Ventilatory adaptations to resistive loading during wakefulness and non-REM sleep

Iber, Con; Berssenbrugge, A.; Skatrud, James B.; Dempsey, Jerome A.

doi:10.1152/jappl.1982.52.3.607

Cited by 90 publications

(37 citation statements)

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“…Similar effects have been demonstrated recently in man in response to chest wall vibration that selectively increases muscle spindle afferent activity (22). In conscious man, however, load compensation depends to a large extent on higher central nervous system structures, active only during consciousness; the importance of reflex responses in the compensation for external loads appears to be rather slight (7,(23)(24)(25).…”

Section: Discussionsupporting

confidence: 79%

Mechanisms underlying CO2 retention during flow-resistive loading in patients with chronic obstructive pulmonary disease.

Oliven¹,

Kelsen²,

Deal³

et al. 1983

J. Clin. Invest.

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A B S T R A C T The present study examined the respiratory responses involved in the maintenance of eucapnea during acute airway obstruction in 12 patients with chronic obstructive disease (COPD) and 3 agematched normal subjects. Acute airway obstruction was produced by application of external flow-resistive loads (2.5 to 30 cm H20/liter per s) throughout inspiration and expiration while subjects breathed 100% 02. Application of loads of increasing severity caused progressive increases in Pco2 in the patients, but the magnitude of the increase in Pco2 varied substantially between subjects. On a resistance of 10 cm H2O/liter per s, the highest load that could be tolerated by all COPD patients, the increase in Pco2 ranged from 1 to 11 mm Hg, while none of the normal subjects retained CO2. Based on the magnitude of the increase in Pco2 the patients could be divided into two groups: seven subjects whose Pco2 increased by <3 mm Hg (group I) and five subjects whose Pco2 increased by >6 mm Hg (group II). Base-line ventilation and the pattern of breathing were similar in the two groups. During loading group I subjects maintained or increased tidal volume while all group II patients decreased tidal volume (VT). The smaller tidal volume in group II subjects was mainly the result of their shorter inspiratory time as the changes in mean inspiratory flow were similar in the two groups. The magnitude of CO2 retention during loading was inversely related to the magnitude of the change in VT (r = -0.91) and inspiratory time (T,) (r = -0.87) but only weakly related to the change in ventilation (r = -0.53). The changes in PCO2, VT, and T, during loading correlated with the subjects' maximum static

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Section: Discussionsupporting

confidence: 79%

Mechanisms underlying CO2 retention during flow-resistive loading in patients with chronic obstructive pulmonary disease.

Oliven¹,

Kelsen²,

Deal³

et al. 1983

J. Clin. Invest.

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“…7), peak phasic GG EMG activity fell significantly in apnea patients but demonstrated little change in the control subjects. In apnea patients, with 5 cm H20 CPAP the EMG fell 46.4% to a level of 21.6% of maximum and with 10 cm H20, the EMG fell 48.2% to a level of 20.1% of maximum. In the controls, with 5 cm H20 CPAP the EMG only fell 2.…”

Section: Resultsmentioning

confidence: 91%

“…There are considerable data which support the concept that respiratory compensatory mechanisms are lost during sleep. The ability to compensate for inspiratory-resistive loads is diminished during NREM sleep (20,21), the cough reflex is lost while asleep (22,23), and the ventilatory responses to chemical stimuli (hypoxia and hypercapnia) are markedly reduced during sleep (24-28). Therefore, it would not be surprising that a local neuromuscular compensatory mechanism active in the pharyngeal airway during wakefulness might also be inhibited during sleep.…”

Section: Introductionmentioning

confidence: 99%

Waking genioglossal electromyogram in sleep apnea patients versus normal controls (a neuromuscular compensatory mechanism).

Mezzanotte¹,

Tangel²,

White³

1992

J. Clin. Invest.

664

389

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Pharyngeal collapse in obstructive sleep apnea patients is likely a product of a sleep-related decrement in pharyngeal dilator muscle activity superimposed upon abnormal airway anatomy. We postulate that during wakefulness, increased pharyngeal dilator muscle activity in apnea patients compensates for diminished airway size thus maintaining patency. We studied the waking genioglossus (GG) electromyogram (EMG) activity in 11 OSA patients and 14 age-matched controls to determine if GG activity is higher in the awake state in apnea patients than controls. To make this determination, we developed a reproducible methodology whereby true maximal GG EMG could be defined and thus basal activity quantitated as a percentage of this maximal value. Therefore, direct comparisons of basal activity between individuals was possible. We observed apnea patients to have significantly greater basal genioglossal activity compared to controls (40.6±5.6% vs. 12.

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“…Moreover, the respiratory pattern may predict the susceptibility and expression of sleep-disordered breathing independent of the upper airway properties. First, diseases of the lungs and chest wall produce resistive and elastic loads to the respiratory system, which impact tI/ttot and fR [44,45]. Because VT/tI responses during UAO are limited (fixed), compensation to defend ventilation are primarily dependent on responses of the tI/ttot and the baseline fR.…”

Section: Discussionmentioning

confidence: 99%

Inspiratory duty cycle responses to flow limitation predict nocturnal hypoventilation

Schneider¹,

Krishnan

Pichard

et al. 2009

Eur Respir J

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Upper airway obstruction (UAO) can elicit neuromuscular responses that mitigate and/or compensate for the obstruction. It was hypothesised that flow-limited breathing elicits specific timing responses that can preserve ventilation due to increases in inspiratory duty cycle rather than respiratory rate.By altering nasal pressure during non-rapid eye movement (non-REM) sleep, similar degrees of UAO were induced in healthy males and females (n510 each). Inspiratory duty cycle, respiratory rate and minute ventilation were determined for each degree of UAO during non-REM sleep and compared with the baseline nonflow-limited condition.A dose-dependent increase in the inspiratory duty cycle and respiratory rate was observed in response to increasing severity of UAO. Increases in the inspiratory duty cycle, but not respiratory rate, helped to acutely maintain ventilation. Heterogeneity in these responses was associated with variable degrees of ventilatory compensation, allowing for the segregation of individuals at risk for hypoventilation during periods of inspiratory airflow limitation.Upper airway obstruction constitutes a unique load on the respiratory system. The inspiratory duty cycle, but not the respiratory rate, determine the individual's ability to compensate for inspiratory airflow limitation during sleep, and may represent a quantitative phenotype for obstructive sleep apnoea susceptibility.KEYWORDS: Nocturnal hypoventilation, obstructive sleep apnoea, sex, sleep-disordered breathing, susceptibility, ventilatory control O bstructive sleep apnoea comprises a spectrum of patients with varying degrees of upper airway obstruction (UAO) as manifested by snoring with intermittent arousals (upper airway resistance syndrome and respiratory effort-related arousals), obstructive hypopnoeas and apnoeas [1][2][3]. While male sex and obesity constitute strong risk factors for the varied manifestation of obstructive sleep apnoea [4-6], heritable factors can also play a significant role in the risk of this disorder [7][8][9][10][11][12][13], contributing to the heterogeneity in the expression of this disorder. Nevertheless, physiological mechanisms that explain the heterogeneity of sleep-disordered breathing severity are not known.UAO during sleep plays a pivotal role in the pathogenesis of obstructive sleep apnoea [14] and is caused by structural defects and disturbances in neuromuscular control [14,15]. UAO can elicit neuromuscular responses that mitigate and/or compensate for the obstruction. Under conditions of UAO (inspiratory airflow limitation), immediate responses in respiratory timing indices can help restore ventilation [16][17][18][19] and blunt disturbances in gas exchange [20]. Nevertheless the impact of respiratory pattern responses on ventilation during periods of UAO remains unclear.The purpose of the current study is to examine ventilatory responses to UAO during sleep in normal males and females. It was hypothesised that flow-limited breathing elicits specific timing responses that can preserve v...

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Ventilatory adaptations to resistive loading during wakefulness and non-REM sleep

Cited by 90 publications

References 0 publications

Mechanisms underlying CO2 retention during flow-resistive loading in patients with chronic obstructive pulmonary disease.

Mechanisms underlying CO2 retention during flow-resistive loading in patients with chronic obstructive pulmonary disease.

Waking genioglossal electromyogram in sleep apnea patients versus normal controls (a neuromuscular compensatory mechanism).

Inspiratory duty cycle responses to flow limitation predict nocturnal hypoventilation

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