Upper airway and respiratory muscle responses to continuous negative airway pressure

To determine upper airway and respiratory muscle responses to nasal continuous negative airway pressure (CNAP), we quantitated the changes in diaphragmatic and genioglossal electromyographic activity, inspiratory duration, tidal volume, minute ventilation, and end-expiratory lung volume (EEL) during CNAP in six normal subjects during wakefulness and five during sleep. During wakefulness, CNAP resulted in immediate increases in electromyographic diaphragmatic and genioglossal muscle activity, and inspiratory duration, preserved or increased tidal volume and minute ventilation, and decreased EEL. During non-rapid-eye-movement and rapid-eye-movement sleep, CNAP was associated with no immediate muscle or timing responses, incomplete or complete upper airway occlusion, and decreased EEL. Progressive diaphragmatic and genioglossal responses were observed during non-rapid-eye-movement sleep in association with arterial O2 desaturation, but airway patency was not reestablished until further increases occurred with arousal. These results indicate that normal subjects, while awake, can fully compensate for CNAP by increasing respiratory and upper airway muscle activities but are unable to do so during sleep in the absence of arousal. This sleep-induced failure of load compensation predisposes the airways to collapse under conditions which threaten airway patency during sleep. The abrupt electromyogram responses seen during wakefulness and arousal are indicative of the importance of state effects, whereas the gradual increases seen during sleep probably reflect responses to changing blood gas composition.

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Metabolic rate and breathing during sleep

Journal of Applied Physiology ◽

10.1152/jappl.1985.59.2.384 ◽

1985 ◽

Vol 59 (2) ◽

pp. 384-391 ◽

Cited By ~ 95

Author(s):

D. P. White ◽

J. V. Weil ◽

C. W. Zwillich

Keyword(s):

Metabolic Rate ◽

Eye Movement ◽

Sleep Stage ◽

Minute Ventilation ◽

Respiratory Control ◽

Normal Subjects ◽

Co2 Production ◽

Sleep Stages ◽

Rapid Eye Movement ◽

Rapid Eye Movement Sleep

Recent investigation suggests that both ventilation (VE) and the chemical sensitivity of the respiratory control system correlate closely with measures of metabolic rate [O2 consumption (VO2) and CO2 production (VCO2)]. However, these associations have not been carefully investigated during sleep, and what little information is available suggests a deterioration of the relationships. As a result we measured VE, ventilatory pattern, VO2, and VCO2 during sleep in 21 normal subjects (11 males and 10 females) between the ages of 21 and 77 yr. When compared with values for awake subjects, expired ventilation decreased 8.2 +/- 2.3% (SE) during sleep and was associated with a 8.5 +/- 1.6% decrement in VO2 and a 12.3 +/- 1.7% reduction in VCO2, all P less than 0.01. The decrease in ventilation was a product primarily of a significant decrease in tidal volume with little change in frequency. None of these findings were dependent on sleep stage with results in rapid-eye-movement (REM) and non-rapid-eye-movement sleep being similar. Through all sleep stages ventilation remained tightly correlated with VO2 and VCO2 both within a given individual and between subjects. Although respiratory rhythmicity was somewhat variable during REM sleep, minute ventilation continued to correlate with VO2 and VCO2. None of the parameters described above were influenced by age or gender, with male and female subjects demonstrating similar findings. Ten of the subjects demonstrated at least occasional apneas. These individuals, however, were not found to differ from those without apnea in any other measure of ventilation or metabolic rate.

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Partitioning of inhaled ventilation between the nasal and oral routes during sleep in normal subjects

Journal of Applied Physiology ◽

10.1152/japplphysiol.00658.2002 ◽

2003 ◽

Vol 94 (3) ◽

pp. 883-890 ◽

Cited By ~ 44

Author(s):

Michael F. Fitzpatrick ◽

Helen S. Driver ◽

Neela Chatha ◽

Nha Voduc ◽

Alison M. Girard

Keyword(s):

Eye Movement ◽

Slow Wave ◽

Sleep Stage ◽

Minute Ventilation ◽

Normal Subjects ◽

Sleep Stages ◽

Rapid Eye Movement ◽

Nasal Mask ◽

Rapid Eye Movement Sleep ◽

Significant Difference

The oral and nasal contributions to inhaled ventilation were simultaneously quantified during sleep in 10 healthy subjects (5 men, 5 women) aged 43 ± 5 yr, with normal nasal resistance (mean 2.0 ± 0.3 cmH2O · l−1 · s−1) by use of a divided oral and nasal mask. Minute ventilation awake (5.9 ± 0.3 l/min) was higher than that during sleep (5.2 ± 0.3 l/min; P < 0.0001), but there was no significant difference in minute ventilation between different sleep stages ( P = 0.44): stage 2 5.3 ± 0.3, slow-wave 5.2 ± 0.2, and rapid-eye-movement sleep 5.2 ± 0.2 l/min. The oral fraction of inhaled ventilation during wakefulness (7.6 ± 4%) was not significantly different from that during sleep (4.3 ± 2%; mean difference 3.3%, 95% confidence interval −2.1–8.8%, P = 0.19), and no significant difference ( P = 0.14) in oral fraction was observed between different sleep stages: stage two 5.1 ± 2.8, slow-wave 4.2 ± 1.8, rapid-eye-movement 3.1 ± 1.7%. Thus the inhaled oral fraction in normal subjects is small and does not change significantly with sleep stage.

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Influence of sleep on response to negative airway pressure of tensor palatini muscle and retropalatal airway

Journal of Applied Physiology ◽

10.1152/jappl.1993.75.5.2117 ◽

1993 ◽

Vol 75 (5) ◽

pp. 2117-2124 ◽

Cited By ~ 88

Author(s):

J. R. Wheatley ◽

D. J. Tangel ◽

W. S. Mezzanotte ◽

D. P. White

Keyword(s):

Eye Movement ◽

Negative Pressure ◽

Upper Airway ◽

Normal Subjects ◽

Rapid Onset ◽

Reflex Response ◽

Rapid Eye Movement ◽

Rapid Eye Movement Sleep ◽

Airway Narrowing ◽

Airway Collapse

Increased retropalatal airway resistance may be caused by a sleep-induced loss of palatal muscle activity and a diminished ability of these muscles to respond to the increasing intrapharyngeal negative pressure that develops during sleep. To investigate these possibilities, in six normal subjects, we determined the effect of non-rapid-eye-movement sleep on 1) the tensor palatini (TP) electromyogram (EMG) response to rapid-onset negative-pressure generations (NPG) in the upper airway and 2) the collapsibility of the retropalatal airway during these NPGs. During wakefulness, the change in TP EMG from basal to peak levels (during NPG) was 19.8 +/- 3.2 arbitrary units (P < 0.005). This was markedly reduced during sleep (3.6 +/- 1.5 arbitrary units; P < 0.001). The latency of the TP EMG response was 48.5 +/- 5.6 ms during wakefulness but was prolonged during sleep (105.0 +/- 12.2 ms; P < 0.02). The peak transpalatal pressure during NPG (a measure of airway collapse) was 2.1 +/- 0.7 cmH2O during wakefulness and increased to 5.3 +/- 0.8 cmH2O during sleep (P < 0.05). We conclude that the brisk reflex response of the TP muscle to negative pressure during wakefulness is markedly reduced during non-rapid-eye-movement sleep, in association with a more collapsible retropalatal airway. We speculate that the reduction in this TP reflex response contributes to retropalatal airway narrowing during sleep in normal subjects.

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An induced blood pressure rise does not alter upper airway resistance in sleeping humans

Journal of Applied Physiology ◽

10.1152/jappl.1998.84.1.269 ◽

1998 ◽

Vol 84 (1) ◽

pp. 269-276 ◽

Cited By ~ 15

Author(s):

Christine R. Wilson ◽

Shalini Manchanda ◽

David Crabtree ◽

James B. Skatrud ◽

Jerome A. Dempsey

Keyword(s):

Blood Pressure ◽

Arterial Pressure ◽

Eye Movement ◽

Airway Resistance ◽

Pressure Rise ◽

Upper Airway ◽

Rapid Eye Movement ◽

Rapid Eye Movement Sleep ◽

Upper Airway Resistance ◽

Blood Pressure Rise

Wilson, Christine R., Shalini Manchanda, David Crabtree, James B. Skatrud, and Jerome A. Dempsey. An induced blood pressure rise does not alter upper airway resistance in sleeping humans. J. Appl. Physiol. 84(1): 269–276, 1998.—Sleep apnea is associated with episodic increases in systemic blood pressure. We investigated whether transient increases in arterial pressure altered upper airway resistance and/or breathing pattern in nine sleeping humans (snorers and nonsnorers). A pressure-tipped catheter was placed below the base of the tongue, and flow was measured from a nose or face mask. During non-rapid-eye-movement sleep, we injected 40- to 200-μg iv boluses of phenylephrine. Parasympathetic blockade was used if bradycardia was excessive. Mean arterial pressure (MAP) rose by 20 ± 5 (mean ± SD) mmHg (range 12–37 mmHg) within 12 s and remained elevated for 105 s. There were no significant changes in inspiratory or expiratory pharyngeal resistance (measured at peak flow, peak pressure, 0.2 l/s or by evaluating the dynamic pressure-flow relationship). At peak MAP, end-tidal CO2 pressure fell by 1.5 Torr and remained low for 20–25 s. At 26 s after peak MAP, tidal volume fell by 19%, consistent with hypocapnic ventilatory inhibition. We conclude that transient increases in MAP of a magnitude commonly observed during non-rapid-eye-movement sleep-disordered breathing do not increase upper airway resistance and, therefore, will not perpetuate subsequent obstructive events.

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

Journal of Applied Physiology ◽

10.1152/jappl.1991.70.6.2574 ◽

1991 ◽

Vol 70 (6) ◽

pp. 2574-2581 ◽

Cited By ~ 134

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)

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Respiratory and cardiovascular responses to increased and decreased carotid sinus pressure in sleeping dogs

Journal of Applied Physiology ◽

10.1152/jappl.1995.78.5.1688 ◽

1995 ◽

Vol 78 (5) ◽

pp. 1688-1698 ◽

Cited By ~ 28

Author(s):

K. W. Saupe ◽

C. A. Smith ◽

K. S. Henderson ◽

J. A. Dempsey

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Eye Movement ◽

Carotid Sinus ◽

Minute Ventilation ◽

Control Level ◽

Cardiovascular Responses ◽

Systemic Blood Pressure ◽

Rapid Eye Movement ◽

Rapid Eye Movement Sleep

The purpose of this study was to determine the effects of changing blood pressure in the carotid sinus (Pcs) on ventilatory output during wakefulness and non-rapid-eye-movement sleep in unanesthetized dogs. Eight dogs were chronically instrumented so that ventilation, heart rate, and blood pressure could be measured while pressure in the isolated carotid sinus was rapidly changed by means of an extracorporeal perfusion circuit. Raising Pcs 35–75 mmHg consistently reduced ventilation 15–40% in a dose-response fashion, with little or no further diminution in minute ventilation as Pcs was further increased > 75 mmHg above control level. This decrease in minute ventilation was immediate, due primarily to a decrease in tidal volume, and was sustained over the 20-s period of elevated Pcs. Increases in Pcs also caused immediate sustained reductions in systemic blood pressure and heart rate, both of which also fell in a dose-dependent fashion. The ventilatory and systemic cardiovascular responses to increased Pcs were the same during wakefulness and non-rapid-eye-movement sleep. Decreasing Pcs 40–80 mmHg caused a sudden carotid chemoreceptor-mediated hyperpnea that was eliminated by hyperoxia. We conclude that increasing Pcs causes a reflex inhibition of ventilation and that this reflex may play a role in sleep-disordered breathing.

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Ventilation during early and late rapid-eye-movement sleep in normal humans

Journal of Applied Physiology ◽

10.1152/jappl.1991.71.4.1201 ◽

1991 ◽

Vol 71 (4) ◽

pp. 1201-1215 ◽

Cited By ~ 10

Author(s):

J. B. Neilly ◽

E. A. Gaipa ◽

G. Maislin ◽

A. I. Pack

Keyword(s):

Eye Movement ◽

Rem Sleep ◽

Minute Ventilation ◽

Inspiratory Flow ◽

Respiratory Frequency ◽

Rapid Eye Movement ◽

Rapid Eye Movement Sleep ◽

Rib Cage ◽

Ventilatory Parameters ◽

Normal Humans

Because successive rapid-eye-movement (REM) sleep periods in the night are longer in duration and have more phasic events, ventilation during late REM sleep might be more affected than in earlier episodes. Despite the increase in eye movement density (EMD) in late REM sleep, average minute ventilation was, however, not reduced compared with that in early REM sleep. Decreases in rib cage motion (mean inspiratory flow of the rib cage) in association with increasing EMD were offset by increments in respiratory frequency. Apart from expiratory time, there were no significant changes in the slopes of the relationships between EMD and specific ventilatory components, from early to late REM sleep periods. However, there was an increase in the number of episodes when ventilation was reduced during late REM sleep. Changes in ventilatory pattern during late REM sleep are due to changes in the underlying nature of REM sleep. The ventilatory response during eye movements is, however, subject specific. Some subjects exhibit large decrements in mean inspiratory flow of the rib cage and increments in respiratory frequency during bursts of eye movement, whereas other individuals demonstrate only small changes in these ventilatory parameters.

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