Airway Muscle Activity Research Articles

Forced oscillation measurements do not affect upper airway muscle tone or sleep in clinical studies.

Upper airway obstruction in the sleep apnoea/hypopnoea syndrome (SAHS) can be easily assessed by measuring respiratory impedance with the forced oscillation technique (FOT). This methodology has been proposed as a useful clinical tool both for the diagnosis of sleep breathing disorders and for continuous positive airway pressure (CPAP) titration. However, previous studies suggest that the application of high-frequency pressure oscillation to the upper airway may induce changes in the electroencephalogram (EEG) or upper airway muscle function. The effect of FOT measurements on upper airway muscle tone and EEG in clinical sleep studies was examined. Seven patients with moderate SAHS were included (age: 54+/-11 yrs; apnoea/hypopnoea index: 43+/-21 events x h(-1); body mass index: 30+/-2 kg x m(-2)). Genioglossus surface electromyogram activity (EMGgg) and EEG signal were analysed with and without FOT application (frequency: 5 Hz and 30 Hz; peak-to-peak pressure oscillation: 1 cmH2O) during stable sleep. Measurements were carried out in two different situations. Step 1: applying FOT during episodes of obstructive events or flow limitation; and step 2: during prolonged periods of normal breathing at optimal CPAP. The root mean square of EMGgg activity and fast Fourier analysis (alpha and delta bands) of the EEG signal were performed. The application of FOT did not increase EMGgg activity in any of the situations studied. In addition, no evidence of the effects on EEG was found: alpha/delta relationship: awake:0.70, baseline sleep:0.13, FOT(5 Hz):0.18, FOT(30 Hz):0.11. The presented results suggest that the use of forced oscillation technique over the ranges of frequency and amplitude proposed for clinical sleep studies does not induce changes in upper airway muscle activity and neurological variables in patients with sleep apnoea/hypopnoea syndrome.

Effect of pulmonary stretch receptor feedback and CO(2) on upper airway and respiratory pump muscle activity in the rat.

1. Our purpose was to examine the effects of chemoreceptor stimulation and lung inflation on neural drive to tongue protrudor and retractor muscles in the rat. 2. Inspiratory flow, tidal volume, transpulmonary pressure, compliance and electromyographic (EMG) activity of genioglossus (GG), hyoglossus (HG) and inspiratory intercostal (IIC) muscles were studied in 11 anaesthetized, tracheotomized and spontaneously breathing rats. Mean EMG activity during inspiration was compared with mean EMG activity during an occluded inspiration, at each of five levels of inspired CO(2) (0, 3, 6, 9 and 12 %). 3. Lung inflation suppressed EMG activity in all muscles, with the effect on both tongue muscles exceeding that of the intercostal muscles. Static elevations of end-expiratory lung volume evoked by 2 cmH(2)O positive end-expiratory pressure (PEEP) had no effect on tongue muscle activity. 4. Despite increasing inspiratory flow, tidal volume and transpulmonary pressure, the inhibition of tongue muscle activity by lung inflation diminished as arterial PCO2 (P(a),CO(2)) increased. 5. The onset of tongue muscle activity relative to the onset of IIC muscle activity advanced with increases in P(a),CO(2) but was unaffected by lung inflation. This suggests that hypoglossal and external intercostal motoneuron pools are controlled by different circuits or have different sensitivities to CO(2), lung inflation and/or anaesthetic agents. 6. We conclude that hypoglossal motoneuronal activity is more strongly influenced by chemoreceptor-mediated facilitation than by lung volume-mediated inhibition. Hypoglossal motoneurons driving tongue protrudor and retractor muscles respond identically to these stimuli.

Chronic intermittent asphyxia impairs rat upper airway muscle responses to acute hypoxia and asphyxia

Sleep disordered breathing (SDB) is characterised by chronic intermittent asphyxia (CIA) due to repetitive apnoeas. We tested the hypothesis that CIA affects upper airway muscle activity and responses to acute hypoxia and asphyxia. Wistar rats were placed in restrainers with their heads in hoods ventilated with air (controls, n = 6) or an air/N2/CO2 mixture intermittently (treated group, n = 6) for 8 h per day, 5 days per week for 5 weeks using timed solenoid valves as previously described [1]. In were added to the the treated group, every 30 s, N2 and CO2 to a minimum of 6–8% and airflow for 15 s reducing hood O2 increasing CO2 to a maximum of 12–14% followed by removal of the N2 and CO2 and recovery to room air values. After 5 weeks, animals were anaesthetised (chloralose and urethane, 100 and 1000 mg/kg respectively IP). Sternohyoid (SH) electromyogram (EMG) activity was measured breathing air, 7.5% O2 in N2 (hypoxia) and 7.5% O2 and 3% CO2 (asphyxia). EMG data were expressed as % of peak activity breathing 9% CO2 (% of reference). Baseline SHEMG activity was significantly elevated in the treated group (28.4 ± 0.3% of reference in the controls vs. 48.5 ± 0.5% of reference in the treated group; means ± SEM, P < 0.05 ANOVA). CIA significantly reduced SHEMG responses to hypoxia and asphyxia. Thus, the increase in EMG activity from baseline values (ΔEMG) during the first minute of hypoxia was +46.2 ± 5.8% in control rats vs. +30.4 ± 6.1% in treated rats. Similarly, ΔEMG during the first minute of asphyxia was +66.3 ± 5.9% in control rats vs. +41.1 ± 11.1% in treated rats. We suggest that the elevated upper airway muscle activity associated with SDB is due to CIA. We propose that a reduction in the response of upper airway dilator muscles to acute asphyxia following upper airway obstruction is likely to cause further asphyxic insult leading to a vicious feed-forward cycle. We further propose that CIA contributes to the pathophysiology of SDB and other conditions of intermittent asphyxia.

Upper airway muscle responsiveness to rising PCO(2) during NREM sleep.

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 CO(2)-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(CO(2))) in 18 subjects during wakefulness, stage 2, and slow-wave sleep (SWS). Responses of ventilation and muscle EMG to administered CO(2) (PET(CO(2)) = 6 Torr above the eupneic level) were also assessed during SWS (n = 9) or stage 2 sleep (n = 7). PET(CO(2)) 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(CO(2)) (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.

Detection of obstructive sleep apnea by analysis of phase angle using the forced oscillation signal

Pharyngeal collapse in patients with obstructive sleep apnea syndrome (OSAS) is linked to decreased upper airway muscle activity. We hypothesised that decreased muscle activity causes decreased stiffness of the upper airway wall and assumed that a decrease in wall stiffness would result in a change point (CP) of the morphology of phase angle time series φ(t) obtained by forced oscillation technique (FOT). We developed an algorithm to detect CPs in φ(t) and investigated φ(t) data measured in parallel to all-night polysomnography in seven patients. A total of 2724 CPs were detected by algorithm. The CPs were marked on the polysomnograms and compared with polysomnogram scoring performed jointly by three sleep expert physicians. A total of 791 (67%) of the 1172 handscored respiratory events showed a CP in φ(t) within a time interval of 8 sec before and 6 sec after the marked onset. A total of 672 (57%) respiratory events were detected at an earlier time by algorithm, and 119 (10%) were algorithmically detected later. The average detection time by the CP algorithm was 4.0±1.1 sec earlier than the manual scoring. We conjecture that a CP in φ(t) indicates a change in upper airway collapsibility and that φ(t) might be a potentially useful parameter for detection of impending upper airway obstruction.

Effects of upper airway carbon dioxide on upper airway resistance and muscle activity in young guinea-pigs.

The upper airway (UA) of adult animals is known to contain carbon dioxide-sensitive receptors and UA CO2 reflexly affects breathing, UA dilator muscle activity and UA resistance. These effects may function in the control of UA patency. There is evidence that some UA reflexes are stronger in young than in adult animals, but it is not known whether CO2-sensitive receptors are present in the UA of young animals, and the effects of UA CO2 on UA resistance and on UA dilator muscle activity have not been investigated in young animals. The responses of ventilation, UA resistance and geniohyoid muscle electromyographic activity to warm air containing 10% CO2 applied to the isolated UA were measured in anaesthetized, vagotomized young guinea-pigs breathing spontaneously through a low-cervical tracheostomy. Upper airway carbon dioxide caused an increase in ventilation (46.7+/-16.3 to 49.9+/-16.8 mL x min(-1) x 100 g body weight(-1)) and upper airway resistance (56.8+/-14.8 to 63.7+/-17.7 cmH2O x L(-1) x s(-1) x kg body weight(-1)). Similar effects were obtained following vagotomy. Geniohyoid activity became apparent following vagotomy and this activity was reduced by upper airway carbon dioxide. These responses were abolished by topical anaesthesia of the upper airway. This suggests that the reflexes seen are due to carbon dioxide-sensitive receptors in the upper airway.

Consequences of periodic augmented breaths on tongue muscle activities in hypoxic rats.

This study was designed to investigate the influence of hypoxia-evoked augmented breaths (ABs) on respiratory-related tongue protrudor and retractor muscle activities and inspiratory pump muscle output. Genioglossus (GG) and hyoglossus (HG) electromyogram (EMG) activities and respiratory-related tongue movements were compared with peak esophageal pressure (Pes; negative change in pressure during inspiration) and minute Pes (Pes x respiratory frequency = Pes/min) before and after ABs evoked by sustained poikilocapnic, isocapnic, and hypercapnic hypoxia in spontaneously breathing, anesthetized rats. ABs evoked by poikilocapnic and isocapnic hypoxia triggered long-lasting (duration at least 10 respiratory cycles) reductions in GG and HG EMG activities and tongue movements relative to pre-AB levels, but Pes was reduced transiently (duration of <10 respiratory cycles) after ABs. Adding 7% CO(2) to the hypoxic inspirate had no effect on the frequency of evoked ABs, but this prevented long-term declines in tongue muscle activities. Bilateral vagotomy abolished hypoxia-induced ABs and stabilized drive to the tongue muscles during each hypoxic condition. We conclude that, in the rat, hypoxia-evoked ABs 1) elicit long-lasting reductions in protrudor and retractor tongue muscle activities, 2) produce short-term declines in inspiratory pump muscle output, and 3) are mediated by vagal afferents. The more prolonged reductions in pharyngeal airway vs. pump muscle activities may lead to upper airway narrowing or collapse after spontaneous ABs.

Effects of CO2 and H+ on laryngeal receptor activity in the perfused larynx in anaesthetized cats.

1. Intralaryngeal CO2 reflexly decreases ventilation and increases upper airway muscle activity. Topical anaesthesia of the laryngeal mucosa or cutting the superior laryngeal nerves (SLNs) abolishes these reflexes, indicating that the receptors responsible are superficially located and that their afferent fibres are in the SLN. Intralaryngeal CO2 affects the activity of receptors recorded from the SLN. 2. An isolated, luminally perfused laryngeal preparation was developed in anaesthetized, paralysed cats in order to compare the effects of solutions with varying levels of pH and PCO2 on pressure-sensitive laryngeal receptor activity. Since the pH of tracheal surface fluid is reported to be approximately 7.0, two neutral (pH 7.4 and 7.0) and two acidic (pH 6.8 and 6.3) solutions were used. 3. Compared with neutral acapnic control solutions, neutral hypercapnic (PCO2 64 mmHg) solutions either excited or inhibited the discharge of 113 out of 211 pressure-sensitive SLN afferents. In 24 receptors, the effects of hypercapnic solutions with either neutral or acidic pH were similar in both direction and magnitude. In 50 receptors affected by neutral hypercapnic solutions, acidic acapnic solutions had no effect on 66 % of units and significantly smaller effects in the remaining units. In 17 receptors, the effects of neutral solutions with a PCO2 of 35 mmHg were significantly less than for neutral solution with a PCO2 of 64 mmHg. 4. These results show that the effects of CO2 on laryngeal pressure-sensitive receptors are independent of the pH of the perfusing media, and suggest that acidification of the receptor cell or its microenvironment is the main mechanism of CO2 chemoreception.

Early detection of upper airway obstructions by analysis of acoustical respiratory input impedance.

Repetitive occurrence of partial or total upper airway obstruction characterizes several respiratory dysfunctions such as the obstructive sleep apnea syndrome (OSAS). In OSAS patients, pharyngeal collapses are linked to a decrease in upper airway muscle activity during sleep which causes decreased upper airway wall stiffness. Continuous positive airway pressure (CPAP) is recommended as the treatment of choice. Advancements in CPAP therapy require early detection of respiratory events in real time to adapt the level of the applied pressure to airway collapsibility. The forced oscillation technique (FOT) is a noninvasive method which reflects patients' airway patency by measuring respiratory impedance. The aim of this study was to evaluate by a mathematical model of the respiratory system if FOT can provide an early detection index of total or partial upper airway obstruction. Furthermore, the simulation should suggest which characteristic features are relevant for early apnea detection in measured clinical data. The respiratory system has been treated as a series of cylindrical segments. The oropharynx analog of the model allows simulation of upper airway collapse, mimicking the situation in patients with OSAS. We calculated the input impedance for different degrees of upper airway obstruction ranging from unobstructed airways to total occlusion. Furthermore, we simulated different upper airway wall compliances. We compared the simulation with real data. The results of the study suggest that FOT is a valuable tool for assessing the degree of upper airway obstruction in patients with OSAS. Especially, the phase angle of the impedance seems to be a potentially useful tool for early apnea detection by assessing the upper airway wall collapsibility.

Resolution of obstructive sleep apnea syndrome after adenoidectomy in congenital central hypoventilation syndrome

We report on a 2½-year-old boy who is currently ventilated at home by positive pressure ventilation through a nasal mask during the night because of congenital central hypoventilation syndrome (CCHS). Up to age 2 he had developed normally. A reevalution was performed because of symptoms suggestive of obstructive sleep apnea syndrome (OSAS), including snoring, nocturnal sweating, frequent nighttime awakenings, speech impairment, daytime fatigue, and failure to thrive. A sleep study indicated obstructive apnea episodes lasting up to 40 s and arterial desaturations below 50% during spontaneous sleep. During mechanical ventilation snoring persisted, and capillary PCO2 rose to 60 mm Hg. Partial upper airway obstruction, leaking around the mask, and arousal movements developed on passive flexion of the neck to 20°. After adenoidectomy, symptoms of OSAS resolved. There were no more obstructive apneas during spontaneous sleep, but obstructive apneas could be provoked by neck flexion to 20°. During ventilation, neck flexion of 20° was tolerated, but a 40° flexion led to partial obstruction. In CCHS patients, the problem of upper airway obstruction is rarely noted because most patients are ventilated through a permanent tracheostomy. Today, noninvasive ventilation strategies are becoming more common. Reduced activity of upper airway muscles and impaired reflex mechanisms could lead to upper airway obstruction during face mask positive pressure ventilation in children with CCHS. Enlarged adenoids worsened this problem in our patient, leading to insufficient ventilation and OSAS. Adenoidectomy resolved symptoms of OSAS and enabled successful nasal mask ventilation. Close follow-up of the patient avoided hypoxia and sequelae from OSAS such as pulmonary hypertension. Pediatr Pulmonol. 1999;27:341–346. © 1999 Wiley-Liss, Inc.

Volume-pressure properties of the upper airway in normal subjects and patients with obstructive sleep apnoea.

The aim of this study was to examine the volume-pressure (V-P) characteristics of isolated upper airways in normal subjects and patients with obstructive sleep apnoea (OSA) and to ascertain whether an increase in upper airway muscle activity affects these characteristics. We studied upper airway pressure changes during volume changes by inflation and deflation of air volumes of 5, 10, 15 and 20 mL without and with submental electrical stimulation, during voluntary closing of the glottis, in seven normal subjects and 13 OSA patients. Volume-pressure properties of the upper airway were assessed by elastance (Euaw) which was obtained from the slope of the regression line of the V-P relationships. Euaw in OSA patients was 0.52 +/- 0.08 cmH2O/mL, which was greater than in normal subjects (0.26 +/- 0.06 cmH2O/mL). Submental stimulation increased Euaw in both OSA patients and normal subjects (0.70 +/- 0.11 cmH2O/mL and 0.41 +/- 0.11 cmH2O/mL, respectively). These results suggest that upper airways of OSA patients during wakefulness are less collapsible than those of normal subjects, and that, in both groups, submental stimulation may stiffen the upper airway.

Differential suppression of upper airway motor activity during carbachol-induced, REM sleep-like atonia.

Microinjections of carbachol into the pontine tegmentum of decerebrate cats have been used to study the mechanisms underlying the suppression of postural and respiratory motoneuronal activity during the resulting rapid eye movement (REM) sleep-like atonia. During REM sleep, distinct respiratory muscles are differentially affected; e.g., the activity of the diaphragm shows little suppression, whereas the activity of some upper airway muscles is quite strong. To determine the pattern of the carbachol-induced changes in the activity of different groups of upper airway motoneurons, we simultaneously recorded the efferent activity of the recurrent laryngeal nerve (RL), pharyngeal branch of the vagus nerve (Phar), and genioglossal branch of the hypoglossal (XII) and phrenic (Phr) nerves in 12 decerebrate, paralyzed, vagotomized, and artificially ventilated cats. Pontine carbachol caused a stereotyped suppression of the spontaneous activity that was significantly larger in Phar expiratory (to 8.3% of control) and XII inspiratory motoneurons (to 15%) than in Phr inspiratory (to 87%), RL inspiratory (to 79%), or RL expiratory motoneurons (to 72%). The suppression in upper airway motor output was significantly greater than the depression caused by a level of hypocapnia that reduced Phr activity as much as carbachol. We conclude that pontine carbachol evokes a stereotyped pattern of suppression of upper airway motor activity. Because carbachol evokes a state having many neurophysiological characteristics similar to those of REM sleep, it is likely that pontine cholinoceptive neurons have similar effects on the activity of upper airway motoneurons during both states.

Evaluation of forced oscillation technique for early detection of airway obstruction in sleep apnea: a model study*

The forced oscillation technique (FOT) is a non-invasive method which may be suitable for assessing upper airway obstruction in obstructive sleep apnea/hypopnea syndrome (OSAS) patients. The aim of this study was to determine in vitro if FOT can provide an early detection index of total or partial upper airway occlusion. A respiratory system analog was developed which includes an upper airway analog that allows simulation of upper airway collapse (thus mimicking the situation in patients with OSAS). We simulated different degrees of upper airway obstructions ranging from 0 (unobstructed airways) to 1 (total occlusion). Furthermore, we imitated the collapsible upper airway wall by means of elastic membranes with ten different wall compliances ranging from 3.3 x 10(-4) to 1 1/mbar. For the two stiffest rubber membranes (Cwall = 0.01 and 3.3 x 10(-4) l/mbar) the absolute value of the impedance (¿Z¿) showed a marked increase for obstructions greater than 0.6. For the two membranes with the highest wall compliances (Cwall = 0.03 and 1 1/mbar) obstructions with an increase in ¿Z¿ could not be detected before the obstruction reached 0.8. For degrees of obstruction less than 0.6 the phase angle of collapsible membranes with low compliance (stiff airway wall) were about 1.5pi which significantly differed from phase angles of 1.77pi measured in membranes with high compliance (elastic airway wall); p < 0.01. We hypothesized that stiffness of upper airway walls corresponds with their muscle tone, i.e., stiff airway walls are related with high muscle tone and vice versa. Thus, a decrease in upper airway muscle activity would cause an increase of upper airway wall elasticity that enables upper airway collapse. As a consequence the phase angle phi could be expected to change from values characterizing stiff membranes to values characterizing more elastic membranes which could be used as early indicator for obstructive respiratory events. We have frequently observed such changes in morphology of phi(t) data obtained from patients with OSAS.

Laryngeal-receptor responses to phasic CO2 in anesthetized cats.

We compared the effects of CO2 applied continuously and during expiration on laryngeal-receptor activity in paralyzed, artificially ventilated and nonparalyzed, spontaneously breathing cats by using an isolated larynx, artificially ventilated to approximate a normal respiratory cycle. The majority of quiescent negative-pressure and all cold receptors were excited by 5 and 9% CO2 applied both continuously and during expiration. In general, quiescent positive-pressure, tonic negative-pressure, and tonic positive-pressure receptors were inhibited by 5 and 9% CO2 applied continuously and during expiration. There were no significant differences between responses to 5 and 9% CO2 or to continuous and expired CO2 or between paralyzed and nonparalyzed preparations. In conclusion, laryngeal receptors respond to changes in CO2 concentration occurring during a normal respiratory cycle. Because laryngeal-receptor stimulation exerts reflex effects on ventilation and upper airway muscle activity, these results suggest that airway CO2 plays a role in reflex regulation of breathing and upper airway patency.

Breathing route dependence of upper airway muscle activity during hyperpnea.

Exercise (Ex) and hypercapnia (HC) both lead to increases in ventilation and upper airway muscle (UAM) activity. To determine whether different breathing routes (nasal vs. oral) or stimuli produced differential UAM activation, electromyographic (EMG) activity of the alae nasi (AN) and genioglossus (GG) were measured in seven normal subjects seated on a bicycle ergometer. Subjects performed paired runs during both progressive Ex and HC while breathing through the nose alone (N) or the mouth alone (O). During hyperpnea, AN EMG was greater when the subjects were breathing via N [81 +/- 6% maximum (HC) and 69 +/- 7% maximum (Ex)] than when they were breathing via O [30 +/- 5% maximum (HC) and 27 +/- 5% maximum (Ex); both P < 0.01], whereas the GG EMG did not differ between N and O. Both AN and GG EMG were similar for Ex and HC when the subjects were breathing via the same route. We conclude that UAM activation was independent of the nature of the stimulus. However, the AN muscle but not the GG muscle demonstrated breathing-route dependence of activity.

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This Month in the Journal

Sites Other Than Ventrolateral Medullary Chemoreceptive Regions Contribute to Hypercapnic Responses During Development. † 1492

During postnatal maturation, development of respiratory activity and hypercapnic responses is controlled by a network of chemosensory cells that senses changes in CO2 and H+ ion concentration. The ventrolateral medulla is considered the primary site for central chemosensitivity, however, brain stem midline neurons have also been shown to contribute to ventilatory control of upper airway and chest wall muscle activities. In this study we sought to characterize the role of specific neurons within the midline brainstem at the so-called raphe obscurus on phrenic and hypoglossal nerve responses to hypercapnia during development. Studies were performed in ten decorticate, vagotomized, paralyzed and mechanically ventilated 14 to 20 day old piglets. Blockade of raphe obscurus neuronal activity induced by microinjections of lidocaine was associated with a significant reduction of phrenic and hypoglossal nerve responses to progressive hypercapnia. At any given end-tidal CO2, peak phrenic and hypoglossal nerve activities were significantly lower following blockade than in the control period. For example, at 7.5% CO2 phrenic activity (in arbitrary units) was 33.9±1.9 vs 18.3±4.1 (p<0.005, mean ± SEM) prior to vs following lidocaine blockade respectively. Corresponding hypoglossal activity was preferentially reduced to a greater degree than phrenic activity. for example, at 7.5% CO2 hypoglossal activity was 20.8±3.6 vs 5.6±2.1 (p<0.005) prior to vs following lidocaine blockade respectively. Injection of saline (control) solution at the same site had no effect. We conclude that impaired function of raphe obscurus midline neurons reduces respiratory responses to central chemosensory stimulation. We speculate that specific neuronal sites within the midline region of the brainstem are required for full expression of ventilatory responses to hypercapnia, and raise the possibility that alteration in their function may contribute to respiratory instability during early postnatal life.

Long-term facilitation of upper airway muscle activities in vagotomized and vagally intact cats.

The primary purpose of the present investigation was to determine whether long-term facilitation (LTF) of upper airway muscle activities occurs in vagotomized and vagally intact cats. Tidal volume and diaphragm, genioglossus, and nasal dilator muscle activities were recorded before, during, and after one carotid sinus nerve was stimulated five times with 2-min trains of constant current. Sixty minutes after stimulation, nasal dilator and genioglossus muscle activities were significantly greater than control in the vagotomized cats but not in the vagally intact cats. Tidal volume recorded from the vagotomized and vagally intact cats was significantly greater than control during the poststimulation period. In contrast, diaphragm activities were not significantly elevated in the poststimulation period in either group of animals. We conclude that 1) LTF of genioglossus and nasal dilator muscle activities can be evoked in vagotomized cats; 2) vagal mechanisms inhibit LTF in upper airway muscles; and 3) LTF can be evoked in accessory inspiratory muscles because LTF of inspired tidal volume was greater than LTF of diaphragm activity.

The effect of the tongue retaining device on awake genioglossus muscle activity in patients with obstructive sleep apnea

Knowledge of how dental appliances alter upper airway muscle activity when they are used for the treatment of snoring and/or obstructive sleep apnea (OSA) is very limited. The purpose of this study was to define the effect of a tongue retaining device (TRD) on awake genioglossus (GG) muscle activity in 10 adult subjects with OSA and in 6 age and body mass index (BMI) matched symptom-free control subjects. The TRD is a custom-made appliance designed to allow the tongue to remain in a forward position between the anterior teeth by holding the tongue in an anterior bulb with negative pressure, during sleep. This pulls the tongue forward to enlarge the volume of the upper airway and to reduce upper airway resistance. In this study, two customized TRDs were used for each subject. The TRD-A did not have an anterior bulb but incorporated lingual surface electrodes to record the GG electromyographic (EMG) activity. The TRD-B contained an anterior bulb and two similar electrodes. The GG EMG activity was also recorded while patients used the TRD-B but were instructed to keep their tongue at rest outside the anterior bulb; this condition is hereafter referred to as TRD-X. The GG EMG activity and nasal airflow were simultaneously recorded while subjects used these customized TRDs during spontaneous awake breathing in both the upright and supine position. The following results were obtained and were consistent whether subjects were in the upright or the supine position. The GG EMG activity was greater with the TRD-B than with the TRD-A in control subjects ( p < 0.05), whereas the GG EMG activity was less with the TRD-B than with the TRD-A in subjects with OSA ( p < 0.01). Furthermore, there was no significant difference between the GG EMG activity of the TRD-A and the TRD-X in control subjects, whereas there was less activity with the TRD-X than with the TRD-A in subjects with OSA ( p < 0.05). On the basis of these findings, it was concluded that the TRD has different effects on the awake GG muscle activity in control subjects and patients with OSA. The resultant change in the anatomic configuration of the upper airway caused by the TRD may be important in the treatment of OSA because such a change may alleviate the impaired upper airway function. (Am J Orthod Dentofac Orthop 1996;110:28-35.)

Upper airway shape: Is it important in the pathogenesis of obstructive sleep apnea?

It is widely accepted that the size of the airway and the level of upper airway muscle activity contribute to the pathogenesis of obstructive sleep apnea (OSA). However, some individuals with normal airway size and apparently normal upper airway muscle activity nonetheless develop OSA. Recent data and analysis suggest that airway shape may also contribute to the development of OSA; patients with OSA tend to have elliptical airways, with the long axis of the ellipse oriented along the anteroposterior axis, and this orientation may adversely affect upper airway muscle function. By incorporating airway shape, airway size, and upper airway muscle activity into a unified hypothesis of the pathogenesis of OSA, it may be possible to reconcile discrepant anatomic and electromyographic findings in patients with OSA, to explain the difficulty of selecting appropriate surgical therapy for patients with OSA using currently available diagnostic tools, and to understand the often disappointing response to upper airway surgery in these patients.