Biomedical subjects

T Zintel

Publications and source records attributed to T Zintel.

10 recordsLinked to original sources

PubMed2000

Ventilatory responses to hypercapnia and hypoxia in relatives of patients with the obesity hypoventilation syndrome.

BACKGROUND: It is unclear why some morbidly obese individuals have waking alveolar hypoventilation while others with similar obesity do not. Some evidence suggests that patients with the obesity hypoventilation syndrome (OHS) may have a measurable premorbid impairment of ventilatory chemoresponsiveness. Such an impairment of ventilatory chemoresponsiveness in OHS, however, may be an acquired and reversible consequence of severe obstructive sleep apnoea (OSA). We hypothesised that, in patients with OHS who do not have coincident severe OSA, there may be a familial impairment in ventilatory responses to hypoxia and hypercapnia. METHODS: Sixteen first degree relatives of seven patients with OHS without severe OSA (mean (SD) age 40 (16) years, body mass index (BMI) 30 (6) kg/m(2)) and 16 subjects matched for age and BMI without OHS or OSA were studied. Selection criteria included normal arterial blood gas tensions and lung function tests and absence of sleep apnoea on overnight polysomnography. Ventilatory responses to isocapnic hypoxia and to hyperoxic hypercapnia were compared between the two groups. RESULTS: The slope of the ventilatory response to hypercapnia was similar in the relatives (mean 2.33 l/min/mm Hg) and in the control subjects (2.12 l/min/mm Hg), mean difference 0.2 l/min/mm Hg, 95% confidence interval (CI) for the difference -0.5 to 0.9 l/min/mm Hg, p=0.5. The hypoxic ventilatory response was also similar between the two groups (slope factor A: 379.1 l/min * mm Hg for relatives and 373.4 l/min * mm Hg for controls; mean difference 5.7 l/min * mm Hg; 95% CI -282 to 293 l/min * mm Hg, p=0.7; slope of the linear regression line of the fall in oxygen saturation and increase in minute ventilation: 2.01 l/min/% desaturation in relatives, 1.15 l/min/% desaturation in controls; mean difference 0. 5 l/min/% desaturation; 95% CI -1.7 to 0.7 l/min/% desaturation, p=0. 8). CONCLUSION: There is no evidence of impaired ventilatory chemoresponsiveness in first degree relatives of patients with OHS compared with age and BMI matched control subjects.

Adult↗

PubMed2000

Evolution of inspiratory and expiratory muscle pressures during endurance exercise.

We investigated the relationship between minute ventilation (VE) and net respiratory muscle pressure (Pmus) throughout the breathing cycle [Total Pmus = mean Pmus, I (inspiratory) + mean Pmus, E (expiratory)] in six normal subjects performing constant-work heavy exercise (CWHE, at approximately 80% maximum) to exhaustion on a cycle ergometer. Pmus was calculated as the sum of chest wall pressure (elastic + resistive) and pleural pressure, and all mean Pmus variables were averaged over the total breath duration. Pmus, I was also expressed as a fraction of volume-matched, flow-corrected dynamic capacity of the inspiratory muscles (P(cap, I)). VE increased significantly from 3 min to the end of CWHE and was the result of a significantly linear increase in Total Pmus (Delta = 43 +/- 9% from 3 min to end exercise, P < 0.005) in all subjects (r = 0. 81-0.99). Although mean Pmus, I during inspiratory flow increased significantly (Delta = 35 +/- 10%), postinspiratory Pmus, I fell (Delta = -54 +/- 10%) and postexpiratory expiratory activity was negligible or absent throughout CWHE. There was a greater increase in mean Pmus, E (Delta = 168 +/- 48%), which served to increase VE throughout CWHE. In five of six subjects, there were significant linear relationships between VE and mean Pmus, I (r = 0.50-0.97) and mean Pmus, E (r = 0.82-0.93) during CWHE. The subjects generated a wide range of Pmus, I/P(cap, I) values (25-80%), and mean Pmus, I/P(cap, I) increased significantly (Delta = 42 +/- 16%) and in a linear fashion (r = 0.69-0.99) with VE throughout CWHE. The progressive increase in VE during CWHE is due to 1) a linear increase in Total Pmus, 2) a linear increase in inspiratory muscle load, and 3) a progressive fall in postinspiratory inspiratory activity. We conclude that the relationship between respiratory muscle pressure and VE during exercise is linear and not curvilinear.

Adult↗

PubMed1999

Effect of high versus low ambient humidity on the severity of obstructive sleep apnoea.

BACKGROUND: Surface tension forces appear to make a significant contribution to upper airway closure in patients with obstructive sleep apnoea (OSA). It is possible that drying of the upper airway mucosa at night might contribute to these surface tension forces and the severity of OSA might therefore change with alteration of the ambient humidity. METHODS: A randomised single blind crossover study of high ambient relative humidity (HRH) versus low ambient relative humidity (LRH) was performed in 12 men of mean (SD) age 49 (9) years with mild OSA (apnoea/hypopnoea index (AHI) 14 (5.2)). On one night patients slept in continuous HRH (85 (4)%, range 80-93%) and on the other in LRH (16 (4)%, range 11-22%). RESULTS: The AHI was similar on the HRH and LRH nights (mean difference 3; 95% CI -2 to 9, p = 0.20 and no statistically significant differences in AHI were observed on the two nights after standardising for body position and sleep stage. Sleep stage distribution and the proportion of time spent in the supine position were similar on the HRH and LRH nights. The number of non-respiratory arousals was also similar on the two nights. CONCLUSION: Altering ambient humidity alone has no significant impact on the severity of OSA.

Humans↗

PubMed1996

Lack of importance of respiratory muscle load in ventilatory regulation during heavy exercise in humans.

1. Seven active subjects (24 +/- 1 years; maximal oxygen uptake (VO2,max), 3.77 +/- 0.2 l min-1; mean +/- S.E.M.) performed constant work rate heavy exercise (CWHE, approximately 80% of maximal incremental work rate) to exhaustion on 2 days, one with (unload) and one without (control) respiratory muscle unloading. 2. With unloading, a special device applied flow-proportional mouth pressure assist (positive with inspiratory (I), negative with expiratory (E) flows) throughout each breath. No pressure assist occurred during control CWHE. To confirm unloading, respiratory muscle pressures (Pmus) were derived (n = 5) from measured pleural pressure and chest wall elastic and resistive pressures. 3. Other than minor differences in early exercise, the temporal course of minute ventilation (VE) was similar in both tests as exercise progressed. The fall in estimated mean alveolar CO2 (PA,CO2) throughout CWHE was identical in both tests. There were no significant differences (ANOVA) in VE, tidal volume, frequency, oxygen consumption rate (VO2), heart rate or PA,CO2, between unload and control CWHE, at matched times (at 50% of control duration and at the end of exercise). Unloading reduced Pmus significantly throughout CWHE; at 50% control duration, peak Pmus,I and Pmus,E fell by 24 and 41%, respectively, with unloading, as did mean Pmus,I and Pmus,E (21 and 44%). 4. The lack of any significant changes in VE, PA,CO2 or breathing pattern, despite a marked reduction in respiratory muscle load throughout CWHE, indicates that the load on the respiratory muscles has only a minor role in the regulation of ventilation during heavy exercise. 5. The absence of improvement in CWHE duration (control, 11.4 +/- 1.2 min; unload, 12.6 +/- 2.1 min, n.s.) with unloading implies that respiratory muscle function does not limit endurance exercise performance during cycling in healthy humans.

Adult↗

PubMed1995

Superior laryngeal nerve blockade and inspiratory resistive load detection in normal subjects.

The site for detection of added inspiratory resistive loads is unknown, but recent evidence suggests that the airways may play an important role. The aim of this study was to discern whether the larynx has an important independent role in conscious detection of added inspiratory resistive loads. A randomized double-blind placebo-controlled study of the effect of superior laryngeal nerve blockade on inspiratory resistive load-detection threshold was carried out in 12 normal subjects (7 women; mean age 27.5 yr; range 18-45 yr). Baseline (preinjection) detection thresholds were similar on the lidocaine [0.58 +/- 0.16 (SE) cmH2O.l-1.s] and saline (0.53 +/- 0.12 cmH2O.l-1.s; P = 0.28) days. There was no significant difference in load-detection thresholds after injection between lidocaine (0.60 +/- 0.15 cmH2O.l-1.s) and saline (0.55 +/- 0.10 cmH2O.l-1.s; P = 0.68). Thus, the larynx does not appear to be an important independent airway site for conscious inspiratory resistive load detection.

Adolescent↗

PubMed1994

Differential ventilatory control during constant work rate and incremental exercise.

The purpose of this study was to determine whether the tachypneic breathing pattern of constant work rate, heavy exercise (CWE) is unique to CWE or whether it represents the usual pattern of the respiratory control system at high levels of ventilation (VI). We compared breathing pattern in ten healthy subjects (age 20-29 years) during CWE and maximal incremental exercise (MIE) on a bicycle ergometer. Work rate was constant at 76% of maximum work rate in CWE and progressively increased by 25 watts/minute until exhaustion during MIE. Breathing pattern was examined at matched levels of VI equivalent to 80% and about 100% of maximum VI during CWE (97.1 and 121.4 L.min-1, respectively). Exercise duration (mean+standard deviation) was 13 +/- 6 and 12 +/- 1 min during CWE and MIE, respectively (P = NS). Tidal volume (VT) fell by an average of 0.20 L towards the end of CWE, but was maintained relatively high and constant towards the end of MIE. At high, but not lower, matched levels of VI breathing pattern during CWE was significantly more rapid and shallow than that during MIE. The tachypnoea of CWE did not correlate with the progressive rise in VI, oxygen uptake or cardiac frequency during CWE. We conclude that (1) CWE is associated with a tachypneic influence that is absent or less during incremental exercise; this tachypnea is most marked at the end of CWE. (2) The tachypnoea of CWE is not part of a generalized rate accelerating process during CWE. The mechanism(s) underlying the tachypnoea are unclear but it may be related to inspiratory muscle fatigue, pulmonary oedema, and/or altered respiratory mechanics.

Adult↗

PubMed1993

Lack of importance of the superior laryngeal nerves in citric acid cough in humans.

The relative importance of laryngeal afferents in the cough reflex in humans is unknown. This study was designed to investigate the importance of superior laryngeal nerve afferents in the cough reflex induced by inhaled nebulized citric acid in awake humans. Nine healthy volunteers had their cough thresholds to inhaled nebulized citric acid measured after superior laryngeal nerve conduction blockade and after a sham nerve block. Of the nine subjects, four showed no change in cough threshold after superior laryngeal nerve anesthesia, three showed increased cough threshold after nerve block compared with no block, and two showed decreased cough threshold after nerve block. The geometric means of the cough thresholds for the nerve block vs. sham block tests were 16 +/- 13 (SD) and 15 +/- 8% citric acid, respectively. There was no statistically significant difference (Wilcoxon signed-rank test) between the cough thresholds with and without superior laryngeal nerve block (P > 0.05). We conclude that, in the awake human, superior laryngeal nerve afferents do not play a necessary role in initiation of citric acid-induced cough.

Administration, Inhalation↗

PubMed1993

Carotid chemoreceptors and respiratory adaptations to dead space loading during incremental exercise.

Dead space (VD) loading has been shown to cause an increase in tidal volume and a decrease in respiratory frequency at moderate to high levels of ventilation (VI) during exercise (J. Appl. Physiol. 70: 55-62, 1991). This study examined the role of carotid chemoreceptors (CC) in the breathing pattern response to added VD during maximal incremental exercise; we used hyperoxia to silence the CC. Nine healthy subjects exercised on a bicycle ergometer on 4 different days while inspiring air with VD (AVD) and without VD [air control (AC)] and while inspiring 100% O2 with VD (O2VD) and without VD (O2C). Equipment resistance for VD and control studies was identical, and the exercise tests were done in a randomized order. At a matched level of VI equivalent to 75% VI at the end of the AC experiments (102 l/min), the breathing pattern in the AVD and O2VD tests was significantly deeper and slower (P < 0.05) than that in the AC and O2C tests. The difference in tidal volume between AVD and AC tests (delta = 0.26 +/- 0.16 liter) was not significantly different from that between O2VD and O2C tests (delta = 0.23 +/- 0.23 liter). The breathing pattern was the same in the AC and O2C tests. It is concluded that the altered breathing pattern with VD loading is not mediated by the CC.

Adaptation, Physiological↗

PubMed1991

Corticosteroid therapy and respiratory muscle function in humans.

We examined the effects of prednisone administration on respiratory muscle function in humans using a double-blind study with a placebo control group. A total of 16 normal subjects were randomized to receive 20 mg prednisone daily (n = 8) or placebo daily (n = 8) for 2 wk. Inspiratory muscle strength (Pimax), expiratory muscle strength (PEmax), diaphragmatic strength (Pdimax), and inspiratory muscle endurance were measured at the beginning and end of the study. There was no significant change with treatment for Pimax (-145 +/- 7 to -138 +/- 6 cm H2O), PEmax (171 +/- 17 to 169 +/- 14 cm H2O), Pdimax (194 +/- 11 to 196 +/- 12 cm H2O), or endurance (76 +/- 3 to 77 +/- 4%) for the prednisone group and no significant difference between the two groups. We conclude that prednisone in moderate dosage has no significant effect on respiratory muscle function in humans, at least in the short term.

Adult↗

PubMed1990

Diagnostic value of maximal exercise tidal volume.

Though breathing pattern is frequently analyzed during clinical exercise testing, there is little information regarding its usefulness in the differential diagnosis of impaired exercise tolerance. This study tested the hypothesis that differences in peak tidal volume during exercise between patients with different cardiorespiratory diseases are related largely to differences in severity of respiratory mechanical impairment (vital capacity), not to differences in disease state. Patients with chronic obstructive pulmonary disease, restrictive lung disease, bronchial asthma, and heart disease (mitral valve disease or left ventricular dysfunction) were studied. Subjects selected had one and only one of the above diagnoses. All subjects performed maximal (symptom-limited) incremental exercise on a cycle ergometer. Multiple linear regression of all subjects (n = 30) in all four groups showed a significant correlation between VTmax and VC: VTmax = 0.55, VC -0.09 L (r = 0.827, p less than 0.0001). The VTmax/VC (x 100) was (mean +/- SD) 44 +/- 15, 54 +/- 11, 56 +/- 11, and 54 +/- 12 for the COPD, RLD, BA and HD patients respectively. There was no significant difference between any of the groups. We concluded that differences in VTmax between different patients are related largely to differences in VC (ie, differences in severity of respiratory mechanical impairment), not to differences in disease state. Measurement of VTmax or the VTmax/VC ratio has little value in the differential diagnosis of exertional dyspnea.

Aged↗