Systematic review: relationships between sleep and gastro-oesophageal reflux.

BACKGROUND: Gastro-oesophageal reflux disease (GERD) adversely impacts on sleep, but the mechanism remains unclear. AIM: To review the literature concerning gastro-oesophageal reflux during the sleep period, with particular reference to the sleep/awake state at reflux onset. METHODS: Studies identified by systematic literature searches were assessed. RESULTS: Overall patterns of reflux during the sleep period show consistently that oesophageal acid clearance is slower, and reflux frequency and oesophageal acid exposure are higher in patients with GERD than in healthy individuals. Of the 17 mechanistic studies identified by the searches, 15 reported that a minority of reflux episodes occurred during stable sleep, but the prevailing sleep state at the onset of reflux in these studies remains unclear owing to insufficient temporal resolution of recording or analysis methods. Two studies, in healthy individuals and patients with GERD, analysed sleep and pH with adequate resolution for temporal alignment of sleep state and the onset of reflux: all 232 sleep period reflux episodes evaluated occurred during arousals from sleep lasting less than 15 s or during longer duration awakenings. Six mechanistic studies found that transient lower oesophageal sphincter relaxations were the most common mechanism of sleep period reflux. CONCLUSIONS: Contrary to the prevailing view, subjective impairment of sleep in GERD is unlikely to be due to the occurrence of reflux during stable sleep, but could result from slow clearance of acid reflux that occurs during arousals or awakenings from sleep. Definitive studies are needed on the sleep/awake state at reflux onset across the full GERD spectrum.

Relationship between body composition, peripheral muscle strength and functional exercise capacity in patients with severe chronic obstructive pulmonary disease.

The influence of body composition and peripheral muscle strength on 6-minute walk distance was assessed by performing dual energy X-ray absorptiometry scanning, spirometry and dynamometry testing in 13 men and 13 women with severe chronic obstructive pulmonary disease. Multivariate modelling showed that 76% of the variance in 6-minute walk distance could be explained by an equation incorporating lung function, quadriceps strength and lean leg mass. These findings indicate an important role for lower limb strength measures in pulmonary rehabilitation training programmes.

Measurement, reconstruction, and flow-field computation of the human pharynx with application to sleep apnea.

Repetitive closure of the upper airway characterizes obstructive sleep apnea. It disrupts sleep causing excessive daytime drowsiness and is linked to hypertension and cardiovascular disease. Previous studies simulating the underlying fluid mechanics are based upon geometries, time-averaged over the respiratory cycle, obtained usually via MRI or CT scans. Here, we generate an anatomically correct geometry from data captured in vivo by an endoscopic optical technique. This allows quantitative real-time imaging of the internal cross section with minimal invasiveness. The steady inhalation flow field is computed using a k-ω shear-stress transport (SST) turbulence model. Simulations reveal flow mechanisms that produce low-pressure regions on the sidewalls of the pharynx and on the soft palate within the pharyngeal section of minimum area. Soft-palate displacement and side-wall deformations further reduce the pressures in these regions, thus creating forces that would tend to narrow the airway. These phenomena suggest a mechanism for airway closure in the lateral direction as clinically observed. Correlations between pressure and airway deformation indicate that quantitative prediction of the low-pressure regions for an individual are possible. The present predictions warrant and can guide clinical investigation to confirm the phenomenology and its quantification, while the overall approach represents an advancement toward patient-specific modeling.

Managing obstruction of the central airways.

Lung cancer is the most common cause of cancer death in Australia, Europe and the USA. Up to 20-30% of these cancers eventually affect the central airways and result in reduced quality of life, dyspnoea, haemoptysis, post-obstructive pneumonia and ultimately death. Non-malignant processes may also lead to central airway obstruction and can have similar symptoms. With the development of newer technologies, the last 20 years have seen the emergence of the field of interventional pulmonology to deal specifically with the diagnosis and management of thoracic malignancy, including obstruction of the central airways. This review discusses the pathology, pre-procedure work-up and management options for obstructing central airway lesions. Several treatment modalities exist for dealing with endobronchial pathology with local availability and expertise guiding choice of treatment. While the literature lacks large, multicentre, randomized studies defining the optimal management strategy for a given problem, there is growing evidence from numerous case studies of improved physiology, of quality of life and possibly of survival with modern interventional techniques.

Measuring airway dimensions during bronchoscopy using anatomical optical coherence tomography.

Airway dimensions are difficult to quantify bronchoscopically because of optical distortion and a limited ability to gauge depth. Anatomical optical coherence tomography (aOCT), a novel imaging technique, may overcome these limitations. This study evaluated the accuracy of aOCT against existing techniques in phantom, excised pig and in vivo human airways. Three comparative studies were performed: 1) micrometer-derived area measurements in 10 plastic tubes were compared with aOCT-derived area; 2) aOCT-derived airway compliance curves from excised pig airways were compared with curves derived using an endoscopic technique; and 3) airway dimensions from the trachea to subsegmental bronchi were measured using aOCT in four anaesthetised patients during bronchoscopy and compared with computed tomography (CT) measurements. Measurements in plastic tubes revealed aOCT to be accurate and reliable. In pig airways, aOCT-derived compliance measurements compared closely with endoscopic data. In human airways, dimensions measured with aOCT and CT correlated closely. Bland-Altman plots showed that aOCT diameter and area measurements were higher than CT measurements by 7.6% and 15.1%, respectively. Airway measurements using aOCT are accurate, reliable and compare favourably with existing imaging techniques. Using aOCT with conventional bronchoscopy allows real-time measurement of airway dimensions and could be useful clinically in settings where knowledge of airway calibre is required.

Quantifying tracheobronchial tree dimensions: methods, limitations and emerging techniques.

The ability to measure airway dimensions is important for clinicians, interventional bronchoscopists and researchers in order to accurately quantify structural abnormalities and track their changes over time or in response to treatment. Most quantitative airway measurements are based on X-ray computed tomography and, more recently, on multidetector computed tomography. Quantitative bronchoscopic techniques have also been developed, although these are less widely employed. Emerging techniques, including magnetic resonance imaging, endoscopic optical coherence tomography, endobronchial ultrasound and confocal endomicroscopy, provide new research tools with potential clinical applications. An understanding of issues related to the acquisition, processing and analysis of images, and how such issues impact on imaging the tracheobronchial tree, is essential in order to assess measurement accuracy and to make effective use of the newer methods. This article contributes to this understanding by providing a comprehensive review of current and emerging techniques for quantifying airway dimensions.

Comparison of incremental and constant load tests of inspiratory muscle endurance in COPD.

The aim of the present study was to determine the relative value of incremental and constant load tests in detecting changes in inspiratory muscle endurance following high-intensity inspiratory muscle training (H-IMT) in chronic obstructive pulmonary disease. In total, 16 subjects (11 males; forced expiratory volume in one second (FEV(1)) 37.4+/-12.5%) underwent H-IMT. In addition, 17 subjects (11 males; FEV(1) 36.5+/-11.5%) underwent sham inspiratory muscle training (S-IMT). Training took place three times a week for 8 weeks. Baseline and post-training measurements were obtained of maximum threshold pressure sustained during an incremental load test (P(th,max)) and time breathing against a constant load (t(lim)). Breathing pattern was unconstrained. H-IMT increased P(th,max) and t(lim) relative to baseline and to any change seen following S-IMT. The effect size for P(th,max) was greater than for t(lim). Post-training tests were accompanied by changes in breathing pattern, including decreased duty cycle, which may have served to decrease inspiratory work and thereby contribute to the increase in P(th,max) and t(lim) in both groups. When assessing inspiratory muscle function in chronic obstructive pulmonary disease via tests in which the pattern of breathing is unconstrained, the current authors recommend incremental load tests be used in preference to constant load tests. However, to attribute changes in these tests to improvements in inspiratory muscle endurance, breathing pattern should be controlled.

High-intensity inspiratory muscle training in COPD.

The aim of the present study was to investigate the effects of an interval-based high-intensity inspiratory muscle training (H-IMT) programme on inspiratory muscle function, exercise capacity, dyspnoea and health-related quality of life (QoL) in subjects with chronic obstructive pulmonary disease. A double-blind randomised controlled trial was performed. Sixteen subjects (11 males, mean forced expiratory volume in one second (FEV(1)) 37.4+/-12.5%) underwent H-IMT performed at the highest tolerable inspiratory threshold load (increasing to 101% of baseline maximum inspiratory pressure). Seventeen subjects (11 males, mean FEV(1 )36.5+/-11.5%) underwent sham inspiratory muscle training (S-IMT) at 10% of maximum inspiratory pressure. Training took place three times a week for 8 weeks and was fully supervised. Pre- and post-training measurements of lung function, maximum inspiratory pressure, maximum threshold pressure, exercise capacity, dyspnoea and QoL (Chronic Respiratory Disease Questionnaire; CRDQ) were obtained. H-IMT increased maximum inspiratory pressure by 29%, maximum threshold pressure by 56%, 6-min walk distance by 27 m, and improved dyspnoea and fatigue (CRDQ) by 1.4 and 0.9 points per item, respectively. These changes were significantly greater than any seen following S-IMT. In conclusion, high-intensity inspiratory muscle training improves inspiratory muscle function in subjects with moderate-to-severe chronic obstructive pulmonary disease, yielding meaningful reductions in dyspnoea and fatigue.

Abnormal ventilatory responses to hypoxia in Type 2 diabetes.

AIMS: The incidence of Type 2 diabetes is increasing, along with its associated micro- and macrovascular disease manifestations. Previous studies indicate that patients with Type 2 diabetes exhibit abnormal cardiopulmonary reflex responses to various stimuli, although the impact of hypoxia, a common physiological stimulus, on ventilatory responses has not previously been studied in humans with Type 2 diabetes. METHODS: Minute ventilation (V(E)) breathing pattern responses (total breath time, T(TOT); expiratory time, T(E); inspiratory time, T(I); inspiratory duty cycle, T(I)/T(TOT)) were measured during 5 min each of normoxia and isocapnic hypoxia (arterial O2 saturation approximately 85%) in eight subjects with Type 2 diabetes and seven age- and body mass index-matched healthy subjects. RESULTS: During normoxia, V(E) was similar in control and diabetic subjects (6.4+/-1.2, 6.4+/-1.1 l/min, respectively). In response to hypoxia, V(E) significantly increased in both groups (to 17.0+/-5.0 and 9.5+/-2.0 l/min, respectively, P<0.05), but the magnitude of increase in V(E) was significantly less in diabetic than in control subjects (P<0.05). In addition, the breathing pattern response to hypoxia differed between groups in terms of T(I)/T(TOT) and T(TOT) (P<0.05), with control subjects significantly decreasing T(TOT) and T(E) (P<0.05) while diabetic subjects tended to increase both. CONCLUSIONS: Relative to matched control subjects, Type 2 diabetic subjects exhibit blunted V(E) responses to acute isocapnic hypoxia, suggesting that this group of diabetic subjects possesses a chemoreflex ill-equipped to respond homeostatically to hypoxic challenge.

The effect of interstate travel on sleep patterns of elite Australian Rules footballers.

The purpose of the current study was to examine the effect of interstate air travel on the quality and quantity of sleep in elite Australian Rules football players. Ten elite male athletes, who were members of a Western Australian-based Australian Football League (AFL) team, participated in the study. Sleep pattern was assessed by measuring sleep duration (SLD), sleep efficiency (SE), number of wakings (NW) and total wake time after sleep onset (WT) using a wrist-worn actigraph. Subjective sleep quality (SQ) was assessed using a scale of sleep rating. Throughout the 2002 AFL season, measurements were obtained on the night before (N1), the night of (N2) and the night after (N3) home and away games. Baseline measurements were obtained from five consecutive non-game nights. Compared to baseline, SLD on N1 was increased when home and away (by 51 and 105 mins respectively, p<0.05), while all other measures of sleep pattern were unchanged. On N2, SLD was decreased to a similar degree whether home or away (by 68 and 64 mins respectively, p<0.05), while all other measures of sleep pattern were unchanged. By N3 all measures of sleep pattern had returned to baseline values. Relative to baseline, perception of SQ was worst on N2 of a home game. This study has shown that interstate travel by elite AFL players has no adverse effects on sleep pattern on the night before a game.

The upper airway during anaesthesia.

Upper airway obstruction is common during both anaesthesia and sleep. Obstruction is caused by loss of muscle tone present in the awake state. The velopharynx, a particularly narrow segment, is especially predisposed to obstruction in both states. Patients with a tendency to upper airway obstruction during sleep are vulnerable during anaesthesia and sedation. Loss of wakefulness is compounded by depression of airway muscle activity by the agents, and depression of the ability to arouse, so they cannot respond adequately to asphyxia. Identifying the patient at risk is vital. Previous anaesthetic history and investigations of the upper airway are helpful, and a history of upper airway compromise during sleep (snoring, obstructive apnoeas) should be sought. Beyond these, risk identification is essentially a search for factors that narrow the airway. These include obesity, maxillary hypoplasia, mandibular retrusion, bulbar muscle weakness and specific obstructive lesions such as nasal obstruction or adenotonsillar hypertrophy. Such abnormalities not only increase vulnerability to upper airway obstruction during sleep or anaesthesia, but also make intubation difficult. While problems with airway maintenance may be obviated during anaesthesia by the use of aids such as the laryngeal mask airway (LMA( dagger )), identification of risk and caution are keys to management, and the airway should be secured before anaesthesia where doubt exists. If tracheal intubation is needed, spontaneous breathing until intubation is an important principle. Every anaesthetist should have in mind a plan for failed intubation or, worse, failed ventilation.

Volume displaced by diaphragm motion in emphysema.

To examine the effect of hyperinflation on the volume displaced by diaphragm motion (DeltaVdi), we compared nine subjects with emphysema and severe hyperinflation [residual volume (RV)/total lung capacity (TLC) 0.65 +/- 0.08; mean +/- SD] with 10 healthy controls. Posteroanterior and lateral chest X rays at RV, functional residual capacity, one-half inspiratory capacity, and TLC were used to measure the length of diaphragm apposed to ribcage (Lap), cross-sectional area of the pulmonary ribcage, DeltaVdi, and volume beneath the lung-apposed dome of the diaphragm. Emphysema subjects, relative to controls, had increased Lap at comparable lung volumes (4.3 vs. 1.0 cm near predicted TLC, 95% confidence interval 3.4-5.2 vs. 0-2.1), pulmonary rib cage cross-sectional area (emphysema/controls 1.22 +/- 0.03, P < 0.001 at functional residual capacity), and DeltaVdi/DeltaLap (0.25 vs. 0.14 liters/cm, P < 0.05). During a vital capacity inspiration, relative to controls, DeltaVdi was normal in five (1.94 +/- 0.51 liters) and decreased in four (0.51 +/- 0.40 liters) emphysema subjects, and volume beneath the dome did not increase in emphysema (0 +/- 0.36 vs. 0.82 +/- 0.80 liters, P < 0.05). We conclude that DeltaVdi can be normal in emphysema because 1) hyperinflation is shared between ribcage and diaphragm, preserving Lap, and 2) the diaphragm remains flat during inspiration.

Inspiratory muscle performance in endurance athletes and sedentary subjects.

OBJECTIVE: The aim of this study was to determine whether whole-body endurance training is associated with increased respiratory muscle strength and endurance. METHODOLOGY: Respiratory muscle strength (maximum inspiratory pressure (PImax)) and endurance (progressive threshold loading of the inspiratory muscles) were measured in six marathon runners and six sedentary subjects. RESULTS: PImax was similar between the two groups of subjects but the maximum threshold pressure achieved was greater in marathon runners (90 +/- 8 vs 78 +/- 10% of PImax, respectively, mean +/- SD, P < 0.05). During progressive threshold loading, marathon runners breathed with lower frequency, higher tidal volume, and longer inspiratory and expiratory time. At maximum threshold pressure, marathon runners had lower arterial O2 saturation, but perceived effort (Borg scale) was maximal in both groups. Efficiency of the respiratory muscles was similar in both groups being 2.0 +/- 1.7% and 2.3 +/- 1.8% for marathon runners and sedentary subjects, respectively. CONCLUSIONS: The apparent increase in respiratory muscle endurance of athletes was a consequence of a difference in the breathing pattern adopted during loaded breathing rather than respiratory muscle strength or efficiency. This implies that sensory rather than respiratory muscle conditioning may be an important mechanism by which whole-body endurance is increased.

Nonchemical elimination of inspiratory motor output via mechanical ventilation in sleep.

In six dogs studied in nonrapid eye movement (NREM) sleep, we found that the frequency, volume, and timing of application of mechanical ventilator breaths had marked and sustained inhibitory effects on diaphragm electromyogram (EMG(di)). Single ventilator breaths of tidal volume (VT) 75-200% of control caused apnea (up to three times eupneic expiratory time [TE]) when applied during the initial 25-65% of expiratory time. When continuous controlled mechanical ventilation (CMV) was applied with ventilator frequency increased as little as 1 cycle/min > eupnea and Pa(CO(2)) and VT maintained at near eupneic control levels, EMG(di) was silenced and triangularis sterni EMG (EMG(ts)) became tonic within 2 to 5 ventilator cycles. On cessation of normocapnic CMV, apnea ensued with TE ranging from 1.2 to five times eupneic TE. The spontaneous VT and EMG(di) determined immediately after these prolonged apneas were also markedly reduced in amplitude. The larger the VT applied during the isocapnic CMV (120-200% of eupnea) and the longer the duration of the CMV (3-90 s), the longer the duration of the postventilator apnea. Significant postventilator apneas and postapneic hypoventilation also occurred even when end-tidal CO(2) pressure (PET(CO(2))) was raised 3-5 mm Hg > eupnea (and 7-10 mm Hg > normal apneic threshold) throughout CMV trials at raised frequency and VT. Our findings demonstrate that the increased frequency of CMV was critical to the elimination of inspiratory motor output and the onset of tonic expiratory muscle activity; furthermore, once EMG(di) was silenced, the tidal volume and duration of the passive mechanical ventilation determined the magnitude of the short-term inhibition of inspiratory motor output after cessation of CMV.

Hemodynamic effects of pressures applied to the upper airway during sleep.

The increase in systemic blood pressure after an obstructive apnea is due, in part, to sympathetically mediated vasoconstriction. We questioned whether upper airway (UA) receptors could contribute reflexly to this vasoconstriction. Four unanesthetized dogs were studied during wakefulness and non-rapid-eye-movement (NREM) sleep. The dogs breathed via a fenestrated tracheostomy tube sealed around the tracheal stoma. The snout was sealed with an airtight mask, thereby isolating the UA when the fenestration was closed and exposing the UA to negative inspiratory intrathoracic pressure when it was open. The blood pressure response to three UA perturbations was studied: 1) square-wave negative pressures sufficient to cause UA collapse with the fenestration closed during a mechanical hyperventilation-induced central apnea; 2) tracheal occlusion with the fenestration open vs. closed; and 3) high-frequency pressure oscillations (HFPO) with the fenestration closed. During NREM sleep, 1) blood pressure response to tracheal occlusion was similar with the fenestration open or closed; 2) collapsing the UA with negative pressures failed to alter blood pressure during a central apnea; and 3) application of HFPO to the UA during eupnea and resistive-loaded breaths increased heart rate and blood pressure. However, these changes were likely to be secondary to the effects of HFPO-induced reflex changes on prolonging expiratory time. These findings suggest that activation of UA pressure-sensitive receptors does not contribute directly to the pressor response associated with sleep-disordered breathing events.

Ventilatory responses to specific CNS hypoxia in sleeping dogs.

Our study was concerned with the effect of brain hypoxia on cardiorespiratory control in the sleeping dog. Eleven unanesthetized dogs were studied; seven were prepared for vascular isolation and extracorporeal perfusion of the carotid body to assess the effects of systemic [and, therefore, central nervous system (CNS)] hypoxia (arterial PO(2) = 52, 45, and 38 Torr) in the presence of a normocapnic, normoxic, and normohydric carotid body during non-rapid eye movement sleep. A lack of ventilatory response to systemic boluses of sodium cyanide during carotid body perfusion demonstrated isolation of the perfused carotid body and lack of other significant peripheral chemosensitivity. Four additional dogs were carotid body denervated and exposed to whole body hypoxia for comparison. In the sleeping dog with an intact and perfused carotid body exposed to specific CNS hypoxia, we found the following. 1) CNS hypoxia for 5-25 min resulted in modest but significant hyperventilation and hypocapnia (minute ventilation increased 29 +/- 7% at arterial PO(2) = 38 Torr); carotid body-denervated dogs showed no ventilatory response to hypoxia. 2) The hyperventilation was caused by increased breathing frequency. 3) The hyperventilatory response developed rapidly (<30 s). 4) Most dogs maintained hyperventilation for up to 25 min of hypoxic exposure. 5) There were no significant changes in blood pressure or heart rate. We conclude that specific CNS hypoxia, in the presence of an intact carotid body maintained normoxic and normocapnic, does not depress and usually stimulates breathing during non-rapid eye movement sleep. The rapidity of the response suggests a chemoreflex meditated by hypoxia-sensitive respiratory-related neurons in the CNS.

Effect of asbestos-related pleural fibrosis on excursion of the lower chest wall and diaphragm.

To examine mechanisms responsible for reduced lung volumes (restriction) in asbestos-related pleural fibrosis (APF), we studied diaphragm function and lower rib-cage excursion in 26 subjects with previous asbestos exposure and no evidence of asbestosis. Using posteroanterior (PA) and lateral chest radiographs taken at residual volume and at 25%, 70%, and 100% vital capacity (VC) during a slow inspiratory maneuver, we measured fractional expansion of the lower rib cage (FErc), fractional shortening of the diaphragm (FSdi), and changes (Delta) in diaphragm dome height (Hdo) and subphrenic volume (Vdi). Vdi was estimated by measuring the major and minor axes of the subphrenic space at 1-cm intervals, assuming an elliptical cross-sectional shape, and correcting for the volume of spinal and paraspinal tissues. Seven subjects had no evidence of APF (control), 12 had pleural plaques (PP), and seven had diffuse pleural thickening with costophrenic obliteration (DPT). Over the range of VC, results (mean +/- SEM, normalized for height) in control subjects were VC = 101.2 +/- 4.0 % predicted and DeltaVdi = 326 +/- 8 ml/m(3), and for the right hemithorax and hemidiaphragm on the PA film, FErc = 0.07 +/- 0.02, FSdi = 0.32 +/- 0.02 and DeltaHdo = 0.8 +/- 0.2 cm/m. Relative to controls: DPT subjects had reduced VC (77.4 +/- 4.9%, p < 0.01), DeltaVdi (256 +/- 2 ml/m(3), p < 0.01), FErc (0.01 +/- 0.02, p < 0.01), FSdi (0.24 +/- 0.01, p < 0.001), and DeltaHdo (-0.9 +/- 0.06 cm/m, p < 0.01); PP subjects had reduced FSdi (0.25 +/- 0.01, p < 0.001) and DeltaVdi (233 +/- 47 ml/m(3), p < 0.01), and no difference in FErc, DeltaHdo, or VC. We conclude that restriction in DPT is due to obliteration of the zone of apposition, and that by limiting separation of the diaphragm from the rib cage during inspiration, this reduces volume contributed by motion of the diaphragm and lower rib cage. Reduction in the latter contribution was the main cause of restriction, because the reduction in volume contributed by the diaphragm was partly compensated by flattening of its dome.

Inhibition of inspiratory motor output by high-frequency low-pressure oscillations in the upper airway of sleeping dogs.

1. We utilized a chronically tracheostomized, unanaesthetized dog model to study the reflex effects on inspiratory motor output of low-amplitude, high-frequency pressure oscillations (HFPOs) applied to the isolated upper airway (UA) during stable non-rapid eye movement (NREM) sleep. 2. HFPOs (30 Hz and +/-2 to +/-4 cmH2O) were applied via a piston pump during eupnoea, inspiratory resistive loading and tracheal occlusion. 3. When applied to the patent UA during expiration, and especially during late expiration, HFPOs prolonged expiratory time (TE) and tonically activated the genioglossus muscle EMG. When applied to the patent UA during inspiration, HFPOs caused tonic activation of the genioglossus muscle EMG and inhibition of inspiratory motor output by either: (a) a shortening of inspiratory time (TI), as inspiration was terminated coincident with the onset of HFPOs; or (b) a prolonged TI accompanied by a decreased rate of rise of diaphragm EMG and rate of fall of tracheal pressure. These effects of HFPOs were observed during eupnoea and inspiratory resistive loading, but were maximal during tracheal occlusion where the additional inhibitory effects of lung inflation reflexes were minimized. 4. During eupnoea, topical anaesthesia of the UA abolished the HFPO-induced prolongation of TE, suggesting that the response was mediated primarily by mechanoreceptors close to the mucosal surface; whereas the TE-prolonging effects of a sustained square wave of negative pressure (range, -4.0 to -14.9 cmH2O) sufficient to close the airway were preserved following anaesthesia. 5. These results demonstrate that high-frequency, low-amplitude oscillatory pressure waves in the UA, similar to those found in snoring, produce reflex inhibition of inspiratory motor output. This reflex may help maintain UA patency by decreasing the collapsing pressure generated by the inspiratory pump muscles and transmitted to the UA.