Long-term Within-Subject Variability of Inspiratory Neural Drive Response to Hypoxia

García‐Río, Francisco; Pino-García, José M.; Racionero, Miguel A.; Terreros-Caro, Javier G.; Gómez-Mendieta, M.A.; Prados, Concepción; Villasante, C.

doi:10.1378/chest.114.2.521

Cited by 7 publications

(4 citation statements)

References 17 publications

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“…Within-subject variability of hypoxic withdrawal response in the OSAHS patients (12.6%) was equal to spontaneous variation estimated by OSANAI et al [7] in healthy subjects. The coefficient of variability for P0.1 response to hypoxia found in the OSAHS patients (8.9%) was also similar to the coefficients of variability described by WHITE et al [28] and the present authors9 [29] in healthy subjects. The mechanism of the reduced peripheral chemosensitivity in OSAHS patients is not well established.…”

Section: Discussionsupporting

confidence: 92%

Inspiratory neural drive response to hypoxia adequately estimates peripheral chemosensitivity in OSAHS patients

García‐Río¹,

Pino²,

Ramı́rez³

et al. 2002

European Respiratory Journal

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The aim of the present study was to examine the relationships between the responses to progressive isocapnic hypoxia and hypoxic withdrawal test in patients with obstructive sleep apnoea-hypopnoea syndrome (OSAHS) and to analyse the determinants of carotid body sensitivity in OSAHS.Nineteen consecutive OSAHS patients and 13 healthy subjects were selected. Ventilatory (DV9I/Sa,O 2 /BSA) and inspiratory neural drive (DP0.1/Sa,O 2 ) responses to progressive isocapnic hypoxia were determined. Peripheral chemosensitivity was evaluated by the hypoxic withdrawal test, which measures the decrease in ventilation caused by two breaths of 100% oxygen (%DV9I).Withdrawal response and ventilatory and inspiratory neural drive responses to hypoxia were lower in OSAHS patients than in control subjects. In patients with OSAHS, %DV9I correlated significantly with DV9I/Sa,O 2 /BSA and with DP0.1/Sa,O 2 . On stepwise multiple linear regression analysis, a strong correlation between %DV9I and DP0.1/Sa,O 2 was found. Moreover, %DV9I, DV9I/Sa,O 2 /BSA and DP0.1/Sa,O 2 were significantly correlated with minimum arterial oxygen saturation and with arousal index.Obstructive sleep apnoea-hypopnoea syndrome patients have a strong relationship between peripheral chemosensitivity and respiratory response to hypoxia, suggesting that hypoxic stimulation of central chemoreceptors is minimally relevant in obstructive sleep apnoea-hypopnoea syndrome. Moreover, sensitivity of the carotid body in patients with obstructive sleep apnoea-hypopnoea syndrome is related to sleep disruption and to nocturnal hypoxia. Eur Respir J 2002; 20: 724-732 The study of peripheral chemosensitivity in patients with obstructive sleep apnoea-hypopnea syndrome (OSAHS) has been of considerable interest over several years [1][2][3][4][5][6][7]. The peripheral chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function [8]. In fact, abnormalities in chemoreflex mechanisms have been implicated in the increased cardiovascular stress in patients with OSAHS. The relationship between peripheral chemosensitivity and blood pressure profile suggests that recurrent obstructive apnoeas may reset the peripheral chemoreceptor output to a higher level, causing a chronic increase in sympathetic tone and initiating hypertension [9,10]. Intersubject variation of heart rate changes during sleep apnoea could also be due to variations in response to hypoxia [11].In spite of these pathophysiological implications, the role of peripheral chemoreception in OSAHS has not been adequately evaluated. The nature of the respiratory response to chemical stimuli in awake patients with OSAHS is still unclear. In these patients, depression of peripheral chemosensitivity has been reported [7]. In contrast, other investigators have concluded that response to hypoxia in OSAHS patients is normal [2][3][4][5][6] These discrepancies in findings concerning chemical sensitivity in OSAHS could be due in part to confounding factors, such as obesity, age, ...

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Section: Discussionsupporting

confidence: 92%

Inspiratory neural drive response to hypoxia adequately estimates peripheral chemosensitivity in OSAHS patients

García‐Río¹,

Pino²,

Ramı́rez³

et al. 2002

European Respiratory Journal

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“…In order to detect significant differences in the inspiratory drive response to progressive isocapnic hypoxia of at least 0.003 kPa/% with an alpha risk of 0.05 and a beta risk of 0.2, a minimum of 15 subjects in each age group was estimated to be necessary. 17 Assuming a loss of 15%, we selected 18 subjects for each group. Moreover, to detect significant differences in the inspiratory drive response to progressive hyperoxic hypercapnia of at least 0.001 kPa/ mmHg 18 with an alpha risk of 0.05, a beta risk of 0.2 and a loss of 15%, a minimum of 11 subjects in each age group was estimated as necessary.…”

Section: Study Subjectsmentioning

confidence: 99%

The progressive effects of ageing on chemosensitivity in healthy subjects

García‐Río

Villamor

Gómez-Mendieta

et al. 2007

Respiratory Medicine

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The aim of this study was to compare the central inspiratory drive (P(0.1)) response to hypoxia and hypercapnia between different age groups of elderly, nonsmoker, healthy subjects and young healthy controls. A random sample, proportionally stratified by age (65-69, 70-74, 75-79 and 80-84 yrs) from a sample of nonsmoker elderly subjects representative of a general population and 47 healthy subjects aged 20-40 were selected. Arterial blood gas, lung volumes, diffusing capacity, maximal respiratory pressure and oxygen uptake measurements were performed. Breathing pattern and mouth occlusion pressure, as well as P(0.1) responses to hyperoxic progressive hypercapnia and isocapnic progressive hypoxia were evaluated. The elderly subjects had lower P0.1 responses to hypoxia (0.017+/-0.006 vs. 0.031+/-0.008 kPa/%, P<0.001) and hypercapnia (0.042+/-0.018 vs. 0.051+/-0.030 kPa/mmHg, P=0.047) than the young healthy controls. Hypoxic sensitivity gradually decreased as age increased to 70-74 and remained unchanged from 75 years of age onward. CO(2) threshold was lower in the elderly groups than in young healthy controls. Lung volumes, inspiratory muscle strength and baseline metabolic rate were the principal determinants of hypoxic sensitivity. In summary, during old age, a progressive decline in hypoxic sensitivity and a decrease in the CO(2) threshold are experienced. These alterations remain stable from the age of 75 onward.

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“…Mean values from at least five measurements were calculated before and after IMST. Garcia-Rio and colleagues (16) showed that baseline P 0.1 did not change between two visits of 2 mo apart in normal subjects. Thus the results support the first hypothesis of this study.…”

mentioning

confidence: 93%

Effect of inspiratory muscle strength training on inspiratory motor drive and RREP early peak components

Huang

Martin

Davenport

2003

Journal of Applied Physiology

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. Effect of inspiratory muscle strength training on inspiratory motor drive and RREP early peak components. J Appl Physiol 94: 462-468, 2003. First published September 20, 2002 10.1152/japplphysiol.00364.2002This study investigated the effect of inspiratory muscle strength training (IMST) on inspiratory motor drive [mouth occlusion pressure at 0.1 s (P0.1)] and respiratory-related evoked potentials (RREP). It was hypothesized that, if IMST increased inspiratory muscle strength, inspiratory motor drive would decrease. If motor drive were related to the RREP, it was further hypothesized that an IMST-related decrease in drive would change RREP latency and/or amplitude. Twenty-three subjects received IMST at 75% of their maximal inspiratory pressure (PImax) with the use of a pressure threshold valve. IMST consisted of four sets of six breaths daily for 4 wk. P0.1 and the RREP were recorded before and after IMST. Posttraining, PImax increased significantly by 36.0 Ϯ 2.7%. P0.1 decreased significantly by 21.9 Ϯ 5.2%. The increase in PImax was significantly correlated to the decrease in P0.1. RREP peaks P1a, Nf, P1, and N1 were identified pre-and post-IMST, and there was no difference in either amplitude or latency for those peaks. These results demonstrate that high-intensity IMST significantly increased PImax, decreased P0.1, but did not change the RREP. maximal inspiratory pressure; mouth occlusion pressure at 0.1 s; mouth occlusion pressure; evoked potential; pressure threshold training; respiratory-related evoked potentials INSPIRATORY MOTOR DRIVE, MEASURED by the pressure generated after the first 0

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Long-term Within-Subject Variability of Inspiratory Neural Drive Response to Hypoxia

Cited by 7 publications

References 17 publications

Inspiratory neural drive response to hypoxia adequately estimates peripheral chemosensitivity in OSAHS patients

Inspiratory neural drive response to hypoxia adequately estimates peripheral chemosensitivity in OSAHS patients

The progressive effects of ageing on chemosensitivity in healthy subjects

Effect of inspiratory muscle strength training on inspiratory motor drive and RREP early peak components

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