Progressive changes in airway resistance during sleep

1996 ◽  
Vol 81 (1) ◽  
pp. 282-292 ◽  
Author(s):  
A. Kay ◽  
J. Trinder ◽  
Y. Kim
Keyword(s):  
Airway Resistance ◽  
Slow Wave Sleep ◽  
Full Range ◽  
Sleep Onset ◽  
Upper Airway ◽  
Young Male ◽  
Nrem Sleep ◽  
Sleep Stages ◽  
Compensatory Mechanisms ◽  
Sleep Period

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.

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.

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
Keyword(s):  
Individual Differences ◽  
Airway Resistance ◽  
Minute Ventilation ◽  
Sleep Onset ◽  
Respiratory Muscles ◽  
Upper Airway ◽  
Compensatory Mechanisms ◽  
Upper Airway Resistance ◽  
Electroencephalographic Activity ◽  
The Relationship

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.

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.

Effect Of Episodic Hypoxia On Upper Airway Resistance In Older Adults During NREM Sleep

2012 ◽  
Author(s):  
Arunima Jayakar ◽  
Sukanya Pranathiageswaran ◽  
Simranjit Narula ◽  
M.S. Badr ◽  
Susmita Chowdhuri
Keyword(s):  
Older Adults ◽  
Airway Resistance ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Upper Airway Resistance ◽  
Episodic Hypoxia

Influence of sleep on tensor palatini EMG and upper airway resistance in normal men

1991 ◽  
Vol 70 (6) ◽  
pp. 2574-2581 ◽  
Author(s):  
D. J. Tangel ◽  
W. S. Mezzanotte ◽  
D. P. White
Keyword(s):  
Eye Movement ◽  
Airway Resistance ◽  
Sleep Stage ◽  
Upper Airway ◽  
Sleep Stages ◽  
Normal Male ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Airway Narrowing ◽  
Upper Airway Resistance

We propose that a sleep-induced decrement in the activity of the tensor palatini (TP) muscle could induce airway narrowing in the area posterior to the soft palate and therefore lead to an increase in upper airway resistance in normal subjects. We investigated the TP to determine the influence of sleep on TP muscle activity and the relationship between changing TP activity and upper airway resistance over the entire night and during short sleep-awake transitions. Seven normal male subjects were studied on a single night with wire electrodes placed in both TP muscles. Sleep stage, inspiratory airflow, transpalatal pressure, and TP moving time average electromyogram (EMG) were continuously recorded. In addition, in two of the seven subjects the activity (EMG) of both the TP and the genioglossus muscle simultaneously was recorded throughout the night. Upper airway resistance increased progressively from wakefulness through the various non-rapid-eye-movement sleep stages, as has been previously described. The TP EMG did not commonly demonstrate phasic activity during wakefulness or sleep. However, the tonic EMG decreased progressively and significantly (P less than 0.05) from wakefulness through the non-rapid-eye-movement sleep stages [awake, 4.6 +/- 0.3 (SE) arbitrary units; stage 1, 2.6 +/- 0.3; stage 2, 1.7 +/- 0.5; stage 3/4, 1.5 +/- 0.8]. The mean correlation coefficient between TP EMG and upper airway resistance across all sleep states was (-0.46). This mean correlation improved over discrete sleep-awake transitions (-0.76). No sleep-induced decrement in the genioglossus activity was observed in the two subjects studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Load compensation and respiratory muscle function during sleep

1992 ◽  
Vol 72 (4) ◽  
pp. 1221-1234 ◽  
Author(s):  
K. G. Henke ◽  
M. S. Badr ◽  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Eye Movement ◽  
Chest Wall ◽  
Muscle Activity ◽  
Respiratory Muscle ◽  
Airway Resistance ◽  
Upper Airway ◽  
Rapid Eye Movement Sleep ◽  
Compensatory Mechanisms ◽  
Ventilatory Control ◽  
Load Compensation

The sleeping state places unique demands on the ventilatory control system. The sleep-induced increase in airway resistance, the loss of consciousness, and the need to maintain the sleeping state without frequent arousals require the presence of complex compensatory mechanisms. The increase in upper airway resistance during sleep represents the major effect of sleep on ventilatory control. This occurs because of a loss of muscle activity, which narrows the airway and also makes it more susceptible to collapse in response to the intraluminal pressure generated by other inspiratory muscles. The magnitude and timing of the drive to upper airway vs. other inspiratory pump muscles determine the level of resistance and can lead to inspiratory flow limitation and complete upper airway occlusion. The fall in ventilation with this mechanical load is not prevented, as it is in the awake state, because of the absence of immediate compensatory responses during sleep. However, during sleep, compensatory mechanisms are activated that tend to return ventilation toward control levels if the load is maintained. Upper airway protective reflexes, intrinsic properties of the chest wall, muscle length-compensating reflexes, and most importantly chemoresponsiveness of both upper airway and inspiratory pump muscles are all present during sleep to minimize the adverse effect of loading on ventilation. In non-rapid-eye-movement sleep, the high mechanical impedance combined with incomplete load compensation causes an increase in arterial PCO2 and augmented respiratory muscle activity. Phasic rapid-eye-movement sleep, however, interferes further with effective load compensation, primarily by its selective inhibitory effects on the phasic activation of postural muscles of the chest wall. The level and pattern of ventilation during sleep in health and disease states represent a compromise toward the ideal goal, which is to achieve maximum load compensation and meet the demand for chemical homeostasis while maintaining sleep state.

Effects of exercise on sleep

1978 ◽  
Vol 44 (6) ◽  
pp. 945-951 ◽  
Author(s):  
J. M. Walker ◽  
T. C. Floyd ◽  
G. Fein ◽  
C. Cavness ◽  
R. Lualhati ◽  
...  
Keyword(s):  
Eye Movement ◽  
Slow Wave Sleep ◽  
Nrem Sleep ◽  
Sleep Stages ◽  
Absolute Amount ◽  
Rapid Eye Movement ◽  
Personality Profiles ◽  
Experimental Conditions ◽  
Strong Trend ◽  
Delta Activity

We tested the hypothesis that EEG sleep stages 3 and 4 (slow-wave sleep, SWS) would be increased as a function of either acute of chronic exercise. Ten distance runners were matched with 10 nonrunners, and their sleep was recorded under both habitual (runners running and nonrunners not running, 3 night) and abruptly changed (runners not running and nonrunners running, 1 night) conditions. Analyses of both visually scored SWS and computer measures of delta activity during non-rapid eye-movement (NREM) sleep failed to support the SWS-exercise hypothesis. The runners showed a significantly higher proportion and a greater absolute amount of NREM sleep than the nonrunners. The runners showed less rapid eye-movement activity during sleep than the nonrunners under both experimental conditions, indicating a strong and unexpected effect of physical fitness on this measure. Modest afternoon exercise in nonrunners was associated with a strong trend toward elevated heart rate during sleep. Mood tests and personality profiles revealed few differences, either between groups or within groups, as a function of exercise.

scholarly journals Effect of age on sleep onset-related changes in respiratory pump and upper airway muscle function

2000 ◽  
Vol 88 (5) ◽  
pp. 1831-1839 ◽  
Author(s):  
Christopher Worsnop ◽  
Amanda Kay ◽  
Young Kim ◽  
John Trinder ◽  
Robert Pierce
Keyword(s):  
Muscle Function ◽  
Airway Resistance ◽  
Sleep Onset ◽  
Upper Airway ◽  
Abrupt Increase ◽  
Age Dependent ◽  
Younger Men ◽  
Surface Electromyograms ◽  
Electroencephalogram Eeg ◽  
Effect Of Age

In normal young men, there is an abrupt fall in ventilation (V˙e), a rise in upper airway resistance (UAR), and falls in the activities of the diaphragm (Di), intercostals (IC), genioglossus (GG), and tensor palatini (TP) at sleep onset. On waking, there is an abrupt increase inV˙e and fall in UAR and an increase in the activities of Di, IC, GG, and TP. The aim of this study was to determine whether these changes are age dependent. Nine men aged 20 to 25 yr were compared with nine men aged 42 to 67 yr. Airflow, UAR, Di, and IC surface electromyograms (EMGs) and the intramuscular EMGs of GG and TP were recorded. It was found that the falls in IC, GG, and TP at the transition from α to θ electroencephalogram (EEG) activity were significantly greater in the older than in the younger men ( P < 0.05) and that the fall in Di was also greater, although this was only marginally significant ( P = 0.15). The rise in GG at θ-to-α transitions was also greater in the older than in the younger men, and there was a trend for TP to be higher.

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.

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