Negative Pharyngeal Pressure Causes Reflex Upper Airway Dilator Muscle Activation in Man

1990 ◽  
Vol 78 (s22) ◽  
pp. 16P-16P
Author(s):  
JA Innes ◽  
RL Horner ◽  
A Guz
Keyword(s):  
Muscle Activation ◽  
Upper Airway ◽  
Pharyngeal Pressure ◽  
Dilator Muscle

Upper airway muscle responsiveness to rising Pco 2 during NREM sleep

2000 ◽  
Vol 89 (4) ◽  
pp. 1275-1282 ◽  
Author(s):  
Giora Pillar ◽  
Atul Malhotra ◽  
Robert B. Fogel ◽  
Josee Beauregard ◽  
David I. Slamowitz ◽  
...  
Keyword(s):  
Muscle Activation ◽  
Slow Wave Sleep ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Dilator Muscle ◽  
Pharyngeal Muscles ◽  
Stage 2 Sleep ◽  
Significant Change ◽  
End Tidal

Although pharyngeal muscles respond robustly to increasing Pco 2 during wakefulness, the effect of hypercapnia on upper airway muscle activation during sleep has not been carefully assessed. This may be important, because it has been hypothesized that CO2-driven muscle activation may importantly stabilize the upper airway during stages 3 and 4 sleep. To test this hypothesis, we measured ventilation, airway resistance, genioglossus (GG) and tensor palatini (TP) electromyogram (EMG), plus end-tidal Pco 2(Pet CO2 ) in 18 subjects during wakefulness, stage 2, and slow-wave sleep (SWS). Responses of ventilation and muscle EMG to administered CO2(Pet CO2 = 6 Torr above the eupneic level) were also assessed during SWS ( n = 9) or stage 2 sleep ( n = 7). Pet CO2 increased spontaneously by 0.8 ± 0.1 Torr from stage 2 to SWS (from 43.3 ± 0.6 to 44.1 ± 0.5 Torr, P < 0.05), with no significant change in GG or TP EMG. Despite a significant increase in minute ventilation with induced hypercapnia (from 8.3 ± 0.1 to 11.9 ± 0.3 l/min in stage 2 and 8.6 ± 0.4 to 12.7 ± 0.4 l/min in SWS, P < 0.05 for both), there was no significant change in the GG or TP EMG. These data indicate that supraphysiological levels of Pet CO2 (50.4 ± 1.6 Torr in stage 2, and 50.4 ± 0.9 Torr in SWS) are not a major independent stimulus to pharyngeal dilator muscle activation during either SWS or stage 2 sleep. Thus hypercapnia-induced pharyngeal dilator muscle activation alone is unlikely to explain the paucity of sleep-disordered breathing events during SWS.

Neostigmine/Glycopyrrolate Administered after Recovery from Neuromuscular Block Increases Upper Airway Collapsibility by Decreasing Genioglossus Muscle Activity in Response to Negative Pharyngeal Pressure

2010 ◽  
Vol 113 (6) ◽  
pp. 1280-1288 ◽  
Author(s):  
Frank Herbstreit ◽  
Daniela Zigrahn ◽  
Christof Ochterbeck ◽  
Jürgen Peters ◽  
Matthias Eikermann
Keyword(s):  
Neuromuscular Blockade ◽  
Lung Volume ◽  
Muscle Activation ◽  
Neuromuscular Block ◽  
Upper Airway ◽  
Acetylcholinesterase Inhibitors ◽  
Genioglossus Muscle ◽  
Pharyngeal Pressure ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

Background Reversal of residual neuromuscular blockade by acetylcholinesterase inhibitors (e.g., neostigmine) improves respiratory function. However, neostigmine may also impair muscle strength. We hypothesized that neostigmine administered after recovery of the train-of-four (TOF) ratio impairs upper airway integrity and genioglossus muscle function. Methods We measured, in 10 healthy male volunteers, epiglottic and nasal mask pressures, genioglossus electromyogram, air flow, respiratory timing, and changes in lung volume before, during (TOF ratio: 0.5), and after recovery of the TOF ratio to unity, and after administration of neostigmine 0.03 mg/kg IV (with glycopyrrolate 0.0075 mg/kg). Upper airway critical closing pressure (Pcrit) was calculated from flow-limited breaths during random pharyngeal negative pressure challenges. Results Pcrit increased significantly after administration of neostigmine/glycopyrrolate compared with both TOF recovery (mean ± SD, by 27 ± 21%; P = 0.02) and baseline (by 38 ± 17%; P = 0.002). In parallel, phasic genioglossus activity evoked by negative pharyngeal pressure decreased (by 37 ± 29%, P = 0.005) compared with recovery, almost to a level observed at a TOF ratio of 0.5. Lung volume, respiratory timing, tidal volume, and minute ventilation remained unchanged after neostigmine/glycopyrrolate injection. Conclusion Neostigmine/glycopyrrolate, when administered after recovery from neuromuscular block, increases upper airway collapsibility and impairs genioglossus muscle activation in response to negative pharyngeal pressure. Reversal with acetylcholinesterase inhibitors may be undesirable in the absence of neuromuscular blockade.

scholarly journals Upper airway collapsibility, dilator muscle activation and resistance in sleep apnoea

2007 ◽  
Vol 30 (2) ◽  
pp. 345-353 ◽  
Author(s):  
R. Pierce ◽  
D. White ◽  
A. Malhotra ◽  
J. K. Edwards ◽  
D. Kleverlaan ◽  
...  
Keyword(s):  
Muscle Activation ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Dilator Muscle ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

scholarly journals Physiology in Medicine: Obstructive sleep apnea pathogenesis and treatment—considerations beyond airway anatomy

2014 ◽  
Vol 116 (1) ◽  
pp. 3-12 ◽  
Author(s):  
Jerome A. Dempsey ◽  
Ailiang Xie ◽  
David S. Patz ◽  
David Wang
Keyword(s):  
Risk Factors ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Muscle Activation ◽  
Upper Airway ◽  
Airway Anatomy ◽  
Output Stability ◽  
Dilator Muscle ◽  
Obstructive Sleep ◽  
Treatment Considerations

We review evidence in support of significant contributions to the pathogenesis of obstructive sleep apnea (OSA) from pathophysiological factors beyond the well-accepted importance of airway anatomy. Emphasis is placed on contributions from neurochemical control of central respiratory motor output through its effects on output stability, upper airway dilator muscle activation, and arousability. In turn, we consider the evidence demonstrating effective treatment of OSA via approaches that address each of these pathophysiologic risk factors. Finally, a case is made for combining treatments aimed at both anatomical and ventilatory control system deficiencies and for individualizing treatment to address a patient 's own specific risk factors.

Changes in upper airway muscle activation and ventilation during phasic REM sleep in normal men

1991 ◽  
Vol 71 (2) ◽  
pp. 488-497 ◽  
Author(s):  
L. Wiegand ◽  
C. W. Zwillich ◽  
D. Wiegand ◽  
D. P. White
Keyword(s):  
Eye Movements ◽  
Tidal Volume ◽  
Rem Sleep ◽  
Muscle Activation ◽  
Sleep Stage ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Respiratory Neurons ◽  
Dilator Muscle ◽  
Normal Men

Several investigators have observed that irregular breathing occurs during rapid-eye-movement (REM) sleep in healthy subjects, with ventilatory suppression being prominent during active eye movements [phasic REM (PREM) sleep] as opposed to tonic REM (TREM) sleep, when ocular activity is absent and ventilation more regular. Inasmuch as considerable data suggest that rapid eye movements are a manifestation of sleep-induced neural events that may importantly influence respiratory neurons, we hypothesized that upper airway dilator muscle activation may also be suppressed during periods of active eye movements in REM sleep. We studied six normal men during single nocturnal sleep studies. Standard sleep-staging parameters, ventilation, and genioglossus and alae nasi electromyograms (EMG) were continuously recorded during the study. There were no significant differences in minute ventilation, tidal volume, or any index of genioglossus or alae nasi EMG amplitude between non-REM (NREM) and REM sleep, when REM was analyzed as a single sleep stage. Each breath during REM sleep was scored as “phasic” or “tonic,” depending on its proximity to REM deflections on the electrooculogram. Comparison of all three sleep states (NREM, PREM, and TREM) revealed that peak inspiratory genioglossus and alae nasi EMG activities were significantly decreased during PREM sleep compared with TREM sleep [genioglossus (arbitrary units): NREM 49 +/- 12 (mean +/- SE), TREM 49 +/- 5, PREM 20 +/- 5 (P less than 0.05, PREM different from TREM and NREM); alae nasi: NREM 16 +/- 4, TREM 38 +/- 7, PREM 10 +/- 4 (P less than 0.05, PREM different from TREM)]. We also observed, as have others, that ventilation, tidal volume, and mean inspiratory airflow were significantly decreased and respiratory frequency was increased during PREM sleep compared with both TREM and NREM sleep. We conclude that hypoventilation occurs in concert with reduced upper airway dilator muscle activation during PREM sleep by mechanisms that remain to be established.

scholarly journals Desipramine improves upper airway collapsibility and reduces OSA severity in patients with minimal muscle compensation

2016 ◽  
Vol 48 (5) ◽  
pp. 1340-1350 ◽  
Author(s):  
Luigi Taranto-Montemurro ◽  
Scott A. Sands ◽  
Bradley A. Edwards ◽  
Ali Azarbarzin ◽  
Melania Marques ◽  
...  
Keyword(s):  
Crossover Trial ◽  
Positive Airway Pressure ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Double Blind ◽  
Healthy Humans ◽  
Dilator Muscle ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

We recently demonstrated that desipramine reduces the sleep-related loss of upper airway dilator muscle activity and reduces pharyngeal collapsibility in healthy humans without obstructive sleep apnoea (OSA). The aim of the present physiological study was to determine the effects of desipramine on upper airway collapsibility and apnoea–hypopnea index (AHI) in OSA patients.A placebo-controlled, double-blind, randomised crossover trial in 14 OSA patients was performed. Participants received treatment or placebo in randomised order before sleep. Pharyngeal collapsibility (critical collapsing pressure of the upper airway (Pcrit)) and ventilation under both passive (V′0,passive) and active (V′0,active) upper airway muscle conditions were evaluated with continuous positive airway pressure (CPAP) manipulation. AHI was quantified off CPAP.Desipramine reduced activePcrit(median (interquartile range) −5.2 (4.3) cmH2O on desipramineversus−1.9 (2.7) cmH2O on placebo; p=0.049) but not passivePcrit(−2.2 (3.4)versus−0.7 (2.1) cmH2O; p=0.135). A greater reduction in AHI occurred in those with minimal muscle compensation (defined asV′0,active−V′0,passive) on placebo (r=0.71, p=0.009). The reduction in AHI was driven by the improvement in muscle compensation (r=0.72, p=0.009).In OSA patients, noradrenergic stimulation with desipramine improves pharyngeal collapsibility and may be an effective treatment in patients with minimal upper airway muscle compensation.

Mechanical effects of pharyngeal constrictor activation on pharyngeal airway function

1999 ◽  
Vol 86 (1) ◽  
pp. 411-417 ◽  
Author(s):  
Samuel T. Kuna ◽  
Christi R. Vanoye
Keyword(s):  
Axial Force ◽  
Airway Pressure ◽  
Muscle Activation ◽  
Upper Airway ◽  
Stimulation Frequency ◽  
Airway Patency ◽  
Pharyngeal Airway ◽  
Mechanical Effects ◽  
Airway Function ◽  
Pharyngeal Branch

The mechanical effects of pharyngeal constrictor (PC) muscle activation on pharyngeal airway function were determined in 20 decerebrate, tracheotomized cats. In 10 cats, a high-compliance balloon attached to a pressure transducer was partially inflated to just occlude the pharyngeal airway. During progressive hyperoxic hypercapnia, changes in pharyngeal balloon pressure were directly related to phasic expiratory hyopharyngeus (middle PC) activity. In two separate protocols in 10 additional cats, the following measurements were obtained with and without bilateral electrical stimulation (0.2-ms duration, threshold voltage) of the distal cut end of the vagus nerve’s pharyngeal branch supplying PC motor output: 1) pressure-volume relationships in an isolated, sealed upper airway at a stimulation frequency of 30 Hz and 2) rostrally directed axial force over a stimulation frequency range of 0–40 Hz. Airway compliance determined from the pressure-volume relationships decreased with PC stimulation at and below resting airway volume. Compared with the unstimulated condition, PC stimulation increased airway pressure at airway volumes at and above resting volume. This constrictor effect progressively diminished as airway volume was brought below resting volume. At relatively low airway volumes below resting volume, PC stimulation decreased airway pressure compared with that without stimulation. PC stimulation generated a rostrally directed axial force that was directly related to stimulation frequency. The results indicate that PC activation stiffens the pharyngeal airway, exerting both radial and axial effects. The radial effects are dependent on airway volume: constriction of the airway at relatively high airway volumes, and dilation of the airway at relatively low airway volumes. The results imply that, under certain conditions, PC muscle activation may promote pharyngeal airway patency.

Effects of hypoxia and hypercapnia on geniohyoid contractility and endurance

1991 ◽  
Vol 71 (2) ◽  
pp. 709-715 ◽  
Author(s):  
R. J. Salmone ◽  
E. Van Lunteren
Keyword(s):  
Force Production ◽  
Upper Airway ◽  
Muscle Performance ◽  
Severe Hypoxia ◽  
Force Frequency ◽  
Force Output ◽  
Frequency Curve ◽  
Dilator Muscle ◽  
Index Ratio ◽  
Mild Hypoxia

Sleep apnea and other respiratory diseases produce hypoxemia and hypercapnia, factors that adversely affect skeletal muscle performance. To examine the effects of these chemical alterations on force production by an upper airway dilator muscle, the contractile and endurance characteristics of the geniohyoid muscle were examined in situ during severe hypoxia (arterial PO2 less than 40 Torr), mild hypoxia (PO2 45–65 Torr), and hypercapnia (PCO2 55–80 Torr) and compared with hyperoxic-normocapnic conditions in anesthetized cats. Muscles were studied at optimal length, and contractile force was assessed in response to supramaximal electrical stimulation of the hypoglossal nerve (n = 7 cats) or geniohyoid muscle (n = 2 cats). There were no significant changes in the twitch kinetics or force-frequency curve of the geniohyoid muscle during hypoxia or hypercapnia. However, the endurance of the geniohyoid, as reflected in the fatigue index (ratio of force at 2 min to initial force in response to 40-Hz stimulation at a duty cycle 0.33), was significantly reduced by severe hypoxia but not by hypercapnia or mild hypoxia. In addition, the downward shift in the force-frequency curve after the repetitive stimulation protocol was greater during hypoxia than hyperoxia, especially at higher frequencies. In conclusion, the ability of the geniohyoid muscle to maintain force output during high levels of activation is adversely affected by severe hypoxia but not mild hypoxia or hypercapnia. However, none of these chemical perturbations affected muscle contractility acutely.

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