in the SPB group than the control group in labPOST. BRS increased only in the SPB group from labPRE to labPOST (12.8±3.2 vs. 15.2±2.8 ms/mmHg). LFsup decreased from hPRE to hPOST and this decrease was greater in SPB than CON. RMSSDstand increased in both groups from hPRE to hPOST and this increase was greater in CON than SPB. LFstand decreased from hPRE to hPOST. This decrease was greater by the end than at the beginning of the intervention and greater in SPB than CON. HFstand increased from hPRE to hPOST, and this increase was greater in SPB than CON. Discussion/Conclusion Four weeks of SPB training led to a larger increase in parasympathetic modulations to the heart in SPB than CON, indicating that such prolonged intervention has beneficial effects on health. These specific benefits were generally significant from week 4 onward. Further studies are required to better explore the underlying mechanisms.

Chronic pain is a prevalent and debilitating condition whose neural mechanisms are incompletely understood. An imbalance of cerebral excitation and inhibition (E/I), particularly in the medial prefrontal cortex (mPFC), is believed to represent a crucial mechanism in the development and maintenance of chronic pain. Thus, identifying a non-invasive, scalable marker of E/I could provide valuable insights into the neural mechanisms of chronic pain and aid in developing clinically useful biomarkers. Recently, the aperiodic component of the electroencephalography (EEG) power spectrum has been proposed to represent a non-invasive proxy for E/I. We, therefore, assessed the aperiodic component in the mPFC of resting-state EEG recordings in 149 people with chronic pain and 115 healthy participants. We found robust evidence against differences in the aperiodic component in the mPFC between people with chronic pain and healthy participants, and no correlation between the aperiodic component and pain intensity. These findings were consistent across different subtypes of chronic pain and were similarly found in a whole-brain analysis. Their robustness was supported by preregistration and multiverse analyses across many different methodological choices. Together, our results suggest that the EEG aperiodic component does not differentiate between people with chronic pain and healthy individuals. These findings and the rigorous methodological approach can guide future studies investigating non-invasive, scalable markers of cerebral dysfunction in people with chronic pain and beyond.