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New Finding: What is the central question of this study?Transition to supine posture induces an inspiratory load associated with cortical activation in awake healthy subjects. Some obstructive sleep apnoea patients exhibit this cortical activity in the sitting position contributing to the arousal‐dependent compensation of their upper airway abnormalities. Does a transition to the supine posture in awake obstructive sleep apnoea patients increase this cortical activity?What is the main finding and its importance?The transition to supine posture induces a reduction in the cortical activity despite evidence of an increase in genioglossus activity, suggesting that genioglossus activation is not driven by cortical activity. The anatomy and mechanical properties of the upper airway (UA) depend on posture. Lying in a supine position causes cephalad fluid shift to the neck, thus narrowing the UA and predisposing the individual to obstructive sleep apnoea (OSA). Increased UA dilator muscle activity during wakefulness prevents the UA collapse but the underlying mechanism has not yet been elucidated. In the sitting position during wakefulness, some OSA patients exhibit preinspiratory cortical activity (preinspiratory potential, PIP) probably related to UA abnormalities. The aim of this study was to investigate changes in the preinspiratory cortical activity and UA dilator muscle in OSA patients during postural challenge. An electroencephalogram was used to detect PIP, and the genioglossus electromyographic activity and ventilation were analysed in 17 awake, male OSA patients while they were sitting, just after lying down, and then in response to leg positive pressure to enhance cephalad fluid shift. The prevalence of PIP decreased from 53% (sitting) to 12% (supine) (P = 0.002) in association with increased genioglossus activity (tonic from median (25th, 75th centiles) 2.3 (1.8, 2.8)% to 3.6 (1.7, 5.0)% of voluntary deglutition, P = 0.019; phasic from 2.3 (1.9, 2.8)% to 3.7 (2.0, 6.1)%, P = 0.024), and with increased transcutaneous carbon dioxide pressure (from 43.0 (42.4, 44.2) to 44.6 (43.5, 45.2) mmHg). No change was observed during leg‐positive‐pressure application. Moving from the sitting position to the supine position reduces respiratory‐related premotor cortical activity in awake OSA patients. The concomitant increase in genioglossus activity, therefore, is not driven by cortical respiratory activity. [ABSTRACT FROM AUTHOR]

Spontaneous ventilation in mammals is driven by automatic brainstem networks that generate the respiratory rhythm and increase ventilation in the presence of increased carbon dioxide production. Hypocapnia decreases the drive to breathe and induces apnea. In humans, this occurs during sleep but not during wakefulness. We hypothesized that hypocapnic breathing would be associated with respiratory-related cortical activity similar to that observed during volitional breathing, inspiratory constraints, or in patients with defective automatic breathing (preinspiratory potentials). Nineteen healthy subjects were studied under passive (mechanical ventilation, n=10) or active (voluntary hyperventilation, n = 9) profound hypocapnia. Ventilatory and electroencephalographic recordings were performed during voluntary sniff maneuvers, normocapnic breathing, hypocapnia, and after return to normocapnia.EEGrecordings were analyzed with respect to the ventilatory flow signal to detect preinspiratory potentials in frontocentral electrodesandto constructtime-frequencymaps.After passive hyperventilation,hypocapnia was associated with apnea in 3 cases and ventilation persisted in 7 cases (3 and 6 after active hyperventilation, respectively). No respiratoryrelated EEG activity was observed in subjects with hypocapnia-related apneas. In contrast, preinspiratory potentials were present at vertex recording sites in 12 of the remaining 13 subjects (p < 0.001). This was corroborated by time-frequency maps. This study provides direct evidence of a cortical substrate to hypocapnic breathing in awake humans and fuels the notion of corticosubcortical cooperation to preserve human ventilation in a variety of situations. Of note, maintaining ventilatory activity at low carbon dioxide levels is among the prerequisites to speech production insofar as speech often induces hypocapnia. [ABSTRACT FROM AUTHOR]

Patients with central respiratory paralysis can benefit from diaphragm pacing to restore respiratory function. However, it would be important to develop a continuous respiratory monitoring method to alert on apnea occurrence, in order to improve the efficiency and safety of the pacing system. In this study, we present a preliminary validation of an acoustic apnea detection method on healthy subjects data. Thirteen healthy participants performed one session of two 2-min recordings, including a voluntary respiratory pause. The recordings were post-processed by combining temporal and frequency detection domains, and a new method was proposed—Phonocardiogram-Derived Respiration (PDR). The detection results were compared to synchronized pneumotachograph, electrocardiogram (ECG), and abdominal strap (plethysmograph) signals. The proposed method reached an apnea detection rate of 92.3%, with 99.36% specificity, 85.27% sensitivity, and 91.49% accuracy. PDR method showed a good correlation of 0.77 with ECG-Derived Respiration (EDR). The comparison of R-R intervals and S-S intervals also indicated a good correlation of 0.89. The performance of this respiratory detection algorithm meets the minimal requirements to make it usable in a real situation. Noises from the participant by speaking or from the environment had little influence on the detection result, as well as body position. The high correlation between PDR and EDR indicates the feasibility of monitoring respiration with PDR. [ABSTRACT FROM AUTHOR]