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• W2930735279 abstract "The human pharyngeal airway is at risk of occlusion during sleep, owing to state-dependent decreases in cranial motor outflow, which result in upper airway muscle hypotonia and narrowing of airway calibre. Obstructive sleep apnoea syndrome (OSAS), a common debilitating condition associated with multisystem morbidity, is characterized by recurrent collapse of the pharyngeal airway that impedes pulmonary gas exchange. The pathogenesis of OSAS is multifactorial, with anatomical and non-anatomical contributory factors. Interestingly, disordered breathing does not present in persons with OSAS whilst awake, revealing the importance of a ‘wakefulness’ drive manifest in multiple motor pathways to dilator muscles of the upper airways, protecting airway patency. Cortical and subcortical circuitry is implicated in motor control of the upper airway. Of interest, there are notable differences in corticomotor control of the genioglossus (the principal airway dilator muscle) during wakefulness in persons with OSAS compared with healthy control subjects (Sériès, Wang, & Similowski, 2009). Moreover, respiratory-related cortical activity is evident in EEG recordings in persons with severe OSAS whilst awake (Launois et al., 2015), whereas this is not usually detected in healthy control subjects. Upper airway collapsibility is posture dependent. Moving from sitting upright to lying supine evokes a number of changes that predispose to airway collapse, including a redistribution of fluid from the legs to the neck. Rostral fluid shift narrows the upper airway, increasing inspiratory load, sufficient to reduce ventilation. Nocturnal rostral fluid shift is implicated in the pathophysiology of OSAS and might be a major factor in some co-morbid diseases, such as chronic heart failure and end-stage renal disease. In this issue of Experimental Physiology, Launois et al. (2019) explored whether experimentally induced rostral fluid shift to the neck elicits respiratory-related cortical activation. Twenty-four healthy participants were studied sitting upright and then lying supine, with a subset also examined during subsequent application of lower-body positive pressure in the supine position. The EEG was measured for the assessment of respiratory-related cortical activation (pre-inspiratory potentials). Ventilation was determined from measurements of nasal airflow. Genioglossus recordings were obtained using surface EMG electrodes. Rostral fluid shift during postural and lower-body positive pressure challenges was calculated from measures of leg fluid volume estimated by bioelectrical impedance. Pre-inspiratory potentials, appearing up to 2 s before the onset of inspiration, were observed in only one of 24 participants while sitting upright, but were evident in 11 participants lying supine, indicative of cortical activation in response to presumed airway narrowing and augmented inspiratory load. The magnitude of rostral fluid shift was significantly higher in participants displaying pre-inspiratory potentials compared with those who did not, suggesting a threshold inspiratory load associated with cortical activation. Movement from sitting upright to lying supine evoked a significant reduction in minute ventilation, with concomitant CO2 retention. Interestingly, responses were transient, dissipating after 15 min in the supine position, such that no pre-inspiratory potentials were observed during application of lower-body positive pressure in the supine position. Of note, however, the majority of the fluid shift occurred during the initial postural adjustment, with considerably less fluid shift during the subsequent lower-body positive pressure challenge. Therefore, inspiratory load might not have been increased during lower-body positive pressure in this particular study design. Oddly, genioglossus EMG activity was not increased in the supine position compared with sitting upright despite rostral fluid shift and other posture-dependent factors. Surprisingly, there were no differences in genioglossus EMG activity when comparing those with and without pre-inspiratory potentials. On the face of it, these observations suggest limited corticomotor activation of the upper airway musculature during postural challenge with confirmed rostral fluid shift. This is unlikely, however, and indeed incongruent with a previous report of increased genioglossus EMG activation in healthy supine participants compared with sitting upright, observed by Vranish & Bailey (2015) using intramuscular wire electrodes, which might be superior to surface electrodes, a point acknowledged by the authors. It is established that airway narrowing evokes reflex activation of the genioglossus in the defence of airway calibre. Assessment of upper airway resistance would have provided a gold-standard measure of airway mechanics, allowing consideration of the consequences of rostral fluid shift on upper airway calibre, which would have benefitted comparisons within and between participants. Notwithstanding the curious EMG findings, the study by Launois et al. (2019) confirms and extends previous work revealing cortical activation during rostral fluid shift, suggesting a cortical contribution to respiratory motor behaviour in circumstances of increased respiratory load. It is plausible to consider that persons with OSAS (and other respiratory conditions characterized by increased respiratory load) develop a greater dependence on cortical control of breathing and airway calibre; indeed, there is evidence of corticomotor plasticity in persons with OSAS (Sériès et al., 2009). One wonders whether compensation is lost in OSAS during the transition to sleep, such that corticomotor facilitation of upper airway muscles might be less effective in the support of airway patency. This potential loss of neuromuscular compensation in persons with OSAS could contribute to the increased propensity for airway collapse. Intriguingly, corticomotor activation of the upper airway can be awakened experimentally. Transcranial magnetic stimulation has been trialled successfully in OSAS, with evidence of reduced flow limitation during sleep (Melo-Silva, Gakwaya, Rousseau, & Sériès, 2013). Moreover, corticomotor pathways may be amenable to facilitation in response to repeated activation (Rousseau, Gakwaya, Melo-Silva, & Sériès, 2015). As such, non-invasive selective motor activation of upper airway muscles could be a viable treatment for OSAS, at least in some sleep stages, providing a realistic alternative strategy for those persons non-compliant with mainstay continuous positive airway pressure therapy. The study by Launois et al. (2019) reminds us that a better understanding of physiological compensation in response to stressors in health can help to inform and guide the development and implementation of interventional therapies in disease. In so doing, it provides plenty to think about! None declared." @default.
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• W2930735279 date "2019-04-11" @default.
• W2930735279 modified "2023-10-16" @default.
• W2930735279 title "Cortical control of upper airway calibre: It's the thought that counts!" @default.
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• W2930735279 doi "https://doi.org/10.1113/ep087681" @default.
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