Individual differences in relationship between upper airway resistance and ventilation during sleep onset

1995 ◽  
Vol 79 (2) ◽  
pp. 411-419 ◽  
Author(s):  
A. Kay ◽  
J. Trinder ◽  
Y. Kim

Sleep-induced hypoventilation is caused partly by inadequate compensation for elevated upper airway resistance (UAR). Some evidence suggests that the effect of UAR on ventilation may vary among individuals. The relationship between minute ventilation (VI) and UAR was examined in 26 healthy young men (average of 10.12 sleep onsets). Variables were analyzed over transitions between wakefulness (defined by alpha electroencephalographic activity) and sleep (theta electroencephalographic activity). Transitions to sleep were associated with increases in UAR in synchrony with reductions in VI, and equally rapid opposite changes occurred with awakenings. The relationship between the magnitudes of the changes in VI and UAR at transitions varied among subjects, accounting for 30% of the variance for alpha-to-theta transitions and 50% of the variance for theta-to-alpha transitions. Results indicated that, although ventilatory changes during sleep onset are partly a consequence of changes in UAR, alterations in UAR do not account fully for alterations in VI. Other factors that may contribute to ventilatory instability during sleep onset include state-related fluctuations in drive to the primary respiratory muscles and variability in compensatory mechanisms.


1994 ◽  
Vol 77 (5) ◽  
pp. 2285-2290 ◽  
Author(s):  
D. W. Hudgel ◽  
H. B. Hamilton

During spontaneous sleep-induced periodic breathing in elderly subjects, we have found that tidal volume oscillations are related to reciprocal oscillations in upper airway resistance. The purpose of this study was to address the mechanism of the relationship between oscillations in tidal volume and upper airway resistance in elderly subjects with sleep-induced periodic breathing. We hypothesized that the spontaneous periodic breathing observed in non-rapid-eye-movement (NREM) sleep in elderly subjects would be closely related to fluctuations in upper airway resistance and not to changes in central motor drive to ventilatory pump muscles. Therefore, in eight healthy elderly subjects, we measured costal margin chest wall peak moving time average electrical inspiratory activity (CW EMG), ventilation variables, and upper airway resistance during sleep. Five of eight subjects had significant sine wave oscillations in upper airway resistance and tidal volume. For these five subjects, there was a reciprocal exponential relationship between peak upper airway inspiratory resistance and tidal volume or minute ventilation [r = -0.60 +/- 0.20 (SD) (P < 0.05) and -0.55 +/- 0.26 (P < 0.05), respectively], such that as resistance increased, ventilation decreased. The relationship between CW EMG and tidal volume or minute ventilation was quite low (r = 0.12 +/- 0.32 and -0.07 +/- 0.27, respectively). This study demonstrated that oscillations in ventilation during NREM sleep in elderly subjects were significantly related to fluctuations in upper airway resistance but were not related to changes in chest wall muscle electrical activity. Therefore, changes in upper airway caliber likely contribute to oscillations in ventilation seen during sleep-induced periodic breathing in the elderly.



1998 ◽  
Vol 30 (1-2) ◽  
pp. 183
Author(s):  
J. Trinder ◽  
C. Worsnop ◽  
A. Kay ◽  
Y. Kim ◽  
R. Pierce


1998 ◽  
Vol 84 (2) ◽  
pp. 486-491 ◽  
Author(s):  
Kathe G. Henke

Henke, Kathe G. Upper airway muscle activity and upper airway resistance in young adults during sleep. J. Appl. Physiol. 84(2): 486–491, 1998.—To determine the relationship between upper airway muscle activity and upper airway resistance in nonsnoring and snoring young adults, 17 subjects were studied during sleep. Genioglossus and alae nasi electromyogram activity were recorded. Inspiratory and expiratory supraglottic resistance (Rinsp and Rexp, respectively) were measured at peak flow, and the coefficients of resistance ( K insp and K exp, respectively) were calculated. Data were recorded during control, with continuous positive airway pressure (CPAP), and on the breath immediately after termination of CPAP. Rinsp during control averaged 7 ± 1 and 10 ± 2 cmH2O ⋅ l−1 ⋅ s and K inspaveraged 26 ± 5 and 80 ± 27 cmH2O ⋅ l−1 ⋅ s−2in the nonsnorers and snorers, respectively ( P = not significant). On the breath immediately after CPAP, K insp did not increase over control in snorers (80 ± 27 for control vs. 46 ± 6 cmH2O ⋅ l−1 ⋅ s−2for the breath after CPAP) or nonsnorers (26 ± 5 vs. 29 ± 6 cmH2O ⋅ l−1 ⋅ s−2). These findings held true for Rinsp. K exp did not increase in either group on the breath immediately after termination of CPAP. Therefore, 1) increases in upper airway resistance do not occur, despite reductions in electromyogram activity in young snorers and nonsnorers, and 2) increases in Rexp and expiratory flow limitation are not observed in young snorers.



1996 ◽  
Vol 81 (1) ◽  
pp. 282-292 ◽  
Author(s):  
A. Kay ◽  
J. Trinder ◽  
Y. Kim

Ventilation (V) decreases during sleep while upper airway resistance (UAR) increases. A number of studies have suggested that in normal healthy individuals the changes in the two variables are reciprocal. Other findings, however, suggest that the relationship between V and UAR may change as non-rapid-eye-movement (NREM) sleep progresses such that most of the change in V occurs early during the sleep period, whereas the most marked changes in UAR occur later during established NREM sleep. However, no study has examined the progressive development of changes in both V and UAR over the NREM sleep period. This study examined V and UAR over one NREM sleep period in two groups of healthy young male subjects: a "slow-wave sleep (SWS) group" (n = 8) in which the subjects obtained the full range of NREM sleep stages from wakefulness to stage 4 NREM sleep and a "no-SWS group" (n = 5) in which the subjects did not attain SWS but spent a prolonged period in stage 2 NREM sleep that was repeatedly interrupted by arousals. Results showed that the most marked changes in V occurred early during the sleep period in association with relatively small increases in UAR. Once NREM sleep became established, further attenuation of V was minimal despite marked and progressive increases in UAR. The progressive increase in UAR occurred in association with increasing delta (0.4- to 3.0-Hz) electroencephalographic activity and did not occur in the no-SWS group. We interpret these findings to indicate that factors in addition to UAR contribute to the reduction in V early in sleep onset, whereas later, during NREM sleep, compensatory mechanisms are activated to allow for maintenance of V in the context of larger increases in UAR.



2013 ◽  
Vol 20 (1) ◽  
pp. e1-e4 ◽  
Author(s):  
Effie J Pereira ◽  
Lauren Sim ◽  
Helen S Driver ◽  
Chris M Parker ◽  
Michael F Fitzpatrick

BACKGROUND: Menthol (l-menthol) is a naturally-occurring cold receptor agonist commonly used to provide symptomatic relief for upper airway congestion. Menthol can also reduce the sensation of dyspnea. It is unclear whether the physiological action of menthol in dyspnea reduction is through its cold receptor agonist effect or whether associated mechanical changes occur in the upper airway.OBJECTIVE: To determine whether menthol inhalation alters upper airway resistance in humans.METHODS: A randomized, sham-controlled, single-blinded crossover study of inhaled menthol on upper airway resistance during semirecumbent quiet breathing in healthy subjects was conducted. Ten healthy participants (eight female) with a mean (± SD) age of 21±1.6 years completed the study.RESULTS: Nasal resistance before testing was similar on both occasions. No differences were found in respiratory frequency (mean ± SEM) (menthol 17.0±1.1 cmH2O/L/s; sham 16.9±0.9 cmH2O/L/s), minute ventilation (menthol 7.7±0.5 cmH2O/L/s; sham 7.9±0.5 cmH2O/L/s) or total inspiratory time/total breath time (menthol 0.4±0.1 cmH2O/L/s; sham 0.4±0.1 cmH2O/L/s). The upper airway resistance was similar during menthol (3.47±0.32 cmH2O/L/s) and sham (3.27±0.28 cmH2O/L/s) (P=0.33) inhalation.CONCLUSION: Inhalation of menthol does not alter upper airway resistance in awake human subjects.



1990 ◽  
Vol 69 (2) ◽  
pp. 617-624 ◽  
Author(s):  
K. G. Henke ◽  
J. A. Dempsey ◽  
J. M. Kowitz ◽  
J. B. Skatrud

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)



1997 ◽  
Vol 83 (6) ◽  
pp. 1986-1997 ◽  
Author(s):  
John Trinder ◽  
Amanda Kay ◽  
Jan Kleiman ◽  
Judith Dunai

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.



1985 ◽  
Vol 58 (5) ◽  
pp. 1489-1495 ◽  
Author(s):  
J. P. Farber

The suckling opossum exhibits an expiration-phased discharge in abdominal muscles during positive-pressure breathing (PPB); the response becomes apparent, however, only after the 3rd-5th wk of postnatal life. The purpose of this study was to determine whether the early lack of activation represented a deficiency of segmental outflow to abdominal muscles or whether comparable effects were observed in cranial outflows to muscles of the upper airways due to immaturity of afferent and/or supraspinal pathways. Anesthetized suckling opossums between 15 and 50 days of age were exposed to PPB; electromyogram (EMG) responses in diaphragm and abdominal muscles were measured, along with EMG of larynx dilator muscles and/or upper airway resistance. In animals older than approximately 30 days of age, the onset of PPB was associated with a prolonged expiration-phased EMG activation of larynx dilator muscles and/or decreased upper airway resistance, along with expiratory recruitment of the abdominal muscle EMG. These effects persisted as long as the load was maintained. Younger animals showed only those responses related to the upper airway; in fact, activation of upper airway muscles during PPB could be associated with suppression of the abdominal motor outflow. After unilateral vagotomy, abdominal and upper airway motor responses to PPB were reduced. The balance between PPB-induced excitatory and inhibitory or disfacilitory influences from the supraspinal level on abdominal motoneurons and/or spinal processing of information from higher centers may shift toward net excitation as the opossum matures.



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