scholarly journals A secondary reflex suppression phase is present in genioglossus but not tensor palatini in response to negative upper airway pressure

2010 ◽  
Vol 108 (6) ◽  
pp. 1619-1624 ◽  
Author(s):  
Danny J. Eckert ◽  
Julian P. Saboisky ◽  
Amy S. Jordan ◽  
David P. White ◽  
Atul Malhotra

On the basis of recent reports, the genioglossus (GG) negative-pressure reflex consists initially of excitation followed by a secondary state-dependent suppression phase. The mechanistic origin and functional role of GG suppression is unknown but has been hypothesized to arise from transient inhibition of respiratory active neurons as a protective reflex to prevent aspiration, as observed in other respiratory muscles (e.g., diaphragm) during airway occlusion. Unlike GG, tensor palatini (TP) is a tonic muscle with minimal respiratory phasic activation during relaxed breathing, although both muscles are important in preserving pharyngeal patency. This study aimed to compare GG vs. TP reflex responses to the same negative-pressure stimulus. We hypothesized that reflex suppression would be present in GG, but not TP. Intramuscular GG and TP EMGs were recorded in 12 awake, healthy subjects (6 female). Reflex responses were generated via 250-ms pulses of negative upper airway pressure (approximately −16 cmH2O mask pressure) delivered in early inspiration. GG and TP demonstrated reflex activation in response to negative pressure (peak latency 31 ± 4 vs. 31 ± 6 ms and peak amplitude 318 ± 55 vs. 314 ± 26% baseline, respectively). A secondary suppression phase was present in 8 of 12 subjects for GG (nadir latency 54 ± 7 ms, nadir amplitude 64 ± 6% baseline), but not in any subject for TP. These data provide further support for the presence of excitatory and inhibitory components of GG (phasic muscle) in response to brief upper airway negative-pressure pulses. Conversely, no reflex suppression below baseline was present in TP (tonic muscle) in response to the same stimuli. These differential responses support the hypothesis that GG reflex suppression may be mediated via inhibition of respiratory-related premotor input.

2015 ◽  
Vol 118 (10) ◽  
pp. 1221-1228 ◽  
Author(s):  
Jayne C. Carberry ◽  
Hanna Hensen ◽  
Lauren P. Fisher ◽  
Julian P. Saboisky ◽  
Jane E. Butler ◽  
...  

This study assessed the effects of inhaled lignocaine to reduce upper airway surface mechanoreceptor activity on 1) basal genioglossus and tensor palatini EMG, 2) genioglossus reflex responses to large pulses (∼10 cmH2O) of negative airway pressure, and 3) upper airway collapsibility in 15 awake individuals. Genioglossus and tensor palatini muscle EMG and airway pressures were recorded during quiet nasal breathing and during brief pulses (250 ms) of negative upper-airway pressure. Lignocaine reduced peak inspiratory (5.6 ± 1.5 vs. 3.8 ± 1.1% maximum; mean ± SE, P < 0.01) and tonic (2.8 ± 0.8 vs. 2.1 ± 0.7% maximum; P < 0.05) genioglossus EMG during quiet breathing but had no effect on tensor palatini EMG (5.0 ± 0.8 vs. 5.0 ± 0.5% maximum; P = 0.97). Genioglossus reflex excitation to negative pressure pulses decreased after anesthesia (60.9 ± 20.7 vs. 23.6 ± 5.2 μV; P < 0.05), but not when expressed as a percentage of the immediate prestimulus baseline. Reflex excitation was closely related to the change in baseline EMG following lignocaine ( r2 = 0.98). A short-latency genioglossus reflex to rapid increases from negative to atmospheric pressure was also observed. The upper airway collapsibility index (%difference) between nadir choanal and epiglottic pressure increased after lignocaine (17.8 ± 3.7 vs. 28.8 ± 7.5%; P < 0.05). These findings indicate that surface receptors modulate genioglossus but not tensor palatini activity during quiet breathing. However, removal of input from surface mechanoreceptors has minimal effect on genioglossus reflex responses to large (∼10 cmH2O), sudden changes in airway pressure. Changes in pressure rather than negative pressure per se can elicit genioglossus reflex responses. These findings challenge previous views and have important implications for upper airway muscle control.


2018 ◽  
Vol 596 (14) ◽  
pp. 2853-2864 ◽  
Author(s):  
Nirupama S. Wijesuriya ◽  
Laura Gainche ◽  
Amy S. Jordan ◽  
David J. Berlowitz ◽  
Mariannick LeGuen ◽  
...  

2008 ◽  
Vol 104 (5) ◽  
pp. 1426-1435 ◽  
Author(s):  
Danny J. Eckert ◽  
R. Doug McEvoy ◽  
Kate E. George ◽  
Kieron J. Thomson ◽  
Peter G. Catcheside

Hypoxia can depress ventilation, respiratory load sensation, and the cough reflex, and potentially other protective respiratory reflexes such as respiratory muscle responses to increased respiratory load. In sleep-disordered breathing, increased respiratory load and hypoxia frequently coexist. This study aimed to examine the effects of hypoxia on the reflex responses of 1) the genioglossus (the largest upper airway dilator muscle) and 2) the scalene muscle (an obligatory inspiratory muscle) to negative-pressure pulse stimuli during wakefulness and sleep. We hypothesized that hypoxia would impair these reflex responses. Fourteen healthy men, 19–42 yr old, were studied on two separate occasions, ∼1 wk apart. Bipolar fine-wire electrodes were inserted orally into the genioglossus muscle, and surface electrodes were placed overlying the left scalene muscle to record EMG activity. In random order, participants were exposed to mild overnight hypoxia (arterial oxygen saturation ∼85%) or medical air. Respiratory muscle reflex responses were elicited via negative-pressure pulse stimuli (approximately −10 cmH2O at the mask, 250-ms duration) delivered in early inspiration during wakefulness and sleep. Negative-pressure pulse stimuli resulted in a short-latency activation followed by a suppression of the genioglossus EMG that did not alter with hypoxia. Conversely, the predominant response of the scalene EMG to negative-pressure pulse stimuli was suppression followed by activation with more pronounced suppression during hypoxia compared with normoxia (mean ± SE suppression duration 64 ± 6 vs. 38 ± 6 ms, P = 0.006). These results indicate differential sensitivity to the depressive effects of hypoxia in the reflex responsiveness to sudden respiratory loads to breathing between these two respiratory muscles.


1995 ◽  
Vol 89 (4) ◽  
pp. 441-445 ◽  
Author(s):  
Rajat Mathur ◽  
Ian L. Mortimore ◽  
Mohammed A. Jan ◽  
Neil J. Douglas

1. Patency of the upper airway is critical to respiration. Although about half of patients with the sleep apnoea/hypopnoea syndrome obstruct their upper airway at the retropalatal level, the respiratory actions of the palatal muscles have been little studied. We have therefore tested the hypothesis that the nasopharyngeal dilator muscle palatoglossus is activated during inspiration and by negative pressure. 2. Using intramuscular wire electrodes inserted perorally, we have compared the response of palatoglossus and genioglossus to breathing, posture change and airway negative pressure in 10 normal awake subjects before and after topical anaesthesia. The results are expressed as a percentage of maximal electromyogram. Data were analysed by repeated-measures analysis of variance. 3. Inspiratory activity was exhibited by both genioglossus [inspiratory, 10% ± 2% (SEM); expiratory, 6% ± 1%, P = 0.001] and palatoglossus (inspiratory, 16% ± 5%, expiratory, 10% ± 3%, P = 0.016), but only genioglossus exhibited increased activity on lying (supine 10% ± 2%, erect 6% ± 1% maximum, P = 0.01). 4. One hundred milliseconds after negative pressure application, activity increased in both genioglossus (7% ± 2% and 13% ± 3% respectively, P = 0.02) and palatoglossus (8% ± 2% and 23% ± 6% respectively, P < 0.001). After lignocaine surface anaesthesia to the nose and pharynx both genioglossus and palatoglossus still increased their activity in response to negative upper airway pressure, the extent of the increase being decreased for palatoglossus (P = 0.02) but not for genioglossus. 5. Thus, palatoglossus has respiratory activity and is activated by negative upper airway pressure.


1988 ◽  
Vol 74 (1) ◽  
pp. 25-34 ◽  
Author(s):  
O.P. Mathew ◽  
F.B. Sant'Ambrogio ◽  
G. Sant'Ambrogio

1994 ◽  
Vol 77 (1) ◽  
pp. 30-36 ◽  
Author(s):  
S. Duara ◽  
G. Silva Neto ◽  
N. Claure

Extrathoracic airway (ETA) narrowing is induced in preterm infants by inspiratory flow-resistive loading (IRL), which reduces intraluminal pressure within the region. Neuromuscular load compensation was evaluated over time in 10 infants [body wt 1.5 +/- 0.17 (SD) kg, gestational age 33 +/- 2.3 wk, age 12 +/- 5.2 days] during quiet sleep. Baseline (BL) studies were followed by IRL (125 cmH2O.l–1.s at 1 l/min). Minute ventilation, changes in esophageal pressure (Pes) and proximal airway pressure, and moving time averages of posterior cricoarytenoid (PCA), submental genioglossus (SM), and diaphragm (DIA) electromyograms were obtained during BL and 1 and 5 min of IRL. Total respiratory resistance was calculated from pressure and flow changes and was used to estimate ETA narrowing: there was an increase in total respiratory resistance from 90 +/- 15 to 120 +/- 34 and 151 +/- 86 cmH2O.l–1.s after 1 and 5 min of IRL, respectively (P < 0.05, 1-min IRL vs. BL), in association with a sustained decline in minute ventilation (P < 0.05) and increases in Pes and proximal airway pressure (P < 0.05). Phasic PCA activity was always present, but its duration was only transiently prolonged with IRL (P < 0.05, 1-min IRL vs. BL). SM activity was present in only one infant during BL and was recruited in two additional infants during IRL. The decline in Pes from 1 to 5 min of IRL occurred despite continuing increases in peak and average activities of the DIA moving time average, which may reflect an onset of DIA fatigue. The transient prolongation of phasic PCA activity and occasional recruitment of SM activity with sustained loading explain, in part, the ETA instability detectable by moderate IRL in sleeping preterm infants.


1994 ◽  
Vol 76 (6) ◽  
pp. 2656-2662 ◽  
Author(s):  
E. B. Gauda ◽  
T. P. Carroll ◽  
A. R. Schwartz ◽  
P. L. Smith ◽  
R. S. Fitzgerald

To investigate the influence of phasic pulmonary stretch receptors (n = 6) and chemoreceptors (n = 7) on the reflex response of the genioglossus (GG) muscle and diaphragm (DIA) to upper airway (UAW) negative pressure, we measured the response of the GG and DIA electromyogram (EMG) to three challenges: 1) negative pressure applied to the UAW during normoxia and hypercapnia, 2) end-expiratory tracheal occlusion, and 3) application of UAW negative pressure simultaneous with tracheal occlusion in spontaneously breathing tracheotomized anesthetized cats. Peak GG EMG was greatest when UAW negative pressure and end-expiratory tracheal occlusion were combined. No GG EMG activity was seen when UAW negative pressure was applied alone unless the animal was vagotomized or hypercapnic. DIA EMG increased in response to UAW negative pressure combined with occlusion. However, the increase in peak GG EMG was significantly greater than for the DIA with the same challenge. DIA EMG amplitude increased in response to occlusion alone but did not change when UAW negative pressure was applied alone. In the cat, phasic feedback from phasic pulmonary stretch receptors is a potent inhibitor of reflex activation of the GG in response to negative pressure applied to the UAW, which can be overridden by an increase in chemoreceptor drive.


1992 ◽  
Vol 73 (6) ◽  
pp. 2283-2288 ◽  
Author(s):  
T. A. Wilson ◽  
A. De Troyer

The chest wall is modeled as a linear system for which the displacements of points on the chest wall are proportional to the forces that act on the chest wall, namely, airway opening pressure and active tension in the respiratory muscles. A standard theorem of mechanics, the Maxwell reciprocity theorem, is invoked to show that the effect of active muscle tension on lung volume, or airway pressure if the airway is closed, is proportional to the change of muscle length in the relaxation maneuver. This relation was tested experimentally. The shortening of the cranial-caudal distance between a rib pair and the sternum was measured during a relaxation maneuver. These data were used to predict the respiratory effect of forces applied to the ribs and sternum. To test this prediction, a cranial force was applied to the rib pair and a caudal force was applied to the sternum, simulating the forces applied by active tension in the parasternal intercostal muscles. The change in airway pressure, with lung volume held constant, was measured. The measured change in airway pressure agreed well with the prediction. In some dogs, nonlinear deviations from the linear prediction occurred at higher loads. The model and the theorem offer the promise that existing data on the configuration of the chest wall during the relaxation maneuver can be used to compute the mechanical advantage of the respiratory muscles.


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