Although compelling evidence has demonstrated considerable neuroplasticity in the respiratory control system, few studies have explored the possibility of altering descending projections to phrenic motoneurons (PMNs) using noninvasive stimulation protocols. The present study was designed to investigate the immediate and long-lasting effects of a single session of transcutaneous spinal direct current stimulation (tsDCS), a promising technique for modulating spinal cord functions, on descending ventilatory commands in healthy humans. Using a double-blind, controlled, randomized, crossover approach, we examined the effects of anodal, cathodal, and sham tsDCS delivered to the C3-C5 level on (1) diaphragm motor-evoked potentials (DiMEPs) elicited by transcranial magnetic stimulation and (2) spontaneous ventilation, as measured by respiratory inductance plethysmography. Both anodal and cathodal tsDCS induced a progressive increase in DiMEP amplitude during stimulation that persisted for at least 15 min after current offset. Interestingly, cathodal, but not anodal, tsDCS induced a persistent increase in tidal volume. In addition, (1) short-interval intracortical inhibition, (2) nonlinear complexity of the tidal volume signal (related to medullary ventilatory command), (3) autonomic function, and (4) compound muscle action potentials evoked by cervical magnetic stimulation were unaffected by tsDCS. This suggests that tsDCS-induced aftereffects did not occur at brainstem or cortical levels and were likely not attributable to direct polarization of cranial nerves or ventral roots. Instead, we argue that tsDCS could induce sustained changes in PMN output. Increased tidal volume after cathodal tsDCS opens up the perspective of harnessing respiratory neuroplasticity as a therapeutic tool for the management of several respiratory disorders.

New Findings What is the central question of this study?Moving to supine induces upper airway modifications and a fluid shift to the neck, which represent inspiratory load that predisposes to upper airway collapse. Is there cortical participation in the response to the load induced by transition to a supine posture in awake healthy subjects? What is the main finding and its importance?Moving to supine induces transient cortical activation in awake healthy subjects, with greater fluid shift, supporting possible cortical participation in the response to upper airway load induced by transition to a supine posture. Our findings open new perspectives in the understanding of the pathogenesis of obstructive sleep apnoea. Abstract Moving from sitting upright to lying supine causes anatomical modifications and a fluid shift to the neck, which represent inspiratory loads that predispose to upper airway collapse. The pre‐inspiratory potential (PIP) corresponds to the cortical activity observed during inspiratory load. In the sitting position during wakefulness, some obstructive sleep apnoea patients exhibit PIP, probably in relationship to upper airway abnormalities. The aim of this study was to investigate whether moving to the supine position induces respiratory‐related cortical activation (PIP) in awake healthy subjects. The ECG was analysed to detect PIP, and EMG activity of the genioglossus muscle and ventilation were measured in the sitting position, immediately after moving to the supine position, and during application of leg positive pressure in the supine position to promote fluid shift, which was measured by bioelectrical impedance. Twenty‐four subjects were included. From sitting to lying, PIP prevalence increased from 1/24 to 11/24 (P = 0.002), and ventilation decreased with no change in genioglossus activity. The fluid shift from sitting to supine was higher in the subjects exhibiting PIP while supine compared with the subjects without PIP [median (25th; 75th centiles) 440 (430; 520) versus 320 (275; 385) ml, P = 0.018], without any other differences. From before to during leg positive pressure, PIP disappeared (P = 0.006). These results indicate that moving from sitting to lying induces transient respiratory‐related cortical activity in awake healthy subjects with greater fluid shift, supporting possible cortical participation in the response to upper airway loading induced by moving from sitting upright to lying supine. This study offers new perspectives in the understanding of obstructive sleep apnoea pathogenesis.

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Introduction La dyspnée semble peu rapportée au cours des pneumopathies causées par le coronavirus 2 du syndrome respiratoire aigu sévère (SARS CoV 2), faisant parfois évoquer le terme d’“hypoxémie silencieuse”. La dyspnée, perception d’informations sensorielles liées à la respiration, est associée à un vécu émotionnel négatif. Elle résulterait de l’activation de structures du système limbique/paralimbique dont, l’insula. Cette dernière serait le centre d’alarme intéroceptif, reliant la perception de sensations viscérales (dont la dyspnée) à l’expérience consciente des émotions. Le potentiel neuroinvasif du SARS CoV 2 via les bulbes olfactifs fait suspecter une atteinte limbique/paralimbique mais aussi du tronc cérébral au cours de l’atteinte respiratoire de la Corona VIrus Disease 2019 (COVID19). Nous formulons l’hypothèse qu’une atténuation de la composante affective de la dyspnée lors de l’hypoxie, résultant de l’atteinte de l’intéroception, est la conséquence d’une atteinte de ces structures neurologiques. Méthodes Une étude observationnelle, DysCovid, a porté sur l’évaluation de l’interoception et de la dyspnée chez des patients hospitalisés en pneumologie et/ou en réanimation. Une étude physiopathologique, CRC COVID, a porté sur l’évaluation de l’interoception et de la dyspnée expérimentalement induite chez des patients présentant une forme neurologique pure de la COVID19. Ces études comportaient un examen neurologique, une évaluation de l’intéroception et de la dyspnée au moyen d’échelles visuelles analogiques (sensorielle et affective) et du questionnaire multidimensional dyspnea profile. Dans CRC-COVID la dyspnée et la réponse ventilatoire ont été évaluées lors de test en hypoxie et en hypercapnie. Résultats et Conclusion Les inclusions et analyses des données, sont en cours.