Long-term facilitation of ventilation is not present during wakefulness in healthy men or women

2002 ◽  
Vol 93 (6) ◽  
pp. 2129-2136 ◽  
Author(s):  
A. S. Jordan ◽  
P. G. Catcheside ◽  
F. J. O'Donoghue ◽  
R. D. McEvoy
Keyword(s):  
Repeated Measures ◽  
Human Subjects ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Menstrual Phase ◽  
Healthy Human ◽  
Dilator Muscle ◽  
Obstructive Sleep ◽  
Long Term Facilitation

Obstructive sleep apnea (OSA) is more common in men than in women for reasons that are unclear. The stability of the respiratory controller has been proposed to be important in OSA pathogenesis and may be involved in the gender difference in prevalence. Repetitive hypoxia elicits a progressive rise in ventilation in animals [long-term facilitation (LTF)]. There is uncertainty whether LTF occurs in humans, but if present it may stabilize respiration and possibly also the upper airway. This study was conducted to determine 1) whether LTF exists during wakefulness in healthy human subjects and, if so, whether it is more pronounced in women than men and 2) whether inspiratory pump and upper airway dilator muscle activities are affected differently by repetitive hypoxia. Twelve healthy young men and ten women in the luteal menstrual phase were fitted with a nasal mask and intramuscular genioglossal EMG (EMGgg) recording electrodes. After 5 min of rest, subjects were exposed to ten 2-min isocapnic hypoxic periods (∼9% O2 in N2, arterial O2 saturation ∼80%) separated by 2 min of room air. Inspired minute ventilation (V˙i) and peak inspiratory EMGgg activity were averaged over 30-s intervals, and respiratory data were compared between genders during and after repetitive hypoxia by using ANOVA for repeated measures. V˙i during recovery from repetitive hypoxia was not different from the resting level and not different between genders. There was no facilitation of EMGgg activity during or after repetitive hypoxia. EMGgg activity was reduced below baseline during recovery from repetitive hypoxia in women. In conclusion, we have found no evidence of LTF of ventilation or upper airway dilator muscle activity in healthy subjects during wakefulness.

scholarly journals Chronic Intermittent Hypoxia Induces the Long-Term Facilitation of Genioglossus Corticomotor Activity

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Ying Zou ◽  
Wei Wang ◽  
Xinshi Nie ◽  
Jian Kang
Keyword(s):  
Obstructive Sleep Apnea ◽  
Intermittent Hypoxia ◽  
Magnetic Stimulation ◽  
Upper Airway ◽  
Emg Activity ◽  
Chronic Intermittent Hypoxia ◽  
Experimental Conditions ◽  
Obstructive Sleep ◽  
Long Term Facilitation

Obstructive sleep apnea (OSA) is characterized by the repetitive collapse of the upper airway and chronic intermittent hypoxia (CIH) during sleep. It has been reported that CIH can increase the EMG activity of genioglossus in rats, which may be related to the neuromuscular compensation of OSA patients. This study aimed to explore whether CIH could induce the long-term facilitation (LTF) of genioglossus corticomotor activity. 16 rats were divided into the air group (n=8) and the CIH group (n=8). The CIH group was exposed to hypoxia for 4 weeks; the air group was subjected to air under identical experimental conditions in parallel. Transcranial magnetic stimulation (TMS) was applied every ten minutes and lasted for 1 h/day on the 1st, 3rd, 7th, 14th, 21st, and 28th days of air/CIH exposure. Genioglossus EMG was also recorded at the same time. Compared with the air group, the CIH group showed decreased TMS latency from 10 to 60 minutes on the 7th, 14th, 21st, and 28th days. The increased TMS amplitude lasting for 60 minutes was only observed on the 21st day. Genioglossus EMG activity increased only on the 28th day of CIH. We concluded that CIH could induce LTF of genioglossus corticomotor activity in rats.

Selected Contribution: Genioglossus muscle activity at rest and in response to brief hypoxia in healthy men and women

2002 ◽  
Vol 92 (1) ◽  
pp. 410-417 ◽  
Author(s):  
A. S. Jordan ◽  
P. G. Catcheside ◽  
F. J. O'Donoghue ◽  
N. A. Saunders ◽  
R. D. McEvoy
Keyword(s):  
Gender Difference ◽  
Repeated Measures ◽  
Neural Control ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Men And Women ◽  
Healthy Men ◽  
Pharyngeal Airway ◽  
Obstructive Sleep ◽  
The Relationship

10.1152/japplphysiol.00461.2001.—Obstructive sleep apnea (OSA) is more common in men than in women for reasons that are not clearly understood. An underlying difference between men and women in the respiratory-related neural control of upper airway dilator muscles has been suggested as a possible reason for the gender difference. We have compared three aspects of upper airway dilator muscle function in healthy men and women: 1) resting inspiratory genioglossus electromyogram (EMGgg) activity, 2) the respiratory EMGgg “afterdischarge” after a brief hypoxic stimulus, and 3) the relationship between the EMGgg and pharyngeal airway pressure. Inspired minute ventilation (V˙i), epiglottic pressure (Pepi), and EMGgg and diaphragm EMG (EMGdi) activity were measured in 24 subjects (12 men, 12 women in the luteal menstrual phase) and were compared between genders while lying supine awake. Every 7–8 min over 2 h, subjects were exposed to 45-s periods of isocapnic hypoxia (9% O2 in N2) that were abruptly terminated with one breath of 100% O2. The relationship between Pepi and EMGgg activity was also compared between genders. The results of 117 trials with satisfactory end-tidal Pco 2 control and no sighs or swallows are reported. There was no gender difference in the resting level of peak inspiratory EMGgg [3.7 ± 0.8 (women) vs. 3.2 ± 0.6% maximal activity (men)]. Repeated-measures ANOVA showed no gender or gender-by-time interaction effect between men and women inV˙i or EMGgg or EMGdi activity during or after the hypoxic stimulus. The relationship between Pepi and EMGgg was not different between men (slope −0.63 ± 0.20) and women (slope −0.69 ± 0.33). These results do not support the hypothesis that the higher prevalence of OSA in men is related to an underlying gender difference in respiratory neural control of upper airway dilator muscles.

The influence of episodic hypoxia on upper airway collapsibility in subjects with obstructive sleep apnea

2007 ◽  
Vol 103 (3) ◽  
pp. 911-916 ◽  
Author(s):  
James A. Rowley ◽  
Ihab Deebajah ◽  
Swapna Parikh ◽  
Ali Najar ◽  
Rajib Saha ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Episodic Hypoxia ◽  
Before And After ◽  
Upper Airway Collapsibility ◽  
Long Term Facilitation

We have previously shown that in subjects with obstructive sleep apnea, repetitive hypoxia is associated with long-term facilitation as manifested by decreased upper airway resistance (Rua). Our objective was to study the influence of long-term facilitation on upper airway collapsibility as measured by the critical closing pressure (Pcrit) model and to determine whether changes in Rua correlated with changes in collapsibility. We studied 13 subjects (10 men, 3 women) with a mean apnea-hypopnea index of 43.9 ± 24.0 events/h. In the first protocol with 11 subjects, we measured collapsibility using a Pcrit protocol before and after episodic hypoxia. Brief (3 min) isocapnic hypoxia (inspired O2 fraction = 8%) followed by 5 min of room air was induced 10 times. A sham study without hypoxia was performed on eight subjects. Ventilatory parameters, Rua, and Pcrit before and after episodic hypoxia were measured. At 20 min of recovery, there was no change in minute ventilation but there was a significant decrease in Rua compared with the control period (control, 8.6 ± 4.8 cmH2O·l−1·s vs. recovery, 5.9 ± 3.8 cmH2O·l−1·s; P < 0.05). However, there was no change in Pcrit between the control (2.3 ± 1.9 cmH2O) and recovery (2.7 ± 3.2 cmH2O) periods. No changes in Rua or Pcrit were observed in the sham protocol. We conclude that long-term facilitation of upper airway dilators is not associated with changes in upper airway collapsibility in subjects with obstructive sleep apnea. These results corroborate previous evidence that changes in upper airway resistance and caliber can be dissociated from changes in upper airway collapsibility.

Long-term facilitation in obstructive sleep apnea patients during NREM sleep

2001 ◽  
Vol 91 (6) ◽  
pp. 2751-2757 ◽  
Author(s):  
Salah E. Aboubakr ◽  
Amy Taylor ◽  
Reason Ford ◽  
Sarosh Siddiqi ◽  
M. Safwan Badr
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Recovery Period ◽  
Upper Airway ◽  
Flow Limitation ◽  
Inspiratory Time ◽  
Nasal Cpap ◽  
Obstructive Sleep ◽  
Long Term Facilitation

Repetitive hypoxia followed by persistently increased ventilatory motor output is referred to as long-term facilitation (LTF). LTF is activated during sleep after repetitive hypoxia in snorers. We hypothesized that LTF is activated in obstructive sleep apnea (OSA) patients. Eleven subjects with OSA (apnea/hypopnea index = 43.6 ± 18.7/h) were included. Every subject had a baseline polysomnographic study on the appropriate continuous positive airway pressure (CPAP). CPAP was retitrated to eliminate apnea/hypopnea but to maintain inspiratory flow limitation (sham night). Each subject was studied on 2 separate nights. These two studies are separated by 1 mo of optimal nasal CPAP treatment for a minimum of 4–6 h/night. The device was capable of covert pressure monitoring. During night 1 (N1), study subjects used nasal CPAP at suboptimal pressure to have significant air flow limitation (>60% breaths) without apneas/hypopneas. After stable sleep was reached, we induced brief isocapnic hypoxia [inspired O2 fraction (Fi O2 ) = 8%] (3 min) followed by 5 min of room air. This sequence was repeated 10 times. Measurements were obtained during control, hypoxia, and at 5, 20, and 40 min of recovery for ventilation, timing ( n = 11), and supraglottic pressure ( n = 6). Upper airway resistance (Rua) was calculated at peak inspiratory flow. During the recovery period, there was no change in minute ventilation (99 ± 8% of control), despite decreased Rua to 58 ± 24% of control ( P < 0.05). There was a reduction in the ratio of inspiratory time to total time for a breath (duty cycle) (0.5 to 0.45, P < 0.05) but no effect on inspiratory time. During night 2 (N2), the protocol of N1 was repeated. N2 revealed no changes compared with N1 during the recovery period. In conclusion, 1) reduced Rua in the recovery period indicates LTF of upper airway dilators; 2) lack of hyperpnea in the recovery period suggests that thoracic pump muscles do not demonstrate LTF; 3) we speculate that LTF may temporarily stabilize respiration in OSA patients after repeated apneas/hypopneas; and 4) nasal CPAP did not alter the ability of OSA patients to elicit LTF at the thoracic pump muscle.

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

1997 ◽  
Vol 82 (2) ◽  
pp. 419-425 ◽  
Author(s):  
J. H. Mateika ◽  
R. F. Fregosi ◽  
Keyword(s):  
Tidal Volume ◽  
Carotid Sinus ◽  
Upper Airway ◽  
Constant Current ◽  
Carotid Sinus Nerve ◽  
Inspiratory Muscles ◽  
Dilator Muscle ◽  
Upper Airway Muscles ◽  
Long Term Facilitation

Mateika, J. H., and R. F. Fregosi. Long-term facilitation of upper airway muscle activities in vagotomized and vagally intact cats. J. Appl. Physiol.82(2): 419–425, 1997.—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.

scholarly journals Pathophysiology of Obstructive Sleep Apnea in Aging Women

2021 ◽  
Author(s):  
Qingchao Qiu ◽  
Jason H. Mateika
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Loop Gain ◽  
Younger Women ◽  
Arousal Threshold ◽  
Obstructive Sleep ◽  
Aging Women ◽  
Long Term Facilitation

AbstractThe following review is designed to explore the pathophysiology of sleep apnea in aging women. The review initially introduces four endotypes (i.e., a more collapsible airway, upper airway muscle responsiveness, arousal threshold, and loop gain) that may have a role in the initiation of obstructive sleep apnea. Thereafter, sex differences in the prevalence of sleep apnea are considered along with differences in the prevalence that exist between younger and older women. Following this discussion, we consider how each endotype might contribute to the increase in prevalence of sleep apnea in aging women. Lastly, we address how modifications in one form of respiratory plasticity, long-term facilitation, that might serve to mitigate apneic events in younger women may be modified in aging women with obstructive sleep apnea. Overall, the published literature indicates that the prevalence of sleep apnea is increased in aging women. This increase is linked primarily to a more collapsible airway and possibly to reduced responsiveness of upper airway muscle activity. In contrast, modifications in loop gain or the arousal threshold do not appear to have a role in the increased prevalence of sleep apnea in aging women. Moreover, we suggest that mitigation of long-term facilitation could contribute to the increased prevalence of sleep apnea in aging women.

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.

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.

scholarly journals Compensatory responses to upper airway obstruction in obese apneic men and women

2012 ◽  
Vol 112 (3) ◽  
pp. 403-410 ◽  
Author(s):  
Chien-Hung Chin ◽  
Jason P. Kirkness ◽  
Susheel P. Patil ◽  
Brian M. McGinley ◽  
Philip L. Smith ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
Airway Obstruction ◽  
Rem Sleep ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Upper Airway Obstruction ◽  
Men And Women ◽  
Compensatory Responses ◽  
Obstructive Sleep

Defective structural and neural upper airway properties both play a pivotal role in the pathogenesis of obstructive sleep apnea. A more favorable structural upper airway property [pharyngeal critical pressure under hypotonic conditions (passive Pcrit)] has been documented for women. However, the role of sex-related modulation in compensatory responses to upper airway obstruction (UAO), independent of the passive Pcrit, remains unclear. Obese apneic men and women underwent a standard polysomnography and physiological sleep studies to determine sleep apnea severity, passive Pcrit, and compensatory airflow and respiratory timing responses to prolonged periods of UAO. Sixty-two apneic men and women, pairwise matched by passive Pcrit, exhibited similar sleep apnea disease severity during rapid eye movement (REM) sleep, but women had markedly less severe disease during non-REM (NREM) sleep. By further matching men and women by body mass index and age ( n = 24), we found that the lower NREM disease susceptibility in women was associated with an approximately twofold increase in peak inspiratory airflow ( P = 0.003) and inspiratory duty cycle ( P = 0.017) in response to prolonged periods of UAO and an ∼20% lower minute ventilation during baseline unobstructed breathing (ventilatory demand) ( P = 0.027). Thus, during UAO, women compared with men had greater upper airway and respiratory timing responses and a lower ventilatory demand that may account for sex differences in sleep-disordered breathing severity during NREM sleep, independent of upper airway structural properties and sleep apnea severity during REM sleep.

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