End-inspiratory Lung Volume Research Articles

Evidence of Ventilatory Constraints in Healthy Exercising Prepubescent Children

We assessed expiratory airflow limitation (exp FL) in 18 healthy prepubescent children (6 girls and 12 boys, 10.1 +/- 0.3 years old), and examined how it might modulate regulation of tidal volume (V(T)) during exercise. The children performed a maximal incremental exercise on a cycle ergometer, preceded and followed by pulmonary function tests. Throughout exercise, breathing flow-volume loops were plotted into the maximal flow-volume loop (MFVL) measured at rest. End-expiratory and end-inspiratory lung volumes were estimated by measuring expiratory reserve volume relative to forced vital capacity (ERV/FVC), and inspiratory reserve volume relative to forced vital capacity (IRV/FVC), respectively. The exp FL, expressed as a percentage of V(T), was defined as the part of the tidal breath meeting the boundary of the MFVL. Ten children (FL) presented an exp FL at peak exercise (range, 16-78% of V(T)), and the remaining 8 constituted a non-flow-limited group (NFL). At peak exercise, FL presented a higher IRV/FVC and lower ERV/FVC (P < 0.01) than NFL children, demonstrating two different exercise breathing patterns. These results suggest that the NFL regulated V(T) at high lung volume, avoiding exp FL, while the FL breathed at low lung volume, leading to exp FL. At peak exercise, FL presented lower values of minute ventilation (P<0.05) and oxygen uptake (P<0.05) than NFL. Nevertheless, oxygen arterial saturation and dyspnea were similar in the two groups. In conclusion, ventilatory constraints may occur in healthy prepubescent children and result in relative dynamic hyperinflation or expiratory flow limitation.

Location of Flow Limitation in Liquid-Filled Rabbit Lungs

The effects of end-inspiratory lung volume (EILV) and expiratory flow rate (Q) on the location of flow limitation in liquid-filled lungs were investigated by measuring pressure along the airways and by radiographic imaging. The lungs of New Zealand white rabbits were filled with perfluorocarbon to the randomly selected EILV of 20, 30, or 40 ml/kg, and the volume was actively drained at one of three Q: 2.5, 5.0, or 7.5 ml/s. The minimum pressures recorded by a movable catheter at locations along the airways show that flow limitation occurred in the main bronchi and trachea, and was independent of EILV and Q. The minimum pressure at the trachea was -80 mm Hg compared with values that were more positive than -10 mm Hg at a location 3 cm distal to the carina for all EILV and Q combinations. This location was confirmed by the lung images. The airway diameters gradually decreased with time, until flow limitation occurred. In airways distal to the collapse, there was not a significant decrease in diameter. Based on these data, we conclude that flow limitation in liquid-filled lungs occurs in the trachea and main bronchi and its location is independent of EILV or Q.

Inspiratory and expiratory CT lung density in infants and young children

There is a lack of information on normal inspiratory and expiratory CT lung density in infants. To describe normal regional CT lung density at end inspiratory and end expiratory lung volumes in children ages 0--5 years. Motionless HRCT images were obtained at 25 cm (inspiratory) and 0 cm (expiratory) water pressure at apical (top of arch) and basal (2 cm above diaphragm) levels in 16 sedated children (mean age 1.5 years) who underwent CT for reasons other than respiratory disease. Density was measured at anterior-posterior and medial-lateral locations at each level in each lung. The influence of level, location, and age was quantified using analysis of variance methods. Lung density declined linearly in the first few years of life and thereafter approximated adult values. Beginning with the anterior-basal location, density at end inspiration (HU)=-835-(16 x age in years)+16 (if apical)+33 (if posterior)+23 (if medial)+14 (if lateral); standard error=38. At resting end exhalation =-616-(41 x age)+50 (if apical)+155 (if posterior)+74 (if medial)+46 (if lateral); standard error=68. We provide an initial basis for employing lung densitometry in infants and young children at end inspiration and resting end exhalation lung volumes.

Simplified Detection of Dynamic Hyperinflation

To detect dynamic hyperinflation by comparing reduction in inspiratory capacity (IC) during both paced hyperventilation and cycle ergometry in patients with moderate-to-severe COPD, studied before and after acute bronchodilation. IC and FEV(1) were measured before and after metronome-paced hyperventilation at twice the resting respiratory rate for 20 s in 16 patients with COPD before and after 54 microg aerosolized ipratropium bromide (IB). We also studied the same 16 patients before and after administration of 54 microg aerosolized IB during symptom-limited incremental cycle ergometry when the final respiratory rate was also twice the resting rate. Resting IC was 2.23 +/- 0.53 L (mean +/- SD), and the mean decrease in IC from baseline was 0.36 +/- 0.25 L after exercise (p < 0.001), and not significantly different (p = 0.64) from mean decrease in IC of 0.40 +/- 0.29 L following hyperventilation. Results following hyperventilation and exercise were similar after bronchodilator. The mean difference for decrease of IC between hyperventilation and exercise was 0.138 L (95% confidence interval, - 0.347 to 0.622; r = 0.66, p = 0.006). The decrease in FEV(1) was 0.01 +/- 0.13 L after exercise and 0.06 +/- 0.18 L after hyperventilation. Separately, baseline and peak end-expiratory and end-inspiratory lung volumes were similar with hyperventilation vs exercise both before and after bronchodilator. Both metronome-paced hyperventilation and incremental cycle ergometry, when resting respiratory rate was doubled, provoked similar significant decrease in IC, even after administration of 54 microg aerosolized IB. The noninvasive simplicity of hyperventilation for 20 s provides a clinically useful screening surrogate to monitor changes in IC following exercise.

Total Liquid Ventilation: Dynamic Airway Pressure and the Development of Expiratory Flow Limitation

Expiratory flow limitation occurs during total liquid ventilation (TLV), and is characterized by the sudden development of excessively negative intratracheal pressures without increases in flow. The purpose of this study was to identify a dynamic signal for the servoregulation of expiratory flow (Ve), by determining the range of dynamic intratracheal pressures [P(T)], which mark the onset of flow limitation during liquid expiration, where choke occurs at the critical pressure (Pc). The lungs of rabbits were filled with perflurocarbon to an end-inspiratory lung volume (EILV) of 20, 30, or 40cc/kg and connected to a piston driven liquid ventilator, which removed perfluorocarbon at a rate (Vs) of 2.5, 5.0, or 7.5 ml/s. Nine animals per EILV group were used (27 animals total), and within each EILV group each (Vs) was used three times. P(T) and (Ve) (T) were measured at the tracheostomy tube, and dP/dT was calculated from P(T). Pc was determined within each EILV/(Vs) group by examining the average dP/dT curve for the first significant change from baseline. Pc ranged from -6.02 +/- 1.83 to -9.02 +/- 3.2 mm Hg. In general, the higher the EILV, the more negative the Pc. We conclude that Pc during TLV varies within a limited range in rabbits. These data may be used to maximize expired volume during TLV by sequentially tapering flow rates as this critical range of pressures is approached.

Measurement of Forced Expiratory Flows and Lung Volumes

After completing this article, readers should be able to: 1. Describe the information that measurements of forced expiratory flow can provide in spontaneously breathing and mechanically ventilated infants. 2. Delineate how lung volume can be measured. The measurements of forced expiratory flows and lung volumes are important to the evaluation of patients who have respiratory symptoms. Until recently, measurements have been restricted to adults and children old enough to cooperate with testing maneuvers. Newer techniques have enabled such measurements to be made in infants and led to improved understanding of normal lung and airway growth during infancy and early childhood, when dramatic changes occur. The measurements have had important clinical uses in the evaluation and treatment of infants who have respiratory disease, but their use has been limited because they require specialized equipment and expertise as well as sedation of the infant. In this article, we discuss the techniques required for measurement of forced expiratory flows and lung volumes, their limitations, and applications in clinical practice. Detection of airflow obstruction, by physical examination or by quantitative measurement techniques, is facilitated by increasing expiratory flow rates. Measurement of forced expiratory flows is useful because flow rates are inversely proportional to the fourth power of the radius of the airway and, therefore, are indicative of airway size when flow is limited. Disease states affecting the airways, including asthma, bronchopulmonary dysplasia (BPD), or congenital lesions such as pulmonary hypoplasia or vascular airway compression, are expected to decrease expiratory flow. Infants typically are sedated for testing to maintain relaxed breathing with a face mask placed over the mouth and nose. This sedation often is perceived by parents and physicians as one of the barriers to such testing. (1) However, sedation can be achieved safely using oral chloral hydrate at a dose of 80 to 100 mg/kg. …

Respiratory control during postural changes in anesthetized cats

The effect of postural changes on respiration was investigated in ten anesthetized cats by applying body tilting during the inspiration phase while recording respiratory patterns, as given by the diaphragmatic EMG, together with either the lung volume or the air flow temperature. The results show that the head-up tilting during inspiration reduced the period of the inspiratory phase and increased the end-inspiratory lung volume. On the other hand, the head-down tilting during inspiration had opposite effects. These effects disappeared after transection of the vagus nerve. However, labyrinthectomy did not diminish the effects, probably because of functional suppression of the vestibular system due to the anesthetic. When correlating the activity of 15 vagal afferents presumably originating from the slowly adapting lung stretch receptors with lung volume changes during tilting, their maximum firing rate (87 +/- 15.7 Hz) was increased with an increase in the lung inflation volume and was attained earlier on head-up tilting and it was reduced with a decrease of the lung volume on head-down tilting (63 +/- 16.6 Hz) as compared with the value in the horizontal position (74 +/- 14.2 Hz). These results suggest that respiratory modulation during head-up or head-down tilting is consistent with the Hering-Breuer reflexes and minimizes the externally induced lung volume changes during postural changes.

Lung volume is a determinant of aerosol bolus dispersion.

The technique of inhaling a small volume element labeled with particles ("aerosol bolus") can be used to assess convective gas mixing in the lung. While a bolus undergoes mixing in the lung, particles are dispersed in an increasing volume of the respired air. However, determining factors of bolus dispersion are not yet completely understood. The present study tested the hypothesis that bolus dispersion is related, among others, to the total volume in which the bolus is allowed to mix--i.e., to the individual lung size. Bolus dispersion was measured in 32 anesthetized, mechanically ventilated dogs with total lung capacities (TLCs) of 1.1-2.5 L. Six-milliliter aerosol boluses were introduced at various preselected time-points during inspiration to probe different volumetric lung depths. Dispersion (SD) was determined by moment analysis of particle concentrations in the expired air. We found linear correlations between SD at a given lung depth and the individual end-inspiratory lung volume (V(L)). The relationship was tightest for boluses inhaled deepest into the lungs: SD(40) = 0.068 V(L) - 1.77, r(2) = 0.59. Normalizing SD to V(L) abolished this dependency and resulted in a considerable reduction of inter-individual variability as compared to the uncorrected measurements. These data indicate that lung size influences measurements of bolus dispersion. It therefore appears reasonable to apply a normalization procedure before interpreting the data. Apart from a reduction in measurement variability, this should help to separate the effects on bolus dispersion of altered lung volumes and altered mixing processes in diseased lungs.

Ventilator-induced lung injury.

During mechanical ventilation, high end-inspiratory lung volume (whether it be because of large tidal volume (VT) and/or high levels of positive end-expiratory pressure) results in a permeability type pulmonary oedema, called ventilator-induced lung injury (VILI). Previous injury sensitises lung to mechanical ventilation. This experimental concept has recently received a resounding clinical illustration after a 22% reduction of mortality was observed in acute respiratory distress syndrome patients whose VT had been reduced. In addition, it has been suggested that repetitive opening and closing of distal units at low lung volume could induce lung injury but this notion has been challenged both conceptually and clinically after the negative results of the Acute Respiratory Distress Syndrome clinical Network Assessment of Low tidal Volume and Elevated end-expiratory volume to Obviate Lung Injury (ARDSNet ALVEOLI) study. Experimentally and clinically, involvement of inflammatory cytokines in VILI has not been unequivocally demonstrated. Cellular response to mechanical stretch has been increasingly investigated, both on the epithelial and the endothelial side. Lipid membrane trafficking has been thought to be a means by which cells respond to stress failure. Alterations in the respiratory system pressure/volume curve during ventilator-induced lung injury that include decrease in compliance and position of the upper inflection point are due to distal obstruction of airways that reduce aerated lung volume. Information from this curve could help avoid potentially harmful excessive tidal volume reduction.

Airflow Limitation and Breathing Strategy in Congestive Heart Failure Patients during Exercise

Background: Congestive heart failure (CHF) patients experience dyspnea on exertion and therefore have decreased exercise tolerance. Objective: This study explores the hypothesis that stable New York Heart Association (NYHA) class III CHF patients without a history of pulmonary disease exhibit airflow limitation with increasing exercise. Methods: We characterized flow limitations and breathing reserves at baseline, during exercise before anaerobic threshold (pre-AT), and after anaerobic threshold (post-AT) in CHF patients and normal subjects. Data were collected in the form of maximal flow volume loops and subsequent tidal flow volume loops at baseline and during exercise. Expiratory flow limitation was expressed as percent of tidal volume that corresponded with overlap of the tidal flow volume loops and maximal flow volume loops during expiration. The area directly between the maximum flow volume loops and the tidal flow volume loops during the expiratory phase is expressed as expiratory flow volume reserve (EFVR). Results: CHF patients experienced expiratory flow limitation during exercise (pre-AT and post-AT) that was significantly increased compared to baseline and to normal subjects at similar exercise levels (CHF, baseline 8.5 ± 7, pre-AT 37 ± 10, post-AT 38 ± 8%, n = 9, p < 0.05). Both CHF patients and normal subjects increased EFVR during exercise, but only the normal subjects increased EFVR to a significantly different value at post-AT exercise levels (normal subjects, 9.5 ± 2, 11 ± 2, 32 ± 4%, n = 7, p < 0.05). Both CHF patients and normal subjects increased end inspiratory lung volume (EILV) during exercise, but only the normal subjects significantly increased EILV at post-AT exercise levels (normal subjects, 49 ± 4, 55 ± 5, 76 ± 4%, p < 0.05). Inspiratory capacity (IC)/forced vital capacity (FVC) ratios were increased in CHF patients compared to normal subjects. However, IC/FVC values did not change during exercise in either group. Conclusions: CHF patients cannot utilize their full respiratory capacity during exercise secondary to expiratory flow limitation and an inability to increase EILV and EFVR.

Chest wall kinematics during chemically stimulated breathing in healthy man.

Chest wall compartment kinematics and respiratory muscle coordinate activity, during either hypercapnia or hypoxia, have not been comparatively assessed in healthy humans. We assessed the displacement volume of the chest wall (Vcw) in 5 normal subjects during hypoxic-normocapnic and hypercapnic-hyperoxic rebreathing by using linearized magnetometers. Vcw was divided into displacement volumes of the rib cage (Vrc) and the abdomen (Vab). Esophageal (Pes) and gastric (Pga) pressures were simultaneously recorded and transdiaphragmatic pressure (Pdi) was calculated by subtracting Pes from Pga. Pressure swings (sw) from end expiration (EE) to end inspiration (EI) were also calculated. During both hypoxia and hypercapnia, from quiet breathing to 40 L/min VE, Vrc,EI increased consistently but Vrc,EE, and Vab,EI did not. Moreover, Vab,EE decreased significantly during hypercapnia and remained unchanged during hypoxia. PesEI decreased (more negative values) and PesEE increased (less negative values) during either stimulus, while PgaEE increased with hypercapnia. Pdisw, calculated as the difference between PdiEE and PdiEI, increased significantly with both hypercapnia and hypoxia ( p = 0.002 for both). On the plot of Pes vs Pga, the slope of a line from end expiratory to end inspiratory lung volume between 20 and 40 L/min VE progressively increased during hypercapnia indicating increasing rib cage muscle (RCM) contribution to inspiratory pressure swings relative to the diaphragm. From these results we conclude that in healthy man: (i) with both chemical stimuli RCM contribution accounts for increase in Vrc displacement; (ii) with hypercapnia, the decrease in Vab,EE displacement indicates abdominal muscle (ABM) contribution to tidal volume; (iii) RCM and ABM assist the diaphragmatic function during hypercapnic stimulation.

Permissive hypercapnia

Although lifesaving, mechanical ventilation can result in lung injury and contribute to the development of bronchopulmonary dysplasia. The most critical determinants of lung injury are tidal volume and end-inspiratory lung volume. Permissive hypercapnia offers to maintain gas exchange with lower tidal volumes and thus decrease lung injury. Further physiologic benefits include improved oxygen delivery and neuroprotection, the latter through both avoidance of accidental hypocapnia, which is associated with a poor neurologic outcome, and direct cellular effects. Clinical trials in adults with acute respiratory failure indicated improved survival and reduced incidence of organ failure in subjects managed with low tidal volumes and permissive hypercapnia. Retrospective studies in low birth weight infants found an association of bronchopulmonary dysplasia with low PaCO2. Randomized clinical trials of low birth weight infants did not achieve sufficient statistical power to demonstrate a reduction of BPD by permissive hypercapnia, but strong trends indicated the possibility of important benefits without increased adverse events. Herein, we review the mechanisms leading to lung injury, the physiologic effects of hypercapnia, the dangers of hypocapnia, and the available clinical data.

Exercise-induced bronchodilation in natural and induced asthma: effects on ventilatory response and performance.

We studied whether bronchodilatation occurs with exercise during the late asthmatic reaction (LAR) to allergen (group 1, n = 13) or natural asthma (NA; group 2, n = 8) and whether this is sufficient to preserve maximum ventilation (VE(max)), oxygen consumption (VO(2 max)), and exercise performance (W(max)). In group 1, partial forced expiratory flow at 30% of resting forced vital capacity increased during exercise, both at control and LAR. W(max) was slightly reduced at LAR, whereas VE(max), tidal volume, breathing frequency, and VO(2 max) were preserved. Functional residual capacity and end-inspiratory lung volume were significantly larger at LAR than at control. In group 2, partial forced expiratory flow at 30% of resting forced vital capacity increased greatly with exercise during NA but did not attain control values after appropriate therapy. Compared with control, W(max) was slightly less during NA, whereas VO(2 max) and VE(max) were similar. Functional residual capacity, but not end-inspiratory lung volume at maximum load, was significantly greater than at control, whereas tidal volume decreased and breathing frequency increased. In conclusion, remarkable exercise bronchodilation occurs during either LAR or NA and allows VE(max) and VO(2 max) to be preserved with small changes in breathing pattern and a slight reduction in W(max).

Ventilator-induced lung injury.

The clinical relevance of experimental ventilator-induced lung injury has recently received a resounding illustration by the Acute Respiratory Distress Syndrome Network trial that showed a 22% reduction of mortality in patients with acute respiratory disease syndrome when lung mechanical stress was lessened by tidal volume reduction during mechanical ventilation. This clinical confirmation of the concept of ventilator-induced lung injury has also undisputedly substantiated the experimental observation that excessive tidal volume and/or end-inspiratory lung volume is the main determinant of ventilator-induced lung injury. More recently, attention has focused on the roles and implication in the pathogenesis of ventilator-induced lung injury of inflammatory cells and mediators that may be activated and released either in the alveolar space or in the systemic circulation because of the rupture of the alveolar-capillary barrier and on the cellular response to mechanical stress.

Cytokines During Ventilator-Induced Lung Injury: A Word of Caution

Cytokines During Ventilator-Induced Lung Injury: A Word of Caution

Diaphragm activation during exercise in chronic obstructive pulmonary disease.

Although it has been postulated that central inhibition of respiratory drive may prevent development of diaphragm fatigue in patients with chronic obstructive pulmonary disease (COPD) during exercise, this premise has not been validated. We evaluated diaphragm electrical activation (EAdi) relative to maximum in 10 patients with moderately severe COPD at rest and during incremental exhaustive bicycle exercise. Flow was measured with a pneumotachograph and volume by integration of flow. EAdi and transdiaphragmatic pressures (Pdi) were measured using an esophageal catheter. End-expiratory lung volume (EELV) was assessed by inspiratory capacity (IC) maneuvers, and maximal voluntary EAdi was obtained during these maneuvers. Minute ventilation (V E) was 12.2 +/- 1.9 L/min (mean +/- SD) at rest, and increased progressively (p < 0.001) to 31.0 +/- 7.8 L/min at end-exercise. EELV increased during exercise (p < 0.001) causing end-inspiratory lung volume to attain 97 +/- 3% of TLC at end-exercise. Pdi at rest was 9.4 +/- 3.2 cm H(2)O and increased during the first two thirds of exercise (p < 0.001) to plateau at about 13 cm H(2)O. EAdi was 24 +/- 6% of voluntary maximal at rest and increased progressively during exercise (p < 0.001) to reach 81 +/- 7% at end-exercise. In conclusion, dynamic hyperinflation during exhaustive exercise in patients with COPD reduces diaphragm pressure-generating capacity, promoting high levels of diaphragm activation.

Flow Limitation and Dynamic Hyperinflation During Exercise in COPD Patients After Single Lung Transplantation

Using the negative expiratory pressure (NEP) method, we have previously shown that patients receiving single lung transplantation (SLT) for COPD do not exhibit expiratory flow limitation and have little dyspnea at rest. In the present study, we assessed whether SLT patients exhibit flow limitation, overall hyperinflation, and dyspnea during exercise. Expiratory flow limitation assessed by the NEP method and inspiratory capacity maneuvers used to determine end-expiratory lung volume (EELV) and end-inspiratory lung volume (EILV) were performed at rest and during symptom-limited incremental cycle exercise in eight SLT patients. At the time of the study, the mean (+/- SD) FEV(1), FVC, functional residual capacity, and total lung capacity (TLC) amounted to 55 +/- 14%, 67 +/- 12%, 137 +/- 16%, and 110 +/- 11% of predicted, respectively. At rest, all patients did not experience expiratory flow limitation and were without dyspnea. At peak exercise, the maximal mechanical power output and maximal oxygen consumption amounted to 72 +/- 20% and 65 +/- 8% of predicted, respectively, with a maximal dyspnea Borg score of 6 +/- 3. All but one patient exhibited flow limitation and dynamic hyperinflation; the EELV and EILV amounted to 74 +/- 5% and 95 +/- 9% TLC, respectively. The patient who did not exhibit flow limitation during exercise had the lowest dyspnea score. Most SLT patients for COPD exhibit expiratory flow limitation and dynamic hyperinflation during exercise, whereas maximal dyspnea is variable.

Effects of the supine and prone position on diaphragm thickness in healthy term infants

BACKGROUNDThe physiological basis underlying the decline in the incidence of sudden infant death syndrome (SIDS) associated with changing the sleep position from prone to supine remains unknown.AIMSTo evaluate diaphragm thickness...

Airway distensibility in healthy and asthmatic subjects: effect of lung volume history.

Anatomic dead space (VD) is known to increase with end-inspiratory lung volume (EILV), and the gradient of the relationship has been proposed as an index of airway distensibility (DeltaVD). The aims of this study were to apply a rapid method for measuring DeltaVD and to determine whether it was affected by lung volume history. VD of 16 healthy and 16 mildly asthmatic subjects was measured at a number of known EILVs by using a tidal breathing, CO(2)-washout method. The effect of lung volume history was assessed by using three tidal breathing regimens: 1) three discrete EILVs (low/medium/high; LMH); 2) progressively decreasing EILVs from total lung capacity (TLC; TLC-RV); and 3) progressively increasing EILVs from residual volume (RV; RV-TLC). DeltaVD was lower in the asthmatic group for the LMH (25.3 +/- 2.24 vs. 21.2 +/- 1.66 ml/l, means +/- SE) and TLC-RV (24. 3 +/- 1.69 vs. 18.7 +/- 1.16 ml/l) regimens. There was a trend for a lower DeltaVD in the asthmatic group for the RV-TLC regimen (23.3 +/- 2.19 vs. 18.8 +/- 1.68 ml/l). There was no difference in DeltaVD between groups. In conclusion, mild asthmatic subjects have stiffer airways than normal subjects, and this is not obviously affected by lung volume history.

Airflow limitation and control of end-expiratory lung volume during exercise

To test the hypothesis that the presence of airflow limitation (AFL) influences the control of end-expiratory lung volume (EELV) during exercise, 11 subjects with normal lung function, performed submaximal exercise (SM) on a cycle ergometer, with and without AFL. AFL was achieved during exercise by increasing the density of the air via a hyperbaric chamber, compressed to a depth of 3 atm (3 ATA; with AFL). Five subjects achieved AFL during SM exercise at 3 ATA while the remaining six subjects did not achieve AFL. SM exercise was performed with the same apparatus in the hyperbaric chamber at sea level pressure with none of the subjects achieving AFL (SL; no-AFL). EELV (% of TLC, BTPS), was significantly larger during exercise at 3 ATA than during exercise at SL for the AFL group (SL=44±6%; 3 ATA–AFL=51±9%, P<0.05; but, was not for the no-AFL group (SL=46±6%; 3 ATA–no AFL=46±7%). End inspiratory lung volume was significantly elevated during exercise at 3 ATA compared with SL in the AFL group (SL=80±6%; 3 ATA–AFL=86±6%; P=0.01) but not in the no-AFL group (SL=82±4%; 3 ATA–no AFL=84±4%). Tidal volume and ventilation were not different for any condition. These data suggest that the occurrence of AFL influences the control of EELV.