Pulmonary and ventilatory responses to pregnancy, immersion, and exercise

To examine the effects of pregnancy, immersion, and exercise during immersion on pulmonary function and ventilation, 12 women were studied at 15, 25, and 35 wk of pregnancy and 8-10 wk postpartum. Pulmonary function and ventilation were measured under three experimental conditions: after 20 min of rest on land (LR), after 20 min of rest during immersion to the level of the xiphoid (IR), and after 20 min of exercise during immersion at 60% of predicted maximal capacity (IE). Forced vital capacity remained relatively constant, except for a decrease at 15 wk, for the duration of pregnancy. Expiratory reserve volume decreased with a change in the pregnancy status and with the duration of pregnancy. However, the forced vital capacity was maintained by an increase in the inspiratory capacity during pregnancy. Forced expiratory volume for 1 s, expressed as percent of forced vital capacity, did not differ significantly between conditions or as a result of pregnancy. Forced vital capacity was lower during the IR trial compared with LR and IE trials. The decreased forced vital capacity of the IR trials was mediated by a decrease in the expiratory reserve volume. Whereas the inspiratory capacity increased during IR and IE compared with LR, the increase was not large enough to offset the decrease in the expiratory reserve volume. Resting immersion resulted in a significant decrease in maximal voluntary ventilation as did pregnancy. Pregnancy resulted in significant increases in minute ventilation (VE), which were related to increases in the O2 consumption.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ozone inhalation effects consequent to continuous exercise in females: comparison to males

Exposure to ozone (O3) at ambient photochemical smog alert levels has been shown to cause alteration in pulmonary function and exercise response in humans, but there is a paucity of data on females. The initial purpose of the present investigation was to study the effects of O3 inhalation on pulmonary function and selected exercise respiratory metabolism and breathing pattern responses in young adult females. Six female subjects exercised continuously on a bicycle ergometer for 1 h on 10 occasions at one of three intensities, while exposed to 0.0, 0.20, 0.30, or 0.40 ppm O3. Forced expiratory volume and flow rates and residual volume (RV) were measured before and immediately following each protocol. During exercise, expired minute ventilation (VE), respiratory frequency (fR), tidal volume, O2 uptake (VO2), and heart rate (HR) were measured every 10 min. O3 dose-dependent decrements were observed for forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1.0), and forced expiratory flow rate during the middle half of FVC, coupled with an increase in RV and altered exercise ventilatory pattern. There was also an increased VE but no significant O3 effect on VO2 or HR. Comparison of the females' responses to those of a group of young adult males (previously studied) at the same total O3 effective dose (i.e., expressed as the simple product of O3 concentration, VE, and exposure time) revealed significantly greater effects on FVC, FEV1.0, and fR for the females. With VE reduced for females as a function of exercise intensity at the same percent of maximum VO2, these differences were considerably attenuated, although not negated.(ABSTRACT TRUNCATED AT 250 WORDS)     

Breathing during exercise in subjects with mild-to-moderate airflow obstruction: effects of physical training.

In this study we explored the effects of physical training on the response of the respiratory system to exercise. Eight subjects with irreversible mild-to-moderate airflow obstruction [forced expiratory volume in 1 s of 85 +/- 14 (SD) % of predicted and ratio of forced expiratory volume in 1 s to forced vital capacity of 68 +/- 5%] and six normal subjects with similar anthropometric characteristics underwent a 2-mo physical training period on a cycle ergometer three times a week for 31 min at an intensity of approximately 80% of maximum heart rate. At this work intensity, tidal expiratory flow exceeded maximal flow at control functional residual capacity [FRC; expiratory flow limitation (EFL)] in the obstructed but not in the normal subjects. An incremental maximum exercise test was performed on a cycle ergometer before and after training. Training improved exercise capacity in all subjects, as documented by a significant increase in maximum work rate in both groups (P < 0.001). In the obstructed subjects at the same level of ventilation at high workloads, FRC was greater after than before training, and this was associated with an increase in breathing frequency and a tendency to decrease tidal volume. In contrast, in the normal subjects at the same level of ventilation at high workloads, FRC was lower after than before training, so that tidal volume increased and breathing frequency decreased. These findings suggest that adaptation to breathing under EFL conditions does not occur during exercise in humans, in that obstructed subjects tend to increase FRC during exercise after experiencing EFL during a 2-mo strenuous physical training period.     

VA/Q distribution during heavy exercise and recovery in humans: implications for pulmonary edema.

Ventilation-perfusion (VA/Q) inequality has been shown to increase with exercise. Potential mechanisms for this increase include nonuniform pulmonary vasoconstriction, ventilatory time constant inequality, reduced large airway gas mixing, and development of interstitial pulmonary edema. We hypothesized that persistence of VA/Q mismatch after ventilation and cardiac output subside during recovery would be consistent with edema; however, rapid resolution would suggest mechanisms related to changes in ventilation and blood flow per se. Thirteen healthy males performed near-maximal cycle ergometry at an inspiratory PO2 of 91 Torr (because hypoxia accentuates VA/Q mismatch on exercise). Cardiorespiratory variables and inert gas elimination patterns were measured at rest, during exercise, and between 2 and 30 min of recovery. Two profiles of VA/Q distribution behavior emerged during heavy exercise: in group 1 an increase in VA/Q mismatch (log SDQ of 0.35 +/- 0.02 at rest and 0.44 +/- 0.02 at exercise; P less than 0.05, n = 7) and in group 2 no change in VA/Q mismatch (n = 6). There were no differences in anthropometric data, work rate, O2 uptake, or ventilation during heavy exercise between groups. Group 1 demonstrated significantly greater VA/Q inequality, lower vital capacity, and higher forced expiratory flow at 25-75% of forced vital capacity for the first 20 min during recovery than group 2. Cardiac index was higher in group 1 both during heavy exercise and 4 and 6 min postexercise. However, both ventilation and cardiac output returned toward baseline values more rapidly than did VA/Q relationships. Arterial pH was lower in group 1 during exercise and recovery. We conclude that greater VA/Q inequality in group 1 and its persistence during recovery are consistent with the hypothesis that edema occurs and contributes to the increase in VA/Q inequality during exercise. This is supported by observation of greater blood flows and acidosis and, presumably therefore, higher pulmonary vascular pressures in such subjects.     

Influence of passive smoking on basic anthropometric characteristics and respiratory function in young athletes

The primary objective of this study is to investigate the maintenance difference in basic anthropometric characteristics and to outline the dynamics of respiratory function change in youngsters athletes exposed to passive smoking (PS) and athletes not exposed to passive smoking in their families (NPS). High and weight were determined as basis anthropometric characteristics. Measured parameters for respiratory function were vital capacity (VC), forced expiratory volume in the first second (FEV1), maximum expiratory flow (PEF), forced expiratory flow at 50% forced vital capacity (MEF 50) and forced expiratory flow at 25% forced vital capacity (MEF 25). Significant statistical differences in separate spirometric variable were found in three variables (FEV1, MEF50, and MEF25) for group older youngsters. Analysis of variance showed statistical differences between athletes unexposed to passive smoking (NPS) and athletes exposed to passive smoking (PS) in even four spirometric variables (VC, FEV1, MEF50 and MEF25).     

Pulmonary function changes in ozone-interaction of concentration and ventilation.

A total of 28 healthy young subjects have been exposed for 2 h to ozone (0.37-0.75 ppm) under conditions of either rest or intermittent light exercise (sufficient to increase the respiratory minute volume by a factor of 2.5). All pulmonary function tests (vital capacity, forced expiratory volume, maximum expiratory flow-volume curve, slope of phase III of alveolar nitrogen plateau) showed a significant deterioration relative to parallel control experiments. Responses were related to the dose of ozone as calculated from the product of concentration, exposure time, and respiratory minute volume during exposure, changes at 1 h averaging approximately one-half those seen at 2 h.     

Ozone and high ventilation effects on pulmonary function and endurance performance

Ozone (O3) toxicity is potentiated by exercise-induced expired minute ventilation (VE) for a given exposure, which may also impair endurance performance. Ten healthy, well-trained long-distance runners were exposed on six occasions for 1 h to O3 concentrations of 0, 0.20, or 0.35 parts per million (ppm), during exercise simulating either training or competition, with mean VE = 77.5 1 X min -1. Standard pulmonary function tests, subjective symptoms, and periodic observations of exercise ventilatory response and respiratory metabolism were obtained. Statistical analyses revealed no significant exercise mode effect for pulmonary function, but a significant O3 effect for forced vital capacity and expiratory volume at 1 s was observed. Altered exercise ventilatory pattern response was noted, but there was no significant O3 effect on exercise oxygen uptake, heart rate, VE, or alveolar ventilation. Subjective symptoms increased with O3 concentration. Statistically significant pulmonary function impairment observed at 0.20 ppm O3 suggests that endurance athletes may be more susceptible to the effects of a given O3 concentration than normal young adult males as a result of sustained high mean VE incurred during training and competition. Three subjects were unable to complete both the training and competitive simulations at 0.35 ppm O3. Performance decrements appeared to be the result of physiologically induced respiratory discomfort rather than decrements in pulmonary gas exchange and/or oxygen transport and delivery.     

Ozone inhalation effects in females varying widely in lung size: comparison with males

It has been suggested that lung size accounts for observed gender differences in responsiveness to the same total inhaled dose of O3. To test the hypothesis that lung size is a determinant of magnitude of response within a gender, two groups of 14 healthy young adult females differing significantly in forced vital capacity [FVC; i.e., small-lung group mean = 3.74 liters (range 3.2-4.0) and large-lung group mean = 5.11 liters (range 4.5-6.2] were exposed for 1 h to filtered air (FA) and to 0.18 and 0.30 ppm O3. On each occasion, subjects exercised continuously on a cycle ergometer at a work rate that elicited a mean minute ventilation of approximately 47 l/min. For the small-lung group [mean total lung capacity (TLC) = 4.52 liters] exercise O2 uptake was 67% of maximal O2 uptake (VO2max), and that for the large-lung group (TLC 6.37 liters) was 61% of VO2max. Statistical analysis revealed significant decrements for both groups in FVC, forced expiratory volume in 1 s (FEV1.0), and forced expiratory flow rate in the middle half of FVC on exposure to 0.18 and 0.30 ppm O3. Exercise respiratory frequency increased, and tidal volume decreased significantly in both groups in response to 0.18 and 0.30 ppm O3 exposure. On exposure to 0.30 ppm O3, the number of individual subjective symptoms reported and their severity were significantly greater for both groups than those reported for the FA and 0.18 ppm O3 exposures. Both groups evidenced similar percent changes in pulmonary function and exercise ventilation response, and in subjective symptom response.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulmonary function in men after oxygen breathing at 3.0 ATA for 3.5 h.

As a pulmonary component of Predictive Studies V, designed to determine O2 tolerance of multiple organs and systems in humans at 3.0-1.5 ATA, pulmonary function was evaluated at 1.0 ATA in 13 healthy men before and after O2 exposure at 3.0 ATA for 3.5 h. Measurements included flow-volume loops, spirometry, and airway resistance (Raw) (n = 12); CO diffusing capacity (n = 11); closing volumes (n = 6); and air vs. HeO2 forced vital capacity maneuvers (n = 5). Chest discomfort, cough, and dyspnea were experienced during exposure in mild degree by most subjects. Mean forced expiratory volume in 1 s (FEV1) and forced expiratory flow at 25-75% of vital capacity (FEF25-75) were significantly reduced postexposure by 5.9 and 11.8%, respectively, whereas forced vital capacity was not significantly changed. The average difference in maximum midexpiratory flow rates at 50% vital capacity on air and HeO2 was significantly reduced postexposure by 18%. Raw and CO diffusing capacity were not changed postexposure. The relatively large change in FEF25-75 compared with FEV1, the reduction in density dependence of flow, and the normal Raw postexposure are all consistent with flow limitation in peripheral airways as a major cause of the observed reduction in expiratory flow. Postexposure pulmonary function changes in one subject who convulsed at 3.0 h of exposure are compared with corresponding average changes in 12 subjects who did not convulse.     

Short-term hypoxic exposure at rest and during exercise reduces lung water in healthy humans.

Hypoxia and hypoxic exercise increase pulmonary arterial pressure, cause pulmonary capillary recruitment, and may influence the ability of the lungs to regulate fluid. To examine the influence of hypoxia, alone and combined with exercise, on lung fluid balance, we studied 25 healthy subjects after 17-h exposure to 12.5% inspired oxygen (barometric pressure = 732 mmHg) and sequentially after exercise to exhaustion on a cycle ergometer with 12.5% inspired oxygen. We also studied subjects after a rapid saline infusion (30 ml/kg over 15 min) to demonstrate the sensitivity of our techniques to detect changes in lung water. Pulmonary capillary blood volume (Vc) and alveolar-capillary conductance (D(M)) were determined by measuring the diffusing capacity of the lungs for carbon monoxide and nitric oxide. Lung tissue volume and density were assessed using computed tomography. Lung water was estimated by subtracting measures of Vc from computed tomography lung tissue volume. Pulmonary function [forced vital capacity (FVC), forced expiratory volume after 1 s (FEV(1)), and forced expiratory flow at 50% of vital capacity (FEF(50))] was also assessed. Saline infusion caused an increase in Vc (42%), tissue volume (9%), and lung water (11%), and a decrease in D(M) (11%) and pulmonary function (FVC = -12 +/- 9%, FEV(1) = -17 +/- 10%, FEF(50) = -20 +/- 13%). Hypoxia and hypoxic exercise resulted in increases in Vc (43 +/- 19 and 51 +/- 16%), D(M) (7 +/- 4 and 19 +/- 6%), and pulmonary function (FVC = 9 +/- 6 and 4 +/- 3%, FEV(1) = 5 +/- 2 and 4 +/- 3%, FEF(50) = 4 +/- 2 and 12 +/- 5%) and decreases in lung density and lung water (-84 +/- 24 and -103 +/- 20 ml vs. baseline). These data suggest that 17 h of hypoxic exposure at rest or with exercise resulted in a decrease in lung water in healthy humans.     

Combined effects of ozone exposure and ambient heat on exercising females

Ten aerobically trained young adult females exercised continuously at 66% of maximum O2 uptake for 1 h while exposed orally to filtered air and 0.15 and 0.30 parts per million (ppm) ozone (O3) in both moderate (24 degrees C) and hot (35 degrees C) ambient conditions. Exposure to 0.30 ppm O3 induced significant impairment in forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1.0), and other pulmonary function variables. Exercise respiratory frequency (fR) increased, whereas tidal volume and alveolar volume (VA) decreased with 0.30 ppm O3 exposure. Significant interactions of O3 and ambient heat were obtained for fR and VA, whereas FVC and FEV1.0 displayed a trend toward an O3-temperature interaction. Although expired ventilation increased, the interactions could not be ascribed to a greater O3 effective dose in the 35 degrees C exposures. However, subjective discomfort increased with both O3 and heat exposure such that three subjects ceased exercise prematurely when O3 and ambient heat were combined. We conclude that accentuation of subjective limitations and certain physiological alterations by ambient heat coinciding with photochemical oxidant episodes is likely to result in more severe impairment of exercise performance, although the mechanisms remain unclear.     

Pulmonary function in asthmatic patients in remission.

Thirty-five asthmatic patients (average age 28 years) who attended a pulmonary function laboratory when their mean ratio of forced expiratory volume in one second: forced vital capacity was 81 per cent (within the normal range for their age group) had arterial hypoxaemia and hypocapnia. These were probably secondary to lung hyperinflation and pulmonary ventilation/perfusion imbalance. The pulmonary abnormalities of bronchial asthma are not always detected by simple spirometric tests and the results of such tests should be interpreted cautiously.     

Gravity effects on regional lung ventilation determined by functional EIT during parabolic flights.

Gravity-dependent changes of regional lung function were studied during normogravity, hypergravity, and microgravity induced by parabolic flights. Seven healthy subjects were followed in the right lateral and supine postures during tidal breathing, forced vital capacity, and slow expiratory vital capacity maneuvers. Regional 1) lung ventilation, 2) lung volumes, and 3) lung emptying behavior were studied in a transverse thoracic plane by functional electrical impedance tomography (EIT). The results showed gravity-dependent changes of regional lung ventilation parameters. A significant effect of gravity on regional functional residual capacity with a rapid lung volume redistribution during the gravity transition phases was established. The most homogeneous functional residual capacity distribution was found at microgravity. During vital capacity and forced vital capacity in the right lateral posture, the decrease in lung volume on expiration was larger in the right lung region at all gravity phases. During tidal breathing, the differences in ventilation magnitudes between the right and left lung regions were not significant in either posture or gravity phase. A significant nonlinearity of lung emptying was determined at normogravity and hypergravity. The pattern of lung emptying was homogeneous during microgravity.     

Evaluation of pulmonary resistance and maximal expiratory flow measurements during exercise in humans.

To evaluate methods used to document changes in airway function during and after exercise, we studied nine subjects with exercise-induced asthma and five subjects without asthma. Airway function was assessed from measurements of pulmonary resistance (RL) and forced expiratory vital capacity maneuvers. In the asthmatic subjects, forced expiratory volume in 1 s (FEV1) fell 24 +/- 14% and RL increased 176 +/- 153% after exercise, whereas normal subjects experienced no change in airway function (RL -3 +/- 8% and FEV1 -4 +/- 5%). During exercise, there was a tendency for FEV1 to increase in the asthmatic subjects but not in the normal subjects. RL, however, showed a slight increase during exercise in both groups. Changes in lung volumes encountered during exercise were small and had no consistent effect on RL. The small increases in RL during exercise could be explained by the nonlinearity of the pressure-flow relationship and the increased tidal breathing flows associated with exercise. In the asthmatic subjects, a deep inspiration (DI) caused a small, significant, transient decrease in RL 15 min after exercise. There was no change in RL in response to DI during exercise in either asthmatic or nonasthmatic subjects. When percent changes in RL and FEV1 during and after exercise were compared, there was close agreement between the two measurements of change in airway function. In the groups of normal and mildly asthmatic subjects, we conclude that changes in lung volume and DIs had no influence on RL during exercise. Increases in tidal breathing flows had only minor influence on measurements of RL during exercise. Furthermore, changes in RL and in FEV1 produce equivalent indexes of the variations in airway function during and after exercise.     

Circulatory and respiratory responses to muscular exercise in Czech and Norwegian children

This paper presents a comparison between Czech and Norwegian rural healthy children with regard to the functional characteristics of the circulatory and respiratory system based upon work physiological variables and measurements of some pulmonary volumes. The study included randomised samples of boys and girls at the age of 8, 12 and 16 years, 66 Czech boys and 63 girls, 54 Norwegian boys and 57 girls. At the age of 8 years the maximal aerobic power was closely similar in both countries, but in the older age groups the Norwegian children exhibited lower physical fitness. The maximal heart rate was close to 200 min-1 on the average without any sex, age or ethnic differences. In agreement with the higher maximal aerobic power the 12 and 16 year old Czech children had lower submaximal heart rates for the same oxygen uptake than the Norwegian children. The forced vital capacity and forced expiratory volume in one second was significantly higher on the average in Czech than in Norwegian children but the latter, expressed in percent age of the former, averaged 87 to 91% without any sex, age or ethnic differences. The maximal ventilation volumes during muscular exercise reached higher values in Czech than in Norwegian children of the same age, but the mean maximal respiratory rate was close to 60 min-1, being independent of age, sex and cultural differences. During heavy exercise only 40 to 50% of the vital capacity and 45 to 55% of the forced expiratory volume were taken into account and this index of pulmonary function did not differ with sex, age or ethnic differences.     

Pulmonary response to threshold levels of sulfur dioxide (1.0 ppm) and ozone (0.3 ppm)

We exposed 22 healthy adult nonsmoking male subjects for 2 h to filtered air, 1.0 ppm sulfur dioxide (SO2), 0.3 ppm ozone (O3), or the combination of 1.0 ppm SO2 + 0.3 ppm O3. We hypothesized that exposure to near-threshold concentrations of these pollutants would allow us to observe any interaction between the two pollutants that might have been masked by the more obvious response to the higher concentrations of O3 used in previous studies. Each subject alternated 30-min treadmill exercise with 10-min rest periods for the 2 h. The average exercise ventilation measured during the last 5 min of exercise was 38 1/min (BTPS). Forced expiratory maneuvers were performed before exposure and 5 min after each of the three exercise periods. Maximum voluntary ventilation, He dilution functional residual capacity, thoracic gas volume, and airway resistance were measured before and after the exposure. After O3 exposure alone, forced expiratory measurements (FVC, FEV1.0, and FEF25-75%) were significantly decreased. The combined exposure to SO2 + O3 produced similar but smaller decreases in these measures. There were small but significant differences between the O3 and the O3 + SO2 exposure for FVC, FEV1.0, FEV2.0, FEV3.0, and FEF25-75% at the end of the 2-h exposure. We conclude that, with these pollutant concentrations, there is no additive or synergistic effect of the two pollutants on pulmonary function.     

Hematological and pulmonary responses to high altitude in Quechuas: a multivariate approach

This study investigates the relationships among hematological variables, pulmonary function, and age in a sample of high-altitude natives. The following anthropometric and physiological variables were examined in 77 adult Quechua males from the Peruvian Central Andes (Huancavelica, 3,680 m): height, weight, sitting height, chest diameters, chest and abdominal circumferences, forced vital capacity (FVC), forced expiratory volume at 1 sec (FEV1), peak expiratory flow (PEF), hemoglobin concentration (Hb), red blood cells (RBC), hematocrit (Htc), diastolic and systolic blood pressure, body temperature, pulmonary rate, and pulse rate. The means of these variables for the Huancavelica sample fall within the range of variability previously observed in Andean populations. Principal components analysis and canonical correlation analysis suggest that in this native Andean population: 1) aging decreases lung function but does not affect hematological features, and 2) there is a negative age-independent correlation between lung function (FVC, FEV1, PEF) and hematological traits (Hb, RBC, Htc).     

Role of the parasympathetic nervous system in acute lung response to ozone

We conducted an ozone (O3) exposure study using atropine, a muscarinic receptor blocker, to determine the role of the parasympathetic nervous system in the acute response to O3. Eight normal subjects with predetermined O3 responsiveness were randomly assigned an order for four experimental exposures. For each exposure a subject inhaled either buffered saline or atropine aerosol followed by exposure either to clean air or 0.4 ppm O3. Measurements of lung mechanics, ventilatory response to exercise, and symptoms were obtained before and after exposure. O3 exposure alone resulted in significant changes in specific airway resistance, forced vital capacity (FVC), forced expiratory flow rates, tidal volume (VT), and respiratory rate (f). Atropine pretreatment prevented the significant increase in airway resistance with O3 exposure and partially blocked the decrease in forced expiratory flow rates but did not prevent a significant fall in FVC, changes in f and VT, or the frequency of reported respiratory symptoms after O3. These results suggest that the increase in pulmonary resistance during O3 exposure is mediated by a parasympathetic mechanism and that changes in other measured variables are mediated, at least partially, by mechanisms not dependent on muscarinic cholinergic receptors of the parasympathetic nervous system.     

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).     

Trachea and lung dimensions in nonsmoking twins: morphological and functional studies

To compare genetic and environmental factors that determine lung function and dimensions, chest radiographs and pulmonary function were measured in 17 pairs of nonsmoking twin adolescent boys (12 monozygotic pairs and 5 dizygotic pairs). Genetic factors dominated in tracheal width and lung dimensions (height, width, and apicofissural and fissurodiaphragmatic distances) at residual volume. Genetic factors also affected forced vital capacity, functional residual capacity, forced expiratory volume in 1 s, maximum expiratory flow at 25% vital capacity, and maximum flow at 50% vital capacity-to-forced vital capacity ratio. Peak expiratory flow correlated with tracheal width at residual volume. Age correlated with lung dimensions (width and depth) but not with tracheal width. These results indicate that genetic factors determine the dimensions and function of central airways, peripheral airways, and lung parenchyma in adolescent males. The effects of genetic factors on some functional measurements (airway resistance, closing volume-to-vital capacity ratio, and phase III in single-breath N2 washout) may be masked because of poor reproducibility of the tests.