Fluctuation in timing of upper airway and chest wall inspiratory muscle activity in obstructive sleep apnea

Hudgel, David W.; Harasick, Theresa

doi:10.1152/jappl.1990.69.2.443

Cited by 96 publications

(47 citation statements)

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“…As an obstructive apnoea approaches and upper airway inspiratory resistance progressively increases, inspiratory EMG activity of the upper airway muscles moves closer to and then falls behind RC EMG inspiratory activity [138]. Activity of the upper airway muscles remains behind the RC muscles during the apnoea, but again begins to precede activity of the RC muscles when the upper airway opens.…”

Section: Relationship Of Upper Airway and Diaphragmatic Emg Activitymentioning

confidence: 98%

“…In addition, it has been speculated that the relative timing of inspiratory EMG activity of the upper airway to DIA and RC activity fluctuates during sleep in OSA [138]. As an obstructive apnoea approaches and upper airway inspiratory resistance progressively increases, inspiratory EMG activity of the upper airway muscles moves closer to and then falls behind RC EMG inspiratory activity [138].…”

Section: Relationship Of Upper Airway and Diaphragmatic Emg Activitymentioning

confidence: 99%

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Pathophysiology of obstructive sleep apnoea

Deegan¹,

McNicholas²

1995

Eur Respir J

264

183

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Arousal plays an important role in the termination of each apnoea, but may also contribute to the development of further apnoea, because of a reduction in respiratory drive related to the hypocapnia which results from postapnoeic hyperventilation. A cyclical pattern of repetitive obstructive apnoeas may result.A better understanding of the integrated pathophysiology of OSA should help in the development of new therapeutic techniques.

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Section: Relationship Of Upper Airway and Diaphragmatic Emg Activitymentioning

confidence: 98%

Section: Relationship Of Upper Airway and Diaphragmatic Emg Activitymentioning

confidence: 99%

Pathophysiology of obstructive sleep apnoea

Deegan¹,

McNicholas²

1995

Eur Respir J

264

183

View full text Add to dashboard Cite

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“…The possibility that a sleep-induced imbalance in both the magnitude and timing of electrical activity between the upper airway and chest wall inspiratory muscles plays a role in the pathogenesis of sleep apnoea was raised long ago [36,37]. Similarly, the muscular-hydrostat model of tongue function proposes a constant coordinated interaction of extrinsic and intrinsic tongue muscles in all tongue movements [38].…”

Section: Sleep-related Disorders Y Dotan Et Almentioning

confidence: 99%

Dissociation of electromyogram and mechanical response in sleep apnoea during propofol anaesthesia

et al. 2012

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Pharyngeal collapsibility during sleep is believed to increase due to a decline in dilator muscle activity. However, genioglossus electromyogram (EMG) often increases during apnoeas and hypopnoeas, often without mechanical effect.17 patients with obstructive sleep apnoea were anaesthetised and evaluated from termination of propofol administration to awakening. Genioglossus EMG, flow and pharyngeal area (pharyngoscopy) were monitored. Prolonged hypopnoeas enabled evaluation of the relationships between genioglossus EMG and mechanical events, before and after awakening. Additional dilator muscle EMGs were recorded and compared to the genioglossus. Electrical stimulation of the genioglossus was used to evaluate possible mechanical dysfunction.Prolonged hypopnoeas during inspiration before arousal triggered an increase in genioglossus EMG, reaching mean¡SD 62.2¡32.7% of maximum. This augmented activity failed to increase flow and pharyngeal area. Awakening resulted in fast pharyngeal enlargement and restoration of unobstructed flow, with marked reduction in genioglossus EMG. Electrical stimulation of the genioglossus under propofol anaesthesia increased the inspiratory pharyngeal area (from 25.1¡28 to 66.3¡75.5 mm 2 ; p,0.01) and flow (from 11.5¡6.5 to 18.6¡9.2 L?min -1 ; p,0.001), indicating adequate mechanical response. All additional dilators increased their inspiratory activity during hypopnoeas. During propofol anaesthesia, pharyngeal occlusion persists despite large increases in genioglossus EMG, in the presence of a preserved mechanical response to electrical stimulation.

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“…In addition, the high expression of NK1 receptors in spinal (particularly phrenic) MN pools relative to moderate or low expression in XII, facial and trigeminal motoneuron pools (Charlton & Helke, 1985;Yashpal et al 1990;Nakaya et al 1994;Manaker & Zucchi, 1998) suggests that actions may differ between motoneuron pools. Given the hypothesis that a mismatch of activity in upper airway and inspiratory pump muscles contributes to apnoea (Hudgel & Harasick, 1990), there is considerable interest in understanding the basis of this differential excitability. The finding that SP is elevated in brains of sudden infant death syndrome (SIDS) victims (Bergstrom et al 1984;Takashima et al 1994) further emphasises its potential importance to respiratory control of the upper airway.…”

mentioning

confidence: 99%

Modulation of hypoglossal motoneuron excitability by NK1 receptor activation in neonatal mice in vitro

Yasuda

Robinson

Selvaratnam

et al. 2001

The Journal of Physiology

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The effects of substance P (SP), acting at NK1 receptors, on the excitability and inspiratory activity of hypoglossal (XII) motoneurons (MNs) were investigated using rhythmically active medullary‐slice preparations from neonatal mice (postnatal day 0‐3). Local application of the NK1 agonist [SAR9,Met (O2)11]‐SP (SPNK1) produced a dose‐dependent, spantide‐ (a non‐specific NK receptor antagonist) and GR82334‐(an NK1 antagonist) sensitive increase in inspiratory burst amplitude recorded from XII nerves. Under current clamp, SPNK1 significantly depolarized XII MNs, potentiated repetitive firing responses to injected currents and produced a leftward shift in the firing frequency‐current relationships without affecting slope. Under voltage clamp, SPNK1 evoked an inward current and increased input resistance, but had no effect on inspiratory synaptic currents. SPNK1 currents persisted in the presence of TTX, were GR82334 sensitive, were reduced with hyperpolarization and reversed near the expected EK. Effects of the α1‐noradrenergic receptor agonist phenylephrine (PE) on repetitive firing behaviour were virtually identical to those of SPNK1. Moreover, SPNK1 currents were completely occluded by PE, suggesting that common intracellular pathways mediate the actions of NK1 and α1‐noradrenergic receptors. In spite of the similar actions of SPNK1 and PE on XII MN responses to somally injected current, α1‐noradrenergic receptor activation potentiated inspiratory synaptic currents and was more than twice as effective in potentiating XII nerve inspiratory burst amplitude. GR82334 reduced XII nerve inspiratory burst amplitude and generated a small outward current in XII MNs. These observations, together with the first immunohistochemical evidence in the newborn for SP immunopositive terminals in the vicinity of SPNK1‐sensitive inspiratory XII MNs, support the endogenous modulation of XII MN excitability by SP. In contrast to phrenic MNs (Ptak et al. 2000), blocking NMDA receptors with AP5 had no effect on the modulation of XII nerve activity by SPNK1. In conclusion, SPNK1 modulates XII motoneuron responses to inspiratory drive primarily through inhibition of a resting, postsynaptic K+ leak conductance. The results establish the functional significance of SP in controlling upper airway tone during early postnatal life and indicate differential modulation of motoneurons controlling airway and pump muscles by SP.

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Fluctuation in timing of upper airway and chest wall inspiratory muscle activity in obstructive sleep apnea

Cited by 96 publications

References 0 publications

Pathophysiology of obstructive sleep apnoea

Pathophysiology of obstructive sleep apnoea

Dissociation of electromyogram and mechanical response in sleep apnoea during propofol anaesthesia

Modulation of hypoglossal motoneuron excitability by NK1 receptor activation in neonatal mice in vitro

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