Healthy humans with a narrow upper airway maintain patency during quiet breathing by dilating the airway during inspiration

Cheng, Shaokoon; Brown, Elizabeth T.; Hatt, Alice; Butler, Jane E.; Gandevia, Simon C.; Bilston, Lynne E.

doi:10.1113/jphysiol.2014.279240

Cited by 46 publications

(31 citation statements)

References 39 publications

(88 reference statements)

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“…A larger study of people without OSA has shown that inspiratory dilatation was larger with increasing BMI (Cheng et al . ). Also in contrast with our results, Brown et al .…”

Section: Discussionmentioning

confidence: 97%

“…In particular, it was found that airway dilatation during inspiration is larger in the presence of a narrow airway in healthy individuals (Cheng et al . ), differs between heathy controls and people with OSA, but differs between people with and without OSA and varies with OSA severity (Brown et al . ).…”

Section: Introductionmentioning

confidence: 99%

“…; Cheng et al . ; Cai et al . ), potentially by varying the neural drive they receive (Bilston & Gandevia, ).…”

Section: Introductionmentioning

confidence: 99%

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Regional respiratory movement of the tongue is coordinated during wakefulness and is larger in severe obstructive sleep apnoea

Jugé

Knapman

Burke

et al. 2020

The Journal of Physiology

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Key points Coordination of the neuromuscular compartments of the tongue is critical to maintain airway patency. Currently, little is known about the extent to which regional tongue dilatory motion is coordinated in heathy people and if this coordination is altered in people with obstructive sleep apnoea (OSA). We show that regional tongue muscle coordination in people with and without OSA during wakefulness is associated with effective airway dilatation during inspiration, using dynamic tagged magnetic resonance imaging. The maximal movement of four compartments of the tongue were correlated and occurred concurrently towards the end of inspiration. If tongue movement was observed, people with more severe OSA had larger movement and moved more compartments (up to four) to maintain airway patency, while people without OSA moved only one compartment. These results suggest that airway patency is preserved during wakefulness in people with OSA via active dilatory movement of the genioglossus. Abstract Maintaining airway patency when supine requires neural drive to the genioglossus horizontal and oblique neuromuscular compartments (superior fan‐like and inferior horizontal genioglossus, regions that are innervated by different branches of the hypoglossal nerve) to be coordinated during breathing, but it is unknown if this coordination is altered in obstructive sleep apnoea (OSA). This study aimed to assess coordination of airway dilatory motion across four mid‐sagittal tongue compartments during inspiration (i.e. anterior and posterior of the horizontal and oblique compartments), and compare it in controls and OSA patients. Fifty‐four participants (12 women, aged 20–73 years) underwent dynamic ‘tagged’ magnetic resonance imaging during wakefulness. Ten participants had no OSA [apnoea hypopnoea index (AHI) < 5 events h–1], 14 had mild OSA (5 < AHI ≤ 15 events h–1), 12 had moderate OSA (15 < AHI ≤ 30 events h–1) and 18 had severe OSA (AHI > 30 events h–1). A higher AHI was associated with a greater anterior movement of the anterior and posterior horizontal compartments (Spearman, r = −0.32, P = 0.02 for both), but not in the oblique compartments. If movement was observed, higher OSA severity was associated with an anterior movement of a greater number of compartments. Controls only moved the posterior horizontal compartment while the anterior horizontal compartment also moved in OSA participants. Oblique compartments moved only in people with severe OSA. The maximal anterior inspiratory movement of the four compartments was highly correlated (Spearman, P < 0.001) and occurred concurrently. The posterior horizontal compartment had the greatest anterior motion. These results suggest that airway patency is preserved during wakefulness in people with OSA via active dilatory movement of the genioglossus.

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“…A larger study of people without OSA has shown that inspiratory dilatation was larger with increasing BMI (Cheng et al . ). Also in contrast with our results, Brown et al .…”

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Regional respiratory movement of the tongue is coordinated during wakefulness and is larger in severe obstructive sleep apnoea

Jugé

Knapman

Burke

et al. 2020

The Journal of Physiology

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“…In healthy humans, the combined phasic inspiratory and tonic components represent less than 2% of maximal spontaneous GG activity (247). Humans who do not meet the clinical criteria for OSA despite having smaller than normal upper airway cross-sectional area produce larger anterior movements of the tongue during inspiration than other control subjects (90). This suggests that, at least in humans studied during wakefulness, a subclinical reduction of upper airway patency elicits a compensatory activation of upper airway dilating muscles during inspiration.…”

Section: Upper Airway Muscles and Their Activity Patternsmentioning

confidence: 99%

Neural Control of the Upper Airway: Respiratory and State‐Dependent Mechanisms

Kubin

2016

Comprehensive Physiology

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Upper airway muscles subserve many essential for survival orofacial behaviors, including their important role as accessory respiratory muscles. In the face of certain predisposition of craniofacial anatomy, both tonic and phasic inspiratory activation of upper airway muscles is necessary to protect the upper airway against collapse. This protective action is adequate during wakefulness, but fails during sleep which results in recurrent episodes of hypopneas and apneas, a condition known as the obstructive sleep apnea syndrome (OSA). Although OSA is almost exclusively a human disorder, animal models help unveil the basic principles governing the impact of sleep on breathing and upper airway muscle activity. This article discusses the neuroanatomy, neurochemistry, and neurophysiology of the different neuronal systems whose activity changes with sleep-wake states, such as the noradrenergic, serotonergic, cholinergic, orexinergic, histaminergic, GABAergic and glycinergic, and their impact on central respiratory neurons and upper airway motoneurons. Observations of the interactions between sleep-wake states and upper airway muscles in healthy humans and OSA patients are related to findings from animal models with normal upper airway, and various animal models of OSA, including the chronic-intermittent hypoxia model. Using a framework of upper airway motoneurons being under concurrent influence of central respiratory, reflex and state-dependent inputs, different neurotransmitters, and neuropeptides are considered as either causing a sleep-dependent withdrawal of excitation from motoneurons or mediating an active, sleep-related inhibition of motoneurons. Information about the neurochemistry of state-dependent control of upper airway muscles accumulated to date reveals fundamental principles and may help understand and treat OSA.

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“…Indeed, in light of recent findings [33,34], morbidly obese individuals who do not have OSA likely have "supranormal" neuromuscular compensatory mechanisms that protect them from OSA. This concept is further supported by >50% of the study participants having a passive Pcrit above −2 cmH 2 O and elevated AHIs during REM sleep into the pathogenic range when neuromuscular compensatory mechanisms are reduced or absent.…”

Section: @Erspublicationsmentioning

confidence: 99%

When insulin has to work hard to keep the sugar at bay the upper airway collapses away

Eckert

Oliven

2016

Eur Respir J

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@ERSpublicationsInsulin resistance may increase upper airway collapsibility and directly contribute to sleep apnoea pathogenesis http://ow.ly/10BTf9Obesity is a major risk factor for both obstructive sleep apnoea (OSA) and metabolic disease. As obesity rates continue to rise, so too does the prevalence of OSA and metabolic disorders. Indeed, recent community sample data from over 2000 adults aged 40-85 years in Switzerland indicate that up to 50% of men and almost a quarter of women have apnoea-hypopnoea indices (AHI) within the moderate to severe range (>15 events·h −1 sleep) [1]. Insulin resistance, a strong predictor for the development of type 2 diabetes [2], is being recognised earlier with prevalence rates in children varying between 3 and 44% [3]. Thus, OSA and insulin resistance are major health issues.Given the shared link with obesity, the connection between metabolic disruption and OSA is not new. Indeed, OSA has been implicated in the pathogenesis of metabolic dysfunction [4][5][6]. Furthermore, a "bidirectional" or "reciprocal" relationship, or the possibility that OSA is a manifestation of the metabolic syndrome, has been discussed in several publications [7][8][9][10]. However, while evidence continues to grow that sleep-disordered breathing and sleep disruption can worsen metabolic function including insulin resistance [11], there is currently limited direct evidence to support the concept that early biomarkers of metabolic dysfunction such as insulin resistance predispose to OSA [12,13]. Thus, the chicken or the egg causality dilemma remains.The new study by LLANOS et al. [14] in this issue of the European Respiratory Journal takes us one step closer to solving this dilemma. Specifically, the authors have provided elegant insight into this question by going to the source; evaluating the relationship between pre-diabetes (i.e. insulin resistance), and "pre-OSA" (i.e. individuals with vulnerable upper airways due to high mechanical load from morbid obesity but without frank OSA (AHI <10 events/h sleep)). This unique approach has allowed the investigators to study upper airway collapsibility during sleep, using the gold standard critical closing pressure or "Pcrit" technique, without the confounding effects of prior exposure to repetitive severe hypoxaemia and sleep fragmentation, both of which contribute to metabolic sequelae [5,15]. Accordingly, consistent with insulin resistance preceding the decline in pharyngeal stability, the reported positive correlation between insulin resistance and upper airway collapsibility and the ∼4 cmH 2 O increase in Pcrit when the group was dichotomised according to high versus low insulin resistance cannot be explained by the presence of severe sleep-disordered breathing.

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Healthy humans with a narrow upper airway maintain patency during quiet breathing by dilating the airway during inspiration

Cited by 46 publications

References 39 publications

Regional respiratory movement of the tongue is coordinated during wakefulness and is larger in severe obstructive sleep apnoea

Regional respiratory movement of the tongue is coordinated during wakefulness and is larger in severe obstructive sleep apnoea

Neural Control of the Upper Airway: Respiratory and State‐Dependent Mechanisms

When insulin has to work hard to keep the sugar at bay the upper airway collapses away

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