Role of expiratory flow limitation in determining lung volumes and ventilation during exercise

1999 ◽  
Vol 86 (4) ◽  
pp. 1357-1366 ◽  
Author(s):  
Steven R. McClaran ◽  
Thomas J. Wetter ◽  
David F. Pegelow ◽  
Jerome A. Dempsey
Keyword(s):  
Lung Volume ◽  
Dead Space ◽  
Maximal Exercise ◽  
Total Lung Capacity ◽  
Esophageal Pressure ◽  
Maximal Flow ◽  
Expiratory Flow Limitation ◽  
Lung Capacity ◽  
Flow Volume Loop

We determined the role of expiratory flow limitation (EFL) on the ventilatory response to heavy exercise in six trained male cyclists [maximal O2 uptake = 65 ± 8 (range 55–74) ml ⋅ kg−1 ⋅ min−1] with normal lung function. Each subject completed four progressive cycle ergometer tests to exhaustion in random order: two trials while breathing N2O2(26% O2-balance N2), one with and one without added dead space, and two trials while breathing HeO2 (26% O2-balance He), one with and one without added dead space. EFL was defined by the proximity of the tidal to the maximal flow-volume loop. With N2O2during heavy and maximal exercise, 1) EFL was present in all six subjects during heavy [19 ± 2% of tidal volume (Vt) intersected the maximal flow-volume loop] and maximal exercise (43 ± 8% of Vt), 2) the slopes of the ventilation (ΔV˙e) and peak esophageal pressure responses to added dead space (e.g., ΔV˙e/[Formula: see text], where [Formula: see text] is end-tidal[Formula: see text]) were reduced relative to submaximal exercise, 3) end-expiratory lung volume (EELV) increased and end-inspiratory lung volume reached a plateau at 88–91% of total lung capacity, and 4) Vt reached a plateau and then fell as work rate increased. With HeO2 (compared with N2O2) breathing during heavy and maximal exercise, 1) HeO2 increased maximal flow rates (from 20 to 38%) throughout the range of vital capacity, which reduced EFL in all subjects during tidal breathing, 2) the gains of the ventilatory and inspiratory esophageal pressure responses to added dead space increased over those during room air breathing and were similar at all exercise intensities, 3) EELV was lower and end-inspiratory lung volume remained near 90% of total lung capacity, and 4) Vt was increased relative to room air breathing. We conclude that EFL or even impending EFL during heavy and maximal exercise and with added dead space in fit subjects causes EELV to increase, reduces the Vt, and constrains the increase in respiratory motor output and ventilation.

Inspiratory muscles during exercise: a problem of supply and demand

1988 ◽  
Vol 64 (6) ◽  
pp. 2482-2489 ◽  
Author(s):  
P. Leblanc ◽  
E. Summers ◽  
M. D. Inman ◽  
N. L. Jones ◽  
E. J. Campbell ◽  
...  
Keyword(s):  
Lung Volume ◽  
Static Pressure ◽  
Total Lung Capacity ◽  
Supply And Demand ◽  
Normal Subjects ◽  
Esophageal Pressure ◽  
Maximum Exercise ◽  
Lung Capacity ◽  
Inspiratory Muscles ◽  
Residual Capacity

The capacity of inspiratory muscles to generate esophageal pressure at several lung volumes from functional residual capacity (FRC) to total lung capacity (TLC) and several flow rates from zero to maximal flow was measured in five normal subjects. Static capacity was 126 +/- 14.6 cmH2O at FRC, remained unchanged between 30 and 55% TLC, and decreased to 40 +/- 6.8 cmH2O at TLC. Dynamic capacity declined by a further 5.0 +/- 0.35% from the static pressure at any given lung volume for every liter per second increase in inspiratory flow. The subjects underwent progressive incremental exercise to maximum power and achieved 1,800 +/- 45 kpm/min and maximum O2 uptake of 3,518 +/- 222 ml/min. During exercise peak esophageal pressure increased from 9.4 +/- 1.81 to 38.2 +/- 5.70 cmH2O and end-inspiratory esophageal pressure increased from 7.8 +/- 0.52 to 22.5 +/- 2.03 cmH2O from rest to maximum exercise. Because the estimated capacity available to meet these demands is critically dependent on end-inspiratory lung volume, the changes in lung volume during exercise were measured in three of the subjects using He dilution. End-expiratory volume was 52.3 +/- 2.42% TLC at rest and 38.5 +/- 0.79% TLC at maximum exercise.

Elastic properties of the lung in acute induced asthma

1983 ◽  
Vol 54 (1) ◽  
pp. 152-158 ◽  
Author(s):  
D. Rodenstein ◽  
D. C. Stanescu
Keyword(s):  
Lung Volume ◽  
Static Pressure ◽  
Total Lung Capacity ◽  
Esophageal Pressure ◽  
Elastic Recoil ◽  
Rapid Loss ◽  
Asthmatic Patients ◽  
Clear Cut ◽  
Lung Capacity ◽  
Significant Change

In acute induced asthma, plethysmographic total lung capacity (TLCm) was reported to increase and lung elastic recoil [Pst(L)] to decrease. The increase in TLC is spurious (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 52: 939–954, 1982), so that the rapid loss in Pst(L) could be due to errors in lung volume. We studied seven asthmatic patients before and during an induced bronchospasm. TLC was derived simultaneously from mouth and esophageal pressure vs. plethysmographic volume plots (TLCm and TLCes, respectively). Before bronchospasm, TLCm and TLCes were similar. During bronchospasm average TLCm increased, from 7.30 +/- 1.34 (SD) to 8.12 +/- 1.49 liters (P less than 0.001), whereas TLCes did not (P greater than 0.60). Static pressure-volume curves, derived from TLCes (P-Ves), were superimposed on prechallenge curves or only slightly shifted to the left, whereas those derived from TLCm (P-Vm) showed a clear-cut parallel shift to the left. At 70% of control TLC there was no significant change in Pst(L) measured from P-Ves curves (7.3 +/- 3.1 cmH2O before bronchospasm; 6.7 +/- 2.3 cmH2O during bronchospasm, P greater than 0.10), whereas Pst(L) measured from P-Vm curves decreased from 7.3 +/- 3.1 to 5.1 +/- 2.4 cmH2O (P less than 0.01). No significant change in Pst(L) at TLC was observed during bronchospasm. We conclude that in our patients acute decrease in Pst(L) during induced asthma was artifactual, secondary to lung volume overestimation by body plethysmography.

Lung volume dependence of esophageal pressure in the neck

1985 ◽  
Vol 59 (6) ◽  
pp. 1849-1854 ◽  
Author(s):  
I. G. Brown ◽  
P. A. McClean ◽  
P. M. Webster ◽  
V. Hoffstein ◽  
N. Zamel
Keyword(s):  
Lung Volume ◽  
Total Lung Capacity ◽  
Balloon Catheter ◽  
Esophageal Pressure ◽  
Lower Esophagus ◽  
Tissue Pressure ◽  
Lung Capacity ◽  
Volume Dependence ◽  
Conflicting Evidence ◽  
Cervical Trachea

There is conflicting evidence in the literature regarding tissue pressure in the neck. We studied esophageal pressure along cervical and intrathoracic esophageal segments in six healthy men to determine extramural pressure for the cervical and intrathoracic airways. A balloon catheter system with a 1.5-cm-long balloon was used to measure intraesophageal pressures. It was positioned at 2-cm intervals, starting 10 cm above the cardiac sphincter and ending at the cricopharyngeal sphincter. We found that esophageal pressures became more negative as the balloon catheter moved from intrathoracic to cervical segments, until the level of the cricopharyngeal sphincter was reached. At total lung capacity, esophageal pressures were -10.5 +/- 2.9 (SE) cmH2O in the lower esophagus, -18.9 +/- 3.0 just within the thorax, and -21.3 +/- 2.73 within 2 cm of the cricopharyngeal sphincter. The variation in mouth minus esophageal pressure with lung volume was similar in cervical and thoracic segments. We conclude that the subatmospheric tissue pressure applied to the posterior membrane of the cervical trachea results in part from transmission of apical pleural pressure into the neck. Transmural pressure for cervical and thoracic tracheal segments is therefore similar.

Lung volumes and expiratory flow limitation during exercise in interstitial lung disease

1994 ◽  
Vol 77 (2) ◽  
pp. 963-973 ◽  
Author(s):  
D. D. Marciniuk ◽  
G. Sridhar ◽  
R. E. Clemens ◽  
T. A. Zintel ◽  
C. G. Gallagher
Keyword(s):  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Lung Volume ◽  
Total Lung Capacity ◽  
Flow Limitation ◽  
Expiratory Flow Limitation ◽  
Lung Volumes ◽  
Lung Capacity ◽  
Ventilatory Capacity ◽  
Expiratory Flow

Lung volumes were measured at rest and during exercise by an open-circuit N2-washout technique in patients with interstitial lung disease (ILD). Exercise tidal flow-volume (F-V) curves were also compared with maximal F-V curves to investigate whether these patients demonstrated flow limitation. Seven patients underwent 4 min of constant work rate bicycle ergometer exercise at 40, 70, and 90% of their previously determined maximal work rates. End-expiratory lung volume and total lung capacity were measured at rest and near the end of each period of exercise. There was no significant change in end-expiratory lung volume or total lung capacity when resting measurements were compared with measurements at 40, 70, and 90% work rates. During exercise, expiratory flow limitation was evident in four patients who reported stopping exercise because of dyspnea. In the remaining patients who discontinued exercise because of leg fatigue, no flow limitation was evident. In all patients, the mean ratio of maximal minute ventilation to maximal ventilatory capacity (calculated from maximal F-V curves) was 67%. We conclude that lung volumes during exercise do not significantly differ from those at rest in this population and that patients with ILD may demonstrate expiratory flow limitation during exercise. Furthermore, because most patients with ILD are not breathing near their maximal ventilatory capacity at the end of exercise, we suggest that respiratory mechanics are not the primary cause of their exercise limitation.

Bronchial airway deposition and retention of particles in inhaled boluses: effect of anatomic dead space

1998 ◽  
Vol 85 (2) ◽  
pp. 685-694 ◽  
Author(s):  
William D. Bennett ◽  
Gerhard Scheuch ◽  
Kirby L. Zeman ◽  
James S. Brown ◽  
Chong Kim ◽  
...  
Keyword(s):  
Lung Volume ◽  
Dead Space ◽  
Gamma Camera ◽  
Total Lung Capacity ◽  
Relative Volume ◽  
Lung Capacity ◽  
Single Breath ◽  
Inhaled Particles ◽  
Insoluble Particles ◽  
R Ratio

The fractional deposition of particles in boluses delivered to shallow lung depths and their subsequent retention in the airways may depend on the relative volume and size of an individual’s airways. To evaluate the effect of variable anatomic dead space (ADS) on aerosol bolus delivery we had healthy subjects inhale radiolabeled, monodisperse aerosol (99mTc-iron oxide, 3.5 μm mean mondispersed aerosol diameter) boluses (40 ml) to a volumetric front depth of 70 ml into the lung at a lung volume of 70% total lung capacity end inhalation. By using filter techniques, aerosol photometry, and gamma camera analysis, we estimated the fraction of the inhaled boluses deposited in intrathoracic airways (IDF). ADS by single-breath N2 washout was also measured from 70% total lung capacity. Results showed that among all subjects IDF was variable (range = 0.04–0.43, coefficient of variation = 0.54) and increased with decreasing ADS ( r = −0.76, P = 0.001, n = 16). We found significantly greater deposition in the left (L) vs. right (R) lungs; mean L/R (ratio of deposition in L lung to R lung, normalized to ratio of L-to-R lung volume) was 1.58 ± 0.42 (SD; P < 0.001 for comparison with 1.0). Retention of deposited particles at 2 h was independent of ADS or IDF. There was significant retention of particles at 24 h postdeposition (0.27 ± 0.05) and slow clearance of these particles continued through 48 h postdeposition. Finally, analysis of central-to-peripheral ratios of initial deposition and 24-h-retention gamma-camera images suggest significant retention of insoluble particles in large bronchial airways at 24 h postdeposition (i.e., 24 h central-to-peripheral ratio = 1.40 ± 0.44 and 1.82 ± 0.54 in the R and L lung, respectively; P < 0.02 for comparison with 1.0). These data may prove useful for 1) designing aerosol delivery techniques to target bronchial airways and 2) understanding airway retention of inhaled particles.

Role of alveolar recruitment in lung inflation: influence on pressure-volume hysteresis

1983 ◽  
Vol 55 (4) ◽  
pp. 1321-1332 ◽  
Author(s):  
G. C. Smaldone ◽  
W. Mitzner ◽  
H. Itoh
Keyword(s):  
Lung Volume ◽  
Linear Dimension ◽  
Total Lung Capacity ◽  
Alveolar Recruitment ◽  
Rapid Cycling ◽  
Lung Inflation ◽  
Lung Capacity ◽  
History Of

The behavior of terminal lung units (alveoli) with changes in lung volume is controversial. For example, different investigators using similar techniques have suggested that alveoli expand homogeneously or, conversely, get smaller with increases in lung volume. We studied this problem by filling excised dog lobes with monodisperse aerosol and observing deposition at zero airflow. Under these conditions, the deposition of particles is inversely proportional to a mean alveolar linear dimension (ALD). With this technique, changes in ALD were assessed as the lung ventilated along its pressure-volume (PV) curve. PV curves were generated using a rapid cycling technique that minimized trapping and allowed reversible regulation of inflation-deflation hysteresis. Irreversible changes in PV hysteresis were assessed by rinsing the lung with Tween. With significant PV hysteresis, the ALD progressively decreased with inflation to total lung capacity (TLC). With deflation from TLC, the ALD was unchanged until low volumes were reached, when it decreased markedly. When PV hysteresis was minimized (reversibly or irreversibly), inflation and deflation ALD were superimposed. These data are consistent with progressive alveolar recruitment with inflation to TLC and derecruitment with deflation. The correlation between alveolar dimensions and PV hysteresis suggests that shifts in the PV curve can be accounted for by changes in the population of units. The number open at any given point is determined by the dynamic history of inflation.

Static Lung Volumes in Singers

1973 ◽  
Vol 82 (1) ◽  
pp. 89-95 ◽  
Author(s):  
Wilbur J. Gould ◽  
Hiroshi Okamura
Keyword(s):  
Lung Volume ◽  
Total Lung Capacity ◽  
The Other ◽  
Lung Volumes ◽  
Lung Capacity ◽  
Vocal Training ◽  
Professional Singers ◽  
Professional Singer ◽  
Singing Ability

It has long been assumed that the superior vocal ability of the trained professional singer arose from a higher than average breathing capacity and consequent above-normal ventilatory efficiency. However, until now, it has not been clear whether this presumed superior pulmonary capacity and breathing efficiency arose from training, from heredity, or from other factors. To clarify the role of training (and by inference that of other factors also) upon the capacity for singing, various indices reflecting static lung volumes, as distinguished from dynamic parameters measured during the act of singing, in trained professional singers, students of voice and subjects with no vocal training, were compared. Results indicated that contrary to reports by others, there were no significant differences in the total lung capacity (TLC) of the trained professional singer and that of the other two groups when allowances were made for age and sex; but when the ability to mobilize or utilize TLC was compared, it was found that the trained singer was much better able to do this than either of the other two groups. Specifically, it was found that the ratio of the residual lung volume (RV) (the amount of air remaining in the lungs at the end of a total voluntary expiration) to TLC was lower in the trained singer than in the students of voice, and that these students, in turn, had a lower RV/TLC ratio than the untrained subjects. These findings, therefore, suggest that the increased singing ability of the trained professional singer arises in large part from the ability to increase breathing efficiency by reducing the residual lung volume and, further, that this ability tends to improve with length of vocal training.

Rib cage and abdominal restrictions have different effects on lung mechanics

1980 ◽  
Vol 49 (6) ◽  
pp. 946-952 ◽  
Author(s):  
C. A. Bradley ◽  
N. R. Anthonisen
Keyword(s):  
Lung Volume ◽  
Total Lung Capacity ◽  
Lung Mechanics ◽  
Elastic Recoil ◽  
Rib Cage ◽  
Lung Capacity ◽  
Single Breath ◽  
Restrictive Procedures ◽  
Maximum Expiratory Flow ◽  
Per Se

The effects of a variety of restrictive procedures on lung mechanics were studied in eight healthy subjects. Rib cage restriction decreased total lung capacity (TLC) by 43% and significantly increased elastic recoil and maximum expiratory flow (MEF). Subsequent immersion of four subjects with rib cage restriction resulted in no further change in either parameter; shifts of blood volume did not reverse recoil changes during rib cage restriction. Abdominal restriction decreased TLC by 40% and increased MEF and elastic recoil, but recoil was increased significantly less than was the case with rib cage restriction. Further, at a given recoil pressure, MEF was less during rib cage restriction than during either abdominal restriction or no restriction. Measurements of the unevenness of inspired gas distribution by the single-breath nitrogen technique showed increased unevenness during rib cage restriction, which was significantly greater than that during abdominal restriction. We conclude that lung volume restriction induces changes in lung function, but the nature of these changes depends on how the restriction is applied and therefore cannot be ascribed to low lung volume breathing per se.

Costal diaphragm curvature in the dog

1993 ◽  
Vol 75 (2) ◽  
pp. 527-533 ◽  
Author(s):  
A. M. Boriek ◽  
S. Liu ◽  
J. R. Rodarte
Keyword(s):  
Mechanical Ventilation ◽  
Muscle Fiber ◽  
Lung Volume ◽  
Spontaneous Breathing ◽  
Total Lung Capacity ◽  
Muscle Fibers ◽  
Transdiaphragmatic Pressure ◽  
Lung Capacity ◽  
Principal Axes ◽  
Quadratic Surface

The curvature of the midcostal region of the diaphragm in seven dogs was determined at functional residual capacity (FRC) and end inspiration during spontaneous breathing and mechanical ventilation and at total lung capacity in the prone and supine positions. Metallic markers were attached to muscle fibers on the abdominal surface of the diaphragm, and the dog was allowed to recover from surgery. The three-dimensional positions of the markers were determined by biplane videofluoroscopy. A quadratic surface was fit to the bead positions. The principal axes of the quadratic surface lie nearly along and perpendicular to the muscle fibers. In both the supine and prone positions, the values of the principal curvatures were similar at FRC and end inspiration during spontaneous breathing, when muscle tension and transdiaphragmatic pressure both increase with increasing lung volume, and during mechanical ventilation and passive inflation to total lung capacity, when both decrease relative to their magnitude at FRC. No abrupt change of curvature, which might be expected at the edge of the zone of apposition, was apparent. The curvature along the muscle fiber was 0.35 +/- 0.07 cm-1; the curvature perpendicular to the muscle fiber was much smaller, 0.06 +/- 0.01 cm-1. The costal region of the diaphragm displaces and shortens as lung volume increases, but its shape, as described by its curvatures, does not change substantially.

Airway responses to inhaled histamine in asymptomatic smokers and nonsmokers

1977 ◽  
Vol 42 (4) ◽  
pp. 508-513 ◽  
Author(s):  
N. E. Brown ◽  
E. R. McFadden ◽  
R. H. Ingram
Keyword(s):  
Vital Capacity ◽  
Total Lung Capacity ◽  
Aerosol Deposition ◽  
Flow Volume ◽  
Maximal Flow ◽  
Airway Reactivity ◽  
Lung Capacity ◽  
Large Airway ◽  
Airway Response ◽  
Airway Responses

Bronchia reactivity to inhaled histamine was assessed in asymptomatic cigarette smokers and in nonsmoking atopic and nonatopic subjects. The only prechallenge between-group difference was the ratio of maximal flow on 80% helium-20% oxygen (Vmax HeO2) to maximal flow on air (Vmax air) from partial expiratory flow volume curves at 25% vital capacity (25% VC PEFV): Mean +/- SEM for smokers 1.18 /+- 0.06, atopics 1.45 +/- 0.08, nonatopics 1.51 +/- 0.03. This suggests that prior to inhalation to total lung capacity, the predominant site of resistance at flow limitation was in smaller airways of the smokers and in larger airways of both groups of nonsmokers. Following inhalation of histamine, smokers and nonatopics had similar changes in lung volumes and Vmax air which were less than in atopics. The Vmax HeO2/Vmax air ratios at 25% VC PEFV increased in smokers and decreased in nonsmokers: smokers 1.48 +/- 0.08, atopics 1.22 +/- 0.10, nontopics 1.16 +/- 0.06. This suggests a predominant large airway response in smokers and a prominent small airway response in nonsmokers. These responses may reflect differences in the predominant site of aerosol deposition rather than in airway reactivity.

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