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.

Influence of sleep on alae nasi EMG and nasal resistance in normal men

1993 ◽  
Vol 75 (2) ◽  
pp. 626-632 ◽  
Author(s):  
J. R. Wheatley ◽  
D. J. Tangel ◽  
W. S. Mezzanotte ◽  
D. P. White
Keyword(s):  
Eye Movement ◽  
Sleep Onset ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Nasal Airway ◽  
Nasal Resistance ◽  
Rapid Eye Movement ◽  
Dilator Muscle ◽  
Stage 2 Sleep ◽  
Normal Men

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.

scholarly journals Control of breathing during sleep assessed by proportional assist ventilation

1998 ◽  
Vol 84 (1) ◽  
pp. 3-12 ◽  
Author(s):  
S. Meza ◽  
E. Giannouli ◽  
M. Younes
Keyword(s):  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Normal Subjects ◽  
Progressive Increase ◽  
Control Of Breathing ◽  
Respiratory Drive ◽  
Proportional Assist Ventilation ◽  
End Tidal

Meza, S., E. Giannouli, and M. Younes. Control of breathing during sleep assessed by proportional assist ventilation. J. Appl. Physiol. 84(1): 3–12, 1998.—We used proportional assist ventilation (PAV) to evaluate the sources of respiratory drive during sleep. PAV increases the slope of the relation between tidal volume (Vt) and respiratory muscle pressure output (Pmus). We reasoned that if respiratory drive is dominated by chemical factors, progressive increase of PAV gain should result in only a small increase in Vt because Pmus would be downregulated substantially as a result of small decreases in[Formula: see text]. In the presence of substantial nonchemical sources of drive [believed to be the case in rapid-eye-movement (REM) sleep] PAV should result in a substantial increase in minute ventilation and reduction in [Formula: see text] as the output related to the chemically insensitive drive source is amplified severalfold. Twelve normal subjects underwent polysomnography while connected to a PAV ventilator. Continuous positive air pressure (5.2 ± 2.0 cmH2O) was administered to stabilize the upper airway. PAV was increased in 2-min steps from 0 to 20, 40, 60, 80, and 90% of the subject’s elastance and resistance. Vt, respiratory rate, minute ventilation, and end-tidal CO2pressure were measured at the different levels, and Pmus was calculated. Observations were obtained in stage 2 sleep ( n = 12), slow-wave sleep ( n = 11), and REM sleep ( n = 7). In all cases, Pmus was substantially downregulated with increase in assist so that the increase in Vt, although significant ( P < 0.05), was small (0.08 liter at the highest assist). There was no difference in response between REM and non-REM sleep. We conclude that respiratory drive during sleep is dominated by chemical control and that there is no fundamental difference between REM and non-REM sleep in this regard. REM sleep appears to simply add bidirectional noise to what is basically a chemically controlled respiratory output.

Changes in upper airway muscle activation and ventilation during phasic REM sleep in normal men

1991 ◽  
Vol 71 (2) ◽  
pp. 488-497 ◽  
Author(s):  
L. Wiegand ◽  
C. W. Zwillich ◽  
D. Wiegand ◽  
D. P. White
Keyword(s):  
Eye Movements ◽  
Tidal Volume ◽  
Rem Sleep ◽  
Muscle Activation ◽  
Sleep Stage ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Respiratory Neurons ◽  
Dilator Muscle ◽  
Normal Men

Several investigators have observed that irregular breathing occurs during rapid-eye-movement (REM) sleep in healthy subjects, with ventilatory suppression being prominent during active eye movements [phasic REM (PREM) sleep] as opposed to tonic REM (TREM) sleep, when ocular activity is absent and ventilation more regular. Inasmuch as considerable data suggest that rapid eye movements are a manifestation of sleep-induced neural events that may importantly influence respiratory neurons, we hypothesized that upper airway dilator muscle activation may also be suppressed during periods of active eye movements in REM sleep. We studied six normal men during single nocturnal sleep studies. Standard sleep-staging parameters, ventilation, and genioglossus and alae nasi electromyograms (EMG) were continuously recorded during the study. There were no significant differences in minute ventilation, tidal volume, or any index of genioglossus or alae nasi EMG amplitude between non-REM (NREM) and REM sleep, when REM was analyzed as a single sleep stage. Each breath during REM sleep was scored as “phasic” or “tonic,” depending on its proximity to REM deflections on the electrooculogram. Comparison of all three sleep states (NREM, PREM, and TREM) revealed that peak inspiratory genioglossus and alae nasi EMG activities were significantly decreased during PREM sleep compared with TREM sleep [genioglossus (arbitrary units): NREM 49 +/- 12 (mean +/- SE), TREM 49 +/- 5, PREM 20 +/- 5 (P less than 0.05, PREM different from TREM and NREM); alae nasi: NREM 16 +/- 4, TREM 38 +/- 7, PREM 10 +/- 4 (P less than 0.05, PREM different from TREM)]. We also observed, as have others, that ventilation, tidal volume, and mean inspiratory airflow were significantly decreased and respiratory frequency was increased during PREM sleep compared with both TREM and NREM sleep. We conclude that hypoventilation occurs in concert with reduced upper airway dilator muscle activation during PREM sleep by mechanisms that remain to be established.

Effects of sleep-induced increases in upper airway resistance on ventilation

1990 ◽  
Vol 69 (2) ◽  
pp. 617-624 ◽  
Author(s):  
K. G. Henke ◽  
J. A. Dempsey ◽  
J. M. Kowitz ◽  
J. B. Skatrud
Keyword(s):  
Airway Resistance ◽  
Minute Ventilation ◽  
Venous Blood ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Esophageal Pressure ◽  
Co2 Partial Pressure ◽  
Upper Airway Resistance ◽  
End Tidal ◽  
End Tidal Co2

To determine the effects of the sleep-induced increases in upper airway resistance on ventilatory output, we studied five subjects who were habitual snorers but otherwise normal while awake (AW) and during non-rapid-eye-movement (NREM) sleep under the following conditions: 1) stage 2, low-resistance sleep (LRS); 2) stage 3-4, high-resistance sleep (HRS) (snoring); 3) with continuous positive airway pressure (CPAP); 4) CPAP + end-tidal CO2 partial pressure (PETCO2) mode isocapnic to LRS; and 5) CPAP + PETCO2 isocapnic to HRS. We measured ventilatory output via pneumotachograph in the nasal mask, PETCO2, esophageal pressure, inspiratory and expiratory resistance (RL,I and RL,E). Changes in PETCO2 were confirmed with PCO2 measurements in arterialized venous blood in all conditions in one subject. During wakefulness, pulmonary resistance (RL) remained constant throughout inspiration, whereas in stage 2 and especially in stage 3-4 NREM sleep, RL rose markedly throughout inspiration. Expired minute ventilation (VE) decreased by 12% in HRS, and PETCO2 increased in LRS (3.3 Torr) and HRS (4.9 Torr). CPAP decreased RL,I to AW levels and increased end-expiratory lung volume 0.25-0.93 liter. Tidal volume (VT) and mean inspiratory flow rate (VT/TI) increased significantly with CPAP. Inspiratory time (TI) shortened, and PETCO2 decreased 3.6 Torr but remained 1.3 Torr above AW. During CPAP (RL,I equal to AW), with PETCO2 returned to the level of LRS, VT/TI and VE were 83 and 52% higher than during LRS alone. Also on CPAP, with PETCO2 made equal to HRS, VT, VT/TI, and VE were 67, 112, and 67% higher than during HRS alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Gender differences in airway resistance during sleep

1997 ◽  
Vol 83 (6) ◽  
pp. 1986-1997 ◽  
Author(s):  
John Trinder ◽  
Amanda Kay ◽  
Jan Kleiman ◽  
Judith Dunai
Keyword(s):  
Slow Wave ◽  
Airway Resistance ◽  
Slow Wave Sleep ◽  
Minute Ventilation ◽  
Sleep Onset ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Progressive Increase ◽  
Sleep Cycle ◽  
Obstructive Sleep

Trinder, John, Amanda Kay, Jan Kleiman, and Judith Dunai.Gender differences in airway resistance during sleep. J. Appl. Physiol. 83(6): 1986–1997, 1997.—At the onset of non-rapid-eye-movement (NREM) sleep there is a fall in ventilation and an increase in upper airway resistance (UAR). In healthy men there is a progressive increase in UAR as NREM sleep deepens. This study compared the pattern of change in UAR and ventilation in 14 men and 14 women (aged 18–25 yr) both during sleep onset and over the NREM phase of a sleep cycle (from wakefulness to slow-wave sleep). During sleep onset, fluctuations between electroencephalographic alpha and theta activity were associated with mean alterations in inspiratory minute ventilation and UAR of between 1 and 4.5 l/min and between 0.70 and 5.0 cmH2O ⋅ l−1 ⋅ s, respectively, with no significant effect of gender on either change ( P > 0.05). During NREM sleep, however, the increment in UAR was larger in men than in women ( P < 0.01), such that the mean levels of UAR at peak flow reached during slow-wave sleep were ∼25 and 10 cmH2O ⋅ l−1 ⋅ s in men and women, respectively. We speculate that the greater increase in UAR in healthy young men may represent a gender-related susceptibility to sleep-disordered breathing that, in conjunction with other predisposing factors, may contribute to the development of obstructive sleep apnea.

Ventilatory dynamics during transient arousal from NREM sleep: implications for respiratory control stability

1996 ◽  
Vol 80 (5) ◽  
pp. 1475-1484 ◽  
Author(s):  
M. C. Khoo ◽  
S. S. Koh ◽  
J. J. Shin ◽  
P. R. Westbrook ◽  
R. B. Berry
Keyword(s):  
Respiratory Control ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Before And After ◽  
Stage 2 Sleep ◽  
Repeated Administrations ◽  
Time Courses ◽  
Control Stability ◽  
Airway Dynamics ◽  
Normal Adults

The polysomnographic and ventilatory patterns of nine normal adults were measured during non-rapid-eye-movement (NREM) stage 2 sleep before and after repeated administrations of a tone (40-72 dB) lasting 5 s. The ventilatory response to arousal (VRA) was determined in data sections showing electrocortical arousal following the start of the tone. Mean inspiratory flow and tidal volume increased significantly above control levels in the first seven breaths after the start of arousal, with peak increases (64.2% > control) occurring on the second breath. Breath-to-breath occlusion pressure 100 ms after the start of inspiration showed significant increases only on the second and third postarousal breaths, whereas upper airway resistance declined immediately and remained below control for > or = 7 consecutive breaths. These results suggest that the first breath and latter portion of the VRA are determined more by upper airway dynamics than by changes in the neural drive to breathe. Computer model simulations comparing different VRA time courses show that sustained periodic apnea is more likely to occur when the fall in the postarousal increase in ventilation is more abrupt.

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.

Effects of almitrine on genioglossal and diaphragmatic electromyograms

1986 ◽  
Vol 61 (6) ◽  
pp. 2122-2128 ◽  
Author(s):  
D. E. Weese-Mayer ◽  
R. T. Brouillette ◽  
L. M. Klemka ◽  
C. E. Hunt
Keyword(s):  
Slow Wave Sleep ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Respiratory Drive ◽  
Peripheral Chemoreceptor ◽  
Obstructive Sleep ◽  
Adult Cats ◽  
Alpha Chloralose ◽  
Spontaneously Breathing ◽  
Dose Dependent

We previously demonstrated dose-dependent increases in both hypoglossal and phrenic electroneurograms after almitrine in anesthetized, paralyzed, and vagotomized cats. We have now investigated the effect of this peripheral chemoreceptor stimulant on diaphragmatic and genioglossal (GG, an upper airway-maintaining muscle) electromyograms in five unanesthetized, chronically instrumented, spontaneously breathing adult cats during slow-wave sleep. In 12 studies almitrine doses of 1.0–6.0 mg/kg increased inspired minute ventilation (VI), frequency (f), and tidal volume (VT) and decreased expiratory time (TE). However, almitrine doses as high as 6.0 mg/kg failed to augment phasic inspiratory GG activity. To determine why almitrine induced phasic inspiratory upper airway activity in anesthetized, vagotomized cats but not in sleeping cats, additional studies were performed. In four dose-response studies in three pentobarbital-anesthetized cats, almitrine, 1.0–6.0 mg/kg, did not produce phasic inspiratory GG activity. Almitrine did induce phasic inspiratory GG activity in two of three studies in three vagotomized, tracheostomized, alpha-chloralose-urethan-anesthetized cats. These results suggest that almitrine would not be useful in obstructive sleep apnea, yet because almitrine markedly increased VI, f, and VT and decreased TE in unanesthetized sleeping cats the drug may be effective in patients who lack normal central neural respiratory drive, such as the preterm infant.

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