Effects of slow wave sleep on ventilatory compensation to inspiratory elastic loading

Wilson, Pamela A.; Skatrud, James B.; Dempsey, Jerome A.

doi:10.1016/0034-5687(84)90120-8

Cited by 27 publications

(11 citation statements)

References 29 publications

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“…Thus, during sleep onset, when the sleep-wake state fluctuates between brief periods of EEG alpha activity (wakefulness) and EEG theta activity (sleep), the compensation reflex is intact during the brief periods of wakefulness but not during brief periods of sleep. This is consistent with, and adds to, previous resistive-and elastic-loading studies that demonstrate immediate compensation in relaxed wakefulness and an absence of compensation during stable NREM sleep (9,10,13,23,24). The mechanisms responsible for immediate load compensation during wakefulness are likely to involve reflex actions mediated by stimulation of airway, lung, and chest wall mechanoreceptors and by the intrinsic properties of the respiratory muscles.…”

Section: Discussionsupporting

confidence: 89%

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Load compensation as a function of state during sleep onset

Gora

Kay

Colrain

et al. 1998

Journal of Applied Physiology

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Ventilation decreases and airway resistance increases with the loss of electroencephalogram alpha activity at sleep onset. The aim of this study was to determine whether reflexive load compensation is lost immediately on the loss of alpha activity. Six healthy male subjects were studied under two conditions (load and control-no load), in three states (continuous alpha, continuous theta, and immediately after a transition from alpha to theta), and in two phases (early and late sleep onset). Ventilation and respiratory timing were measured. A comparison of loaded with control conditions indicated that loading had no effect on inspiratory minute ventilation during continuous alpha (differential effect of 0.00 l/min) and only a small, nonsignificant effect in theta immediately after phase 2 transitions (0.31 l/min), indicating a preservation of load compensation at these times. However, there were significant decreases in inspiratory minute ventilation on loaded trials during continuous theta in phase 2 (0.77 l/min) and phase 3 (1.15 l/min) and during theta immediately after a transition in phase 3 (0.87 l/min), indicating a lack of reflexive load compensation. The results indicate that, because reflex load compensation is state dependent, state-related changes in airway resistance contribute to state-related changes in ventilation during sleep onset. However, this effect was slightly delayed with transitions into theta early in sleep.

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Section: Discussionsupporting

confidence: 89%

“…Thus, during wakefulness, an increase in airway resistance is immediately compensated for, resulting in a maintenance in the level of ventilation (13). During sleep, however, this immediate reflexive component of resistive load compensation is effectively absent (4,10,13,23,24). Furthermore, the sensitivity of chemical responsiveness is reduced (19).…”

mentioning

confidence: 99%

Load compensation as a function of state during sleep onset

Gora

Kay

Colrain

et al. 1998

Journal of Applied Physiology

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“…However, this wakefulness input has no fixed magnitude. Rather, its most important characteristic is its marked variability, as opposed to the highly reproducible responses obtained in NREM sleep, in response to such perturbations as changes in airway resistance or hypocapnia (Skatrud & Dempsey, 1983; Wilson et al 1984). ) Second, sleep state is not constant, which greatly enhances the opportunity for changing respiratory drives and airway resistance.…”

Section: Sleep Effects On Ventilatory Control Stabilitymentioning

confidence: 99%

The ventilatory responsiveness to CO₂ below eupnoea as a determinant of ventilatory stability in sleep

Dempsey

Smith

Przybylowski

et al. 2004

The Journal of Physiology

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199

112

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Sleep unmasks a highly sensitive hypocapnia-induced apnoeic threshold, whereby apnoea is initiated by small transient reductions in arterial CO 2 pressure (P aCO 2 ) below eupnoea and respiratory rhythm is not restored until P aCO 2 has risen significantly above eupnoeic levels. We propose that the 'CO 2 reserve' (i.e. the difference in P aCO 2 between eupnoea and the apnoeic threshold (AT)), when combined with 'plant gain' (or the ventilatory increase required for a given reduction in P aCO 2 ) and 'controller gain' (ventilatory responsiveness to CO 2 above eupnoea) are the key determinants of breathing instability in sleep. The CO 2 reserve varies inversely with both plant gain and the slope of the ventilatory response to reduced CO 2 below eupnoea; it is highly labile in non-random eye movement (NREM) sleep. With many types of increases or decreases in background ventilatory drive and P aCO 2 , the slope of the ventilatory response to reduced P aCO 2 below eupnoea remains unchanged from control. Thus, the CO 2 reserve varies inversely with plant gain, i.e. it is widened with hyperventilation and narrowed with hypoventilation, regardless of the stimulus and whether it acts primarily at the peripheral or central chemoreceptors. However, there are notable exceptions, such as hypoxia, heart failure, or increased pulmonary vascular pressures, which all increase the slope of the CO 2 response below eupnoea and narrow the CO 2 reserve despite an accompanying hyperventilation and reduced plant gain. Finally, we review growing evidence that chemoreceptor-induced instability in respiratory motor output during sleep contributes significantly to the major clinical problem of cyclical obstructive sleep apnoea.

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“…Normal subjects can fully compensate for external resistive loads [91,[181][182][183] and external elastic loads [184] during wakefulness by immediate adjustments in ventilatory timing, and minute ventilation is maintained at preloading levels. During NREM sleep, however, there is an immediate fall in minute ventilation following load application, largely due to a reduction in tidal volume.…”

Section: Response To Breath Loadingmentioning

confidence: 99%

“…During NREM sleep, however, there is an immediate fall in minute ventilation following load application, largely due to a reduction in tidal volume. This fall becomes less marked with time due to a rise in Pa,CO 2 that results in augmented ventilatory effort [183,184].…”

Section: Response To Breath Loadingmentioning

confidence: 99%

Pathophysiology of obstructive sleep apnoea

Deegan¹,

McNicholas²

1995

Eur Respir J

263

183

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Arousal plays an important role in the termination of each apnoea, but may also contribute to the development of further apnoea, because of a reduction in respiratory drive related to the hypocapnia which results from postapnoeic hyperventilation. A cyclical pattern of repetitive obstructive apnoeas may result.A better understanding of the integrated pathophysiology of OSA should help in the development of new therapeutic techniques.

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Effects of slow wave sleep on ventilatory compensation to inspiratory elastic loading

Cited by 27 publications

References 29 publications

Load compensation as a function of state during sleep onset

Load compensation as a function of state during sleep onset

The ventilatory responsiveness to CO₂ below eupnoea as a determinant of ventilatory stability in sleep

Pathophysiology of obstructive sleep apnoea

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Effects of slow wave sleep on ventilatory compensation to inspiratory elastic loading

Cited by 27 publications

References 29 publications

Load compensation as a function of state during sleep onset

Load compensation as a function of state during sleep onset

The ventilatory responsiveness to CO2 below eupnoea as a determinant of ventilatory stability in sleep

Pathophysiology of obstructive sleep apnoea

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Product

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The ventilatory responsiveness to CO₂ below eupnoea as a determinant of ventilatory stability in sleep