Control of nasal dilator muscle activities during exercise: role of nasopharyngeal afferents

1996 ◽  
Vol 80 (5) ◽  
pp. 1520-1527 ◽  
Author(s):  
J. Sullivan ◽  
D. Fuller ◽  
R. F. Fregosi

Our primary aim was to determine whether reducing the activity of nasal airway receptors would influence drive to the nasal dilator muscles (NDMs) during exercise. We used lidocaine (2%) or nasal splints to diminish afferent airway receptor activity and measured the electromyogram (EMG) activity of the NDMs during incremental bicycle exercise in subjects who breathed nasally. NDM EMG activities increased as a function of exercise intensity but were not changed by lidocaine and were only slightly reduced by splinting. Similarly, neither intervention altered the normal decrease in NDM EMG activity associated with reductions in airway resistance evoked by He-O2 breathing. We also compared the NDM EMG response to exercise with that evoked by CO2 rebreathing at rest to determine whether the nature of the ventilatory stimulus influences drive to the NDMs; comparisons were made at constant levels of nasal inspired ventilation and, therefore, constant total ventilatory output. The increase in EMG activity was much higher during exercise compared with hyperoxic hypercapnia. In conclusion, 1) desensitizing the nasal airway does not alter NDM activity significantly during exercise and 2) exercise results in much greater increases in NDM activity compared with hypercapnia, indicating that different ventilatory stimuli can evoke more or less activation of upper airway motoneurons, even when comparisons are made at constant levels of total ventilatory output.

1998 ◽  
Vol 84 (6) ◽  
pp. 2115-2122 ◽  
Author(s):  
Avram R. Gold ◽  
Philip L. Smith ◽  
Alan R. Schwartz

The upper airway is a complicated structure that is usually widely patent during inspiration. However, on inspiration during certain physiological and pathophysiological states, the nares, pharynx, and larynx may collapse. Collapse at these locations occurs when the transmural pressure (Ptm) at a flow-limiting site (FLS) falls below a critical level (Ptm′). On airway collapse, inspiratory airflow is limited to a maximal level (V˙i max) determined by (−Ptm′)/Rus, where Rus is the resistance upstream to the FLS. The airflow dynamics of the upper airway are affected by the activity of its associated muscles. In this study, we examine the modulation ofV˙i maxby muscle activity in the nasal airway under conditions of inspiratory airflow limitation. Each of six subjects performed sniffs through one patent nostril (pretreated with an alpha agonist) while flaring the nostril at varying levels of dilator muscle (alae nasi) EMG activity (EMGan). For each sniff, we located the nasal FLS with an airway catheter and determinedV˙i max, Ptm′, and Rus. Activation of the alae nasi from the lowest to the highest values of EMGan increasedV˙i maxfrom 422 ± 156 to 753 ± 291 ml/s ( P < 0.01) and decreased Ptm′ from −3.6 ± 3.0 to −6.0 ± 4.7 cmH2O ( P < 0.05). Activation of the alae nasi had no consistent effect on Rus.V˙i maxwas positively correlated with EMGan, and Ptm′ was negatively correlated with EMGan in all subjects. Our findings demonstrate that alae nasi activation increasesV˙i maxthrough the nasal airway by decreasing airway collapsibility.


1998 ◽  
Vol 84 (3) ◽  
pp. 1055-1062 ◽  
Author(s):  
Rainer M. Popovic ◽  
David P. White

Obstructive sleep apnea is a disorder with a strong male predominance. One possible explanation could be an effect of female hormones on pharyngeal dilator muscle activity. Therefore, we determined the level of awake genioglossus electromyogram (EMGgg) and upper airway resistance in 12 pre- and 12 postmenopausal women under basal conditions and during the application of an inspiratory resistive load (25 cmH2O ⋅ l−1 ⋅ s). In addition, a subgroup of eight postmenopausal women were studied a second time after 2 wk of combined estrogen and progesterone replacement in standard doses. Peak phasic and tonic genioglossus activity, expressed as a percentage of maximum, were highest in the luteal phase of the menstrual cycle (phasic 23.9 ± 3.8%, tonic 10.2 ± 1.0%), followed by the follicular phase (phasic 15.5 ± 2.2%, tonic 7.3 ± 0.8%), and were lowest in the postmenopausal group (phasic 11.3 ± 1.6%, tonic of 5.0 ± 0.6), whereas upper airway resistance did not differ. There was a weak but significant positive correlation between progesterone levels and both peak phasic ( P < 0.05) and tonic ( P < 0.01) EMGgg. Finally, there was a significant increase in EMGgg in the postmenopausal group restudied after hormone therapy. In conclusion, female hormones (possibly progesterone) have a substantial impact on upper airway dilator muscle activity.


1982 ◽  
Vol 52 (6) ◽  
pp. 1432-1437 ◽  
Author(s):  
K. P. Strohl ◽  
C. F. O'Cain ◽  
A. S. Slutsky

To investigate the effect of alae nasi (AN) activation on nasal resistance, we monitored AN electromyographic (EMG) activity in 17 healthy subjects using surface electrodes placed on either side of the external nares and measured inspiratory nasal resistance utilizing the method of posterior rhinometry. With CO2 inhalation (6 subj), AN EMG activity increased as nasal resistance fell 23 +/- 5% (P less than 0.01). In the same subjects, voluntary flaring of the external nares also increased AN EMG and decreased nasal resistance by 29 +/- 5% (P less than 0.01). Nasal resistance was altered by nasal flaring and CO2 inhalation even after administration of a topical nasal vasoconstrictive spray (8 subj). In six subjects, voluntary nasal flaring or inhibition with the mouth closed produced a 21 +/- 12% change (P less than 0.01) in total airway resistance as measured by body plethysmography. We conclude that activation of the alae nasi will decrease nasal and total airway resistance during voluntary nasal flaring and during CO2 inhalation and thus should be considered in any studies of upper airway resistance.


2009 ◽  
Vol 101 (2) ◽  
pp. 558-568 ◽  
Author(s):  
Kori Schmitt ◽  
Christiana DelloRusso ◽  
Ralph F. Fregosi

Human upper airway and facial muscles support breathing, swallowing, speech, mastication, and facial expression, but their endurance performance in sustained contractions is poorly understood. The muscular fatigue typically associated with task failure during sustained contractions has both central and intramuscular causes, with the contribution of each believed to be task dependent. Previously we failed to show central fatigue in the nasal dilator muscles of subjects that performed intermittent maximal voluntary contractions (MVCs). Here we test the hypothesis that central mechanisms contribute to the fatigue of submaximal, sustained contractions in nasal dilator muscles. Nasal dilator muscle force and EMG activities were recorded in 11 subjects that performed submaximal contractions (20, 35, and 65% MVC) until force dropped to ≤90% of the target force for ≥3 s, which we defined as task failure. MVC and twitch forces (the latter obtained by applying supramaximal shocks to the facial nerve) were recorded before the trial and at several time points over the first 10 min of recovery. The time to task failure was inversely related to contraction intensity. MVC force was depressed by roughly 30% at task failure in all three trials, but recovered within 2 min. Twitch force fell by 30–44% depending on contraction intensity and remained depressed after 10 min of recovery, consistent with low-frequency fatigue. Average EMG activity increased with time, but never exceeded 75% of the maximal, pretrial level despite task failure. EMG mean power frequency declined by 20–25% in all trials, suggesting reduced action potential conduction velocity at task failure. In contrast, the maximal evoked potential did not change significantly in any of the tasks, indicating that the EMG deficit at task failure was due largely to mechanisms proximal to the neuromuscular junction. Additional experiments using the interpolated twitch technique suggest that subjects can produce about 92% of the maximal evocable force with this muscle, which is not a large enough deficit to explain the entire shortfall in the EMG at task failure. These data show that the nervous system fails to fully activate the nasal dilator muscles during sustained, submaximal contractions; putative mechanisms are discussed.


1973 ◽  
Vol 82 (6) ◽  
pp. 827-830 ◽  
Author(s):  
John Cavo ◽  
Joseph H. Ogura ◽  
Donald G. Sessions ◽  
J. Roger Nelson

The role of the upper airway (the breathing passage above the trachea) in maintaining the normal junction of the respiratory system has been suggested by previous investigators. During a tracheotomy the upper airway is by-passed by a prosthetic metal or plastic tube which is placed into the trachea through the neck. In order to determine which, among the most commonly used tracheotomy tubes, most closely simulate the flow resistance of the adult human upper airway, a series of varying flow rates were passed through different sized tubes. Pressure drops were recorded and resistance values were thereby determined. Our data was compared with previously determined values for flow resistance of the adult human upper airway. Resistance related to turbulent and laminar flow was considered. On the basis of our data we have suggested that large caliber tracheotomy tubes be used in adult patients in whom the prolonged need for a tracheotomy is anticipated.


1993 ◽  
Vol 75 (2) ◽  
pp. 626-632 ◽  
Author(s):  
J. R. Wheatley ◽  
D. J. Tangel ◽  
W. S. Mezzanotte ◽  
D. P. White

The influence of sleep on the upper airway musculature varies considerably, with some muscles maintaining their activity at waking levels and others falling substantially. The influence of sleep on the alae nasi (AN), a dilator muscle of the nasal airway, has been minimally studied to date. Thus we determined the effect of non-rapid-eye-movement (NREM) sleep on the AN electromyogram and its relationship to nasal resistance (Rn) in nine normal supine males. Phasic inspiratory AN activity decreased from 20 +/- 6 arbitrary units during wakefulness to 5 +/- 1 arbitrary units (P < 0.001) at the onset of stage 2 NREM sleep and remained unchanged for two subsequent hours of NREM sleep. However, the Rn at the onset of NREM sleep remained similar to awake values (5.7 +/- 0.9 cmH2O.l-1 x s) and increased only after 1 h of NREM sleep (8.6 +/- 1.7 cmH2O.l-1 x s, P < 0.05), thus demonstrating little relationship to AN activity. We conclude that Rn increases slightly after 1 h of sleep, whereas AN activity decreases at stage 2 sleep onset. Thus AN activity has little influence on Rn during sleep.


1985 ◽  
Vol 58 (4) ◽  
pp. 1252-1256 ◽  
Author(s):  
P. M. Suratt ◽  
R. McTier ◽  
S. C. Wilhoit

The alae nasi is an accessible dilator muscle of the upper airway located in the nose. We measured electromyograms (EMG) of the alae nasi to determine the relationship between their activity and timing to contraction of the rib cage muscles and diaphragm during obstructive apnea in nine patients. Alae nasi EMG were measured with surface electrodes and processed to obtain a moving time average. Contraction of the rib cage and diaphragm during apneas was detected with esophageal pressure. During non-rapid-eye-movement (NREM) sleep, there was a significant correlation in each patient between alae nasi EMG activity and the change in esophageal pressure. During rapid-eye-movement (REM) sleep, correlations were significantly lower than during NREM sleep. As the duration of each apnea increased, the activation of alae nasi EMG occurred progressively earlier than the change in esophageal pressure. We conclude that during obstructive apneas in NREM sleep, activity of the alae nasi increases when diaphragm and rib cage muscle force increases and the activation occurs earlier as each apneic episode progresses.


1987 ◽  
Vol 63 (2) ◽  
pp. 603-608 ◽  
Author(s):  
D. W. Hudgel ◽  
M. Mulholland ◽  
C. Hendricks

The purposes of this study were 1) to characterize the immediate inspiratory muscle and ventilation responses to inspiratory resistive loading during sleep in humans and 2) to determine whether upper airway caliber was compromised in the presence of a resistive load. Ventilation variables, chest wall, and upper airway inspiratory muscle electromyograms (EMG), and upper airway resistance were measured for two breaths immediately preceding and immediately following six applications of an inspiratory resistive load of 15 cmH2O.l–1 X s during wakefulness and stage 2 sleep. During wakefulness, chest wall inspiratory peak EMG activity increased 40 +/- 15% (SE), and inspiratory time increased 20 +/- 5%. Therefore, the rate of rise of chest wall EMG increased 14 +/- 10.9% (NS). Upper airway inspiratory muscle activity changed in an inconsistent fashion with application of the load. Tidal volume decreased 16 +/- 6%, and upper airway resistance increased 141 +/- 23% above pre-load levels. During sleep, there was no significant chest wall or upper airway inspiratory muscle or timing responses to loading. Tidal volume decreased 40 +/- 7% and upper airway resistance increased 188 +/- 52%, changes greater than those observed during wakefulness. We conclude that 1) the immediate inspiratory muscle and timing responses observed during inspiratory resistive loading in wakefulness were absent during sleep, 2) there was inadequate activation of upper airway inspiratory muscle activity to compensate for the increased upper airway inspiratory subatmospheric pressure present during loading, and 3) the alteration in upper airway mechanics during resistive loading was greater during sleep than wakefulness.


1993 ◽  
Vol 102 (8) ◽  
pp. 631-638 ◽  
Author(s):  
David S. James ◽  
William E. Lambert ◽  
Christine A. Stidley ◽  
Thomas W. Chick ◽  
Christine M. Mermier ◽  
...  

Sources of variability in nasal airway resistance measured by posterior rhinomanometry were studied in 5 subjects tested on 5 different days and 56 subjects tested on 2 different days. On each day, a questionnaire on upper airway health and nasal symptoms was completed. The mean individual difference in nasal airway resistance between the 2 test days in the group of 56 subjects was 5.3% (SD 52.7%). Between-subject variability accounted for 74.9% and 72.5% of the total variability in the group of 5 and the group of 56 subjects, respectively. For the 5 subjects, by accounting for a change in upper airway symptoms or upper respiratory tract infection that occurred over the 5 test days, there was a significant decrease in the between-subject variability. The difference in sources of variation due to a change in upper airway symptoms was not seen in the group of 56 subjects. We conclude that the largest source of variability in nasal airway resistance is due to between-subject differences.


1984 ◽  
Vol 92 (3) ◽  
pp. 302-307 ◽  
Author(s):  
Janet S. Mertz ◽  
Thomas V. Mccaffrey ◽  
Eugene B. Kern

Posterior mask rhinomanometry was used to measure nasal resistance during exercise and hypercapnia in 10 healthy adult volunteers. Exercise was produced by peddling a stationary bicycle at three loads. Hypercapnia was produced by breathing O2 mixtures containing 5%, 6%, and 8% CO2. The results showed that (1) nasal resistance decreases linearly as expired CO2 levels and exercise levels increase, (2) minute ventilation increases linearly as expired CO2 levels and exercise levels increase, and (3) nasal resistance varies inversely with minute ventilation during both hypercapnia and exercise. The constant relationship between nasal resistance and minute ventilation during hypercapnia and exercise suggests that nasal resistance is regulated by the respiratory center to match the level of respiratory demand.


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