Exercise-induced Bronchodilation Research Articles

Respiratory oscillometry testing in relation to exercise in healthy and asthmatic Thoroughbreds.

Racehorses may experience exercise-induced bronchodilation or bronchoconstriction, with potential differences between healthy and asthmatic individuals. To identify exercise-related lung function variations by oscillometry in racehorses, compare lung function between healthy and mild equine asthma (MEA) horses, assess oscillometry's potential as a predictor of racing fitness. Prospective case-control clinical study. Fourteen Thoroughbred racehorses (5 healthy, 9 MEA) underwent a protocol including respiratory oscillometry at rest, exercise with fitness monitoring, oscillometry at 15 and 45 min post-exercise, and bronchoalveolar lavage fluid (BALf) cytology. Oscillometry parameters (resistance [Rrs] and reactance [Xrs]) were compared within and between healthy and MEA groups at different timepoints. Associations between Rrs and Xrs at rest and 15 min post-exercise and BALf cytology and fitness indices were evaluated. MEA horses showed higher Rrs at 15 min post-exercise (0.6 ± 0.2 cmH2 O/L/s) than healthy horses (0.3 ± 0.1 cmH2 O/L/s) (p < 0.01). In healthy horses, Rrs decreased at 15 min post-exercise compared with resting values (0.5 ± 0.1 cmH2 O/L/s) (p = 0.04). In MEA horses, oscillometry parameters did not vary with time. Post-exercise Xrs inversely correlated with total haemosiderin score (p < 0.01, r2 = 0.51). Resting Rrs inversely correlated with speed at 200 bpm (p = 0.03, r2 = -0.61), and Xrs with maximum heart rate (HR) during exercise (p = 0.02, r2 = -0.62). Post-exercise Rrs inversely correlated with mean (p = 0.04, r2 = -0.60) and maximum speed (p = 0.04, r2 = -0.60), and HR variability (p < 0.01, r2 = -0.74). Small sample size, oscillometry repeatability not assessed, potential interference of upper airway obstructions, external variables influencing fitness indices. Oscillometry identified lung function differences between healthy and MEA horses at 15 min post-exercise. Only healthy horses exhibited exercise-induced bronchodilation. Oscillometry showed potential in predicting subclinical airway obstruction.

Exercise induced bronchodilation: a phenomenon more common, greater magnitude and more prolonged in older adults than in adolescents

Objective There are few studies in clinically healthy subjects describing and quantifying exercise-induced bronchodilation (EIBd). This study aimed to describe and compare the magnitude and time course changes in post-exercise forced expired volume at the first second (FEV1) in healthy adolescents, younger adults, and older adults. Methods Adolescent (n = 73, aged 10–17 years), younger adult (n = 35, aged 18–25 years), and older adult (n = 25, aged 35–66 years) subjects with normal spirometry z-scores completed a maximal cardiopulmonary exercise test using the standardized exponential exercise test protocol on a cycle ergometer performed at stable temperature and humidity. Spirometry was performed pre-exercise and at 1-, 3-, 5-, and 10-minutes post-exercise to determine the percentage change in FEV1 compared to baseline. EIBd was defined as a ≥ 5% increase in post-exercise FEV1. Results Increases in FEV1 at one-minute post-exercise were observed in the adolescents (1.3%) and young adults (6.0%) with FEV1 returning to baseline after ten minutes. Compared to the adolescents, the older adults showed significantly greater and sustained increases in FEV1 at 1-, 3-, 5-, and 10-minutes post-exercise (6.4, 4.6, 4.7, and 3.8%, p < 0.05). At 1-minute post exercise a significantly greater proportion of younger adults (54%, p < 0.01) and older adults (64%, p < 0.01) demonstrated EIBd compared to the adolescent group (15%). Conclusion Healthy older adults had a higher prevalence, greater magnitude and more prolonged EIBd compared to healthy adolescent and young adult subjects.

Exercise-induced bronchoconstriction and bronchodilation: investigating the effects of age, sex, airflow limitation and FEV1.

Exercise-induced bronchoconstriction (EIBc) is a recognised response to exercise in asthmatic subjects and athletes but is less well understood in an unselected broad population. Exercise-induced bronchodilation (EIBd) has received even less attention. The objective of this study was to investigate the effects of age, sex, forced expiratory volume in 1 s (FEV1) and airflow limitation (FEV1/forced vital capacity (FVC) <0.7) on the prevalence of EIBc and EIBd.This was a retrospective study based on incremental cardiopulmonary exercise testing on cycle ergometry to symptom limitation performed between 1988 and 2012. FEV1 was measured before and 10 min after exercise. EIBc was defined as a percentage fall in FEV1 post-exercise below the 5th percentile, while EIBd was defined as a percentage increase in FEV1 above the 95th percentile.35 258 subjects aged 6-95 years were included in the study (mean age 53 years, 60% male) and 10.3% had airflow limitation (FEV1/FVC <0.7). The lowest 5% of subjects demonstrated a ≥7.6% fall in FEV1 post-exercise (EIBc), while the highest 5% demonstrated a >11% increase in FEV1 post-exercise (EIBd). The probability of both EIBc and EIBd increased with age and was highest in females across all ages (OR 1.76, 95% CI 1.60-1.94; p<0.0001). The probability of EIBc increased as FEV1 % pred declined (<40%: OR 4.38, 95% CI 3.04-6.31; p<0.0001), with a >2-fold increased likelihood in females (OR 2.31, 95% CI 1.71-3.11; p<0.0001), with a trend with airflow limitation (p=0.06). The probability of EIBd increased as FEV1 % pred declined, in the presence of airflow limitation (OR 1.55, 95% CI 1.24-1.95; p=0.0001), but sex had no effect.EIBc and EIBd can be demonstrated at the population level, and are influenced by age, sex, FEV1 % pred and airflow limitation.

Pitfalls in Expiratory Flow Limitation Assessment at Peak Exercise in Children: Role of Thoracic Gas Compression.

Thoracic gas compression and exercise-induced bronchodilation can influence the assessment of expiratory flow limitation (EFL) during cardiopulmonary exercise tests. The purpose of this study was to examine the effect of thoracic gas compression and exercise-induced bronchodilation on the assessment of EFL in children with and without obesity. Forty children (10.7 ± 1.0 yr; 27 obese; 15 with EFL) completed pulmonary function tests and incremental exercise tests. Inspiratory capacity maneuvers were performed during the incremental exercise test for the placement of tidal flow volume loops within the maximal expiratory flow volume (MEFV) loops, and EFL was calculated as the overlap between the tidal and the MEFV loops. MEFV loops were plotted with volume measured at the lung using plethysmography (MEFVp), with volume measured at the mouth using spirometry concurrent with measurements in the plethysmograph (MEFVm), and from spirometry before (MEFVpre) and after (MEFVpost) the incremental exercise test. Only the MEFVp loops were corrected for thoracic gas compression. Not correcting for thoracic gas compression resulted in incorrect diagnosis of EFL in 23% of children at peak exercise. EFL was 26% ± 15% VT higher for MEFVm compared with MEFVp (P < 0.001), with no differences between children with and without obesity (P = 0.833). The difference in EFL estimation using MEFVpre (37% ± 30% VT) and MEFVpost (31% ± 26% VT) did not reach statistical significance (P = 0.346). Not correcting the MEFV loops for thoracic gas compression leads to the overdiagnosis and overestimation of EFL. Because most commercially available metabolic measurement systems do not correct for thoracic gas compression during spirometry, there may be a significant overdiagnosis of EFL in cardiopulmonary exercise testing. Therefore, clinicians must exercise caution while interpreting EFL when the MEFV loop is derived through spirometry.

Sex, Lungs, And Forced Expiratory Flows

Women display lower maximal, forced expiratory flows (FEFs) across the vital capacity range compared with height- and age-matched men. This sex-difference on FEFs is believed to increase the prevalence of ventilatory constraint in women compared with men at a given ventilation during exercise. It remains unclear whether this sex-difference in FEFs is evident when absolute lung size is taken into account. Purpose: To investigate the influences of sex, TLC and residual volume on FEFs at rest, and during exercise in healthy adults. METHODS: Forty-seven untrained adults (24 women; 29 ± 6 yrs) with normal pulmonary function (>90% pred.) participated in this study. Subjects completed 9 min of constant-load cycling at 75% of the peak work rate achieved during an incremental cycling test. TLC and RV were obtained at rest and at the end of exercise using He-dilution, and inspiratory and forced vital capacity manoeuvres. FEFs were obtained at 25, 50 and 75% of vital capacity (FEF25%, FEF50% and FEF75%, respectively). Multivariate analyses of covariance (MANCOVA) were used to examine the effect of sex on FEFs after controlling for RV and TLC. RESULTS: Height, TLC and RV were larger for men than women (P < 0.05), as expected. The TLC to height ratio was greater in men than women (45 ± 9 ml·cm-1 v 35 ± 5 ml·cm-1, P < 0.05). FEFs increased during exercise for both sexes (P < 0.05), suggesting bronchodilation. The MANCOVA revealed a main-effect of sex on FEFs at rest and during exercise, where FEFs were systematically higher for men than women (P < 0.05). Importantly, however, the main-effect of sex on FEFs disappeared when TLC and RV were entered into the model as covariates. CONCLUSIONS: The differences in FEFs of our subjects could not be explained on the basis of sex alone. Instead, our analyses suggests that FEFs appear similar between young men and women if one controls for static lung volumes - a result that was also observed in the presence of exercise-induced bronchodilation. Thus, the higher prevalence of ventilatory constraint during exercise in women compared with height-matched men is likely the result of women having a smaller TLC relative to their height, as opposed to a sexual dimorphism in airway size/caliber for a given lung size (dysanapsis). Supported by NIH Grant HL71478

Pulmonary Function And Heart Rate Variability Responses To Low- And High-intensity Cycling In Diesel Exhaust

INTRODUCTION: Exposure to diesel exhaust (DE) prior to exercise increases exercise heart rate and attenuates exercise-induced bronchodilation. However, the effects of exercise combined with air pollution on pulmonary function and heart rate variability (HRV) are unclear. Furthermore, it is often assumed that increases in exercise intensity will increase the dose of air pollution, thus magnifying the resultant health effects. However, how the effects of DE on pulmonary function and HRV are modulated by exercise intensity is unknown. PURPOSE: To determine the effects to low- and high-intensity cycling in DE on pulmonary function and HRV. METHODS: Eighteen males performed 30-minute trials of low (30% VO2peak power) and high-intensity (60% VO2peak power) cycling and a resting control condition. For each subject, each trial was performed once breathing filtered air (FA) and once breathing DE (300ug/m3 of PM2.5), for a total of 6 trials. Pulmonary function and HRV were measured before, immediately after, and 1 h, and 2 h post-exposure to DE or FA. Time domain measures of HRV included the standard deviation of normal-to-normal intervals (SDNN), the root mean square of the mean differences in successive N-N intervals (RMSSD), and the HRV triangular index. Frequency domain analysis included low frequency power (LFP: 0.04–0.15 Hz), high frequency power (HFP: 0.15–0.40 Hz) as well as total power (TP). Additionally, LF and HF normalized units (LFnu, HFnu), and LF/HF ratios were determined. RESULTS: Exposure to DE had no significant effect on pulmonary function or HRV (p<0.05). As expected all time and frequency domain indices of HRV significantly decreased following high-intensity exercise (p<0.05; Pre to post high-intensity exercise: SDNN 1018.7 vs. 730.1 ms, RMSSD 65.2 vs. 19.5 ms, HRV triangular index 14.3 vs. 7.2, LFP 1408.8 vs. 455.7 ms2, HFP 1487.0 vs. 391.1 ms2, TP 4949.0 vs. 1152.8 ms2, HFnu 44.5 vs. 19.8). The exception to this pattern was LFnu and LF/HF ratio, which significantly increased following high-intensity exercise (p<0.05; Pre to post high-intensity exercise: LFnu 51.7 vs. 71.8, LF/HF 1.49 vs. 4.52). CONCLUSION: These data suggest that acute exposure to DE during exercise does not affect pulmonary function or HRV. Furthermore, performing high intensity exercise does not potentiate the effects of DE.

Tracheal epithelium cell volume responses to hyperosmolar, isosmolar and hypoosmolar solutions: relation to epithelium-derived relaxing factor (EpDRF) effects.

In asthmatic patients, inhalation of hyperosmolar saline or D-mannitol (D-M) elicits bronchoconstriction, but in healthy subjects exercise causes bronchodilation. Hyperventilation causes drying of airway surface liquid (ASL) and increases its osmolarity. Hyperosmolar challenge of airway epithelium releases epithelium-derived relaxing factor (EpDRF), which relaxes the airway smooth muscle. This pathway could be involved in exercise-induced bronchodilation. Little is known of ASL hyperosmolarity effects on epithelial function. We investigated the effects of osmolar challenge maneuvers on dispersed and adherent guinea-pig tracheal epithelial cells to examine the hypothesis that EpDRF-mediated relaxation is associated with epithelial cell shrinkage. Enzymatically-dispersed cells shrank when challenged with ≥10 mOsM added D-M, urea or NaCl with a concentration-dependence that mimics relaxation of the of isolated perfused tracheas (IPT). Cells shrank when incubated in isosmolar N-methyl-D-glucamine (NMDG) chloride, Na gluconate (Glu), NMDG-Glu, K-Glu and K2SO4, and swelled in isosmolar KBr and KCl. However, isosmolar challenge is not a strong stimulus of relaxation in IPTs. In previous studies amiloride and 4,4′-diisothiocyano-2,2′-stilbenedisulfonic acid (DIDS) inhibited relaxation of IPT to hyperosmolar challenge, but had little effect on shrinkage of dispersed cells. Confocal microscopy in tracheal segments showed that adherent epithelium is refractory to low hyperosmolar concentrations that induce dispersed cell shrinkage and relaxation of IPT. Except for gadolinium and erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA), actin and microtubule inhibitors and membrane permeabilizing agents did not affect on ion transport by adherent epithelium or shrinkage responses of dispersed cells. Our studies dissociate relaxation of IPT from cell shrinkage after hyperosmolar challenge of airway epithelium.

The effect of pre-exercise diesel exhaust exposure on cycling performance and cardio-respiratory variables

Purpose: To determine the effect of pre-exercise exposure to diesel exhaust (DE) on 20-km cycling performance, pulmonary function, and cardio-respiratory variables during exercise.Methods: Eight endurance-trained males participated in the study. Test days consisted of a 60-min exposure to either filtered air (FA) or DE, followed by a 20 km cycling time trial. Exposures to DE were at a concentration of 300 µg/m3 of PM2.5. Forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) were measured before and after exposure, and after exercise. Oxygen consumption (VO2) and carbon dioxide production (VCO2), minute ventilation (VE), tidal volume (VT), breathing frequency (FB), heart rate and oxyhemoglobin saturation (SpO2), were collected during the time trials. The effect of condition on time trial duration, an order effect, and mean cardio-respiratory variables were each analysed using paired T-tests. Repeated-measures ANOVA were used to assess the effect of DE exposure on pulmonary function.Results: There was a main effect of condition (FA vs. DE) on the change in FEV1 from baseline, and in exercise heart rate. Post hoc tests revealed that exercise-induced bronchodilation was significantly attenuated following DE compared to FA. There were no main effects of condition on 20 km cycling performance, or VO2, VCO2, VE, VT, FB and SpO2 during a 20 km time trial.Conclusion: A 60-min exposure to DE prior to exercise significantly attenuated exercise-induced bronchodilation and significantly increased heart rate during exercise. Pre-exercise exposure to diesel exhaust did not significantly impair 20 km cycling time trial performance.

Contribution of β-adrenergic receptors to exercise-induced bronchodilatation in healthy humans

Exercise in healthy subjects is usually associated with progressive bronchodilatation. Though the decrease in vagal tone is deemed to be the main underlying mechanism, activation of bronchial β2-receptors may constitute an additional cause. To examine the contribution of β2-adrenergic receptors to bronchodilatation during exercise in healthy humans, we studied 15 healthy male volunteers during maximum exercise test at control conditions and after a non-selective β-adrenergic blocker (carvedilol 12.5mg twice a day until heart rate decreased at least by 10beats/min) and inhaled β2-agonist (albuterol 400μg). Airway caliber was estimated from the partial flow at 40% of control forced vital capacity (V˙part40) and its changes during exercise from the slope of linear regression analysis of V˙part40 values against the corresponding minute ventilation during maximal exercise until exhaustion. At control, V˙part40 increased progressively and significantly with exercise. After albuterol, resting V˙part40 was significantly larger than at control increased but did not further increase during exercise. After carvedilol, V˙part40 was similar to control but its increase with exercise was significantly attenuated. These findings suggest that β2-adrenergic system plays a major role in exercise-induced bronchodilation in healthy subjects.

Effects Of An Aging Pulmonary System On Expiratory Flow Limitation Susceptibility During Exercise In Healthy Women

Aging is associated with a decline in lung function, primarily because of a loss of elastic recoil which acts to reduce maximal expiratory flow rates. Aging related changes in pulmonary function might make older women more susceptible to developing expiratory flow limitation (EFL) relative to their younger counterparts, despite having lower levels of minute ventilation (VE) during exercise. PURPOSE: To determine if there are aging related differences in the susceptibility and severity of EFL during exercise in healthy women. METHODS: Healthy young (YW; n=8; 29±7 (20-39) yrs) and old (OW; n=8; 64±3 (60-68) yrs) women participated in this study and were matched for %predicted forced vital capacity (115±5 vs. 122±14 %, respectively, P>0.05) and forced expiratory volume in 1 second (104±7 vs. 108±20 %, respectively, P>0.05). EFL was calculated as the percent overlap between tidal flow-volume loops during maximal exercise and the maximal expiratory flow-volume (MEFV) curve. The MEFV curve was generated by having subjects perform several expirations from total lung capacity to residual volume at different efforts before and after exercise to account for both thoracic gas compression and exercise-induced bronchodilation. RESULTS: Maximal O2 consumption was lower in the OW (29.4±3.6 ml·kg-1·min-1) compared to the YW (49.1±8.9 ml·kg-1·min-1, P<0.05). Maximal VE during exercise was also lower in the OW (73.7±18.4 l·min-1) compared to the YW (108.7±14.1 l·min-1, P<0.05). EFL at maximal exercise was present in 2 of 8 YW (25%) and in 5 of 8 OW (63%). There were no differences in the magnitude of EFL between OW (23±24 (0-69) %EFL) and YW (9±18 (0-46) %EFL, P>0.05). The magnitude of EFL in OW appeared to be inversely related to %predicted forced vital capacity (r=-0.70, P=0.05). CONCLUSION: OW tend to be more susceptible to EFL than YW despite having lower levels of VE during exercise. Funding by: BC Lung Association and NSERC

Effect of Albuterol on Maximal Exercise Capacity in Cystic Fibrosis

Inhaled, short-acting beta-adrenergic agonists (SAbetaAs) are widely prescribed in cystic fibrosis (CF) subjects, despite a lack of convincing data for efficacy and the potential for these agents to result in airway instability. We tested the hypothesis that inhaled albuterol would improve maximal exercise performance in CF subjects with airflow obstruction, as a result of acute bronchodilation. Randomized, double-blind, placebo-controlled crossover study of the effect of inhaled albuterol on maximal exercise performance in 20 stable adult CF patients (mean +/- SD age, 23.3 +/- 6.1 years; FEV(1), 57.65 +/- 17.13% of predicted). Ventilatory limitation to exercise was demonstrated in 16 subjects (80%). Significant bronchodilation occurred with exercise alone (end-exercise FEV(1), 2.24 +/- 0.8 L; vs preexercise FEV(1), 2.09 +/- 0.77 L; p < 0.0001), but albuterol resulted in significantly greater exercise-induced bronchodilation than placebo (change in FEV(1), 0.3 +/- 0.15 L vs 0.15 +/- 0.11 L; 95% confidence interval [CI], + 0.07 to + 0.23; p < 0.001). However, there was no difference in maximal workload achieved (albuterol, 158 +/- 46 W; vs placebo, 158 +/- 45 W; 95% CI, - 4.41 to + 4.71; p = 0.95), nor any other measure of exercise performance including maximal oxygen uptake. Despite causing significant acute bronchodilation, inhaled albuterol did not improve maximal exercise performance in ventilatory-limited CF adults, adding to the body of literature that fails to show any clinical benefit of SAbetaAs in CF subjects. The current results provide further evidence to question the widespread use of these agents, although the potential for adrenergic beta-agonists to instead improve submaximal exercise performance merits further investigation.

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).

COPD exercise-induced bronchodilation

COPD exercise-induced bronchodilation

981-53 Impaired Ventilatory Adaptations to Submaximal Exercise in Patients with Chronic Heart Failure

The physiologic determinants limiting maximal exercise performance in patients with congestive heart failure (CHF) have not been completely characterized. Cardiac, peripheral, and ventilatory responses to exercise are attenuated in patients with CHF. While ventilatory factors are not believed to limit maximal exercise, several abnormalities of pulmonary function have been documented. Maximal voluntary ventilation (MVV) is a brief hyperventilatory maneuver that is usually performed at rest. We hypothesized that this maneuver performed during exercise could further elucidate exercise-induced pulmonary abnormalities in patients with CHF. Accordingly, MVV (in L/min, determined by a 12-second maximal hyperventilatory effort) was measured at rest and during 10 minutes of submaximal bicycle exercise (at 55% of a previously determined maximal effort) in 9 normal subjects (NL) and 9 patients with CHF (mean EF 0.23). VO 2 max Peak V E Rest MVV Exercise MVV NL 38.3 ± 7.1 132 ± 32 175 ± 42 193 ± 36 CHF 15.4 ± 1.9 * 73 ± 13 * 143 ± 28 143 ± 25 * Peak V E = peak ventilation during maximal exercise * P &lt; 0.05. CHF vs normals Although ventilatory factors did not appear to limit exercise (since MVV &gt;&gt; peak V E in both NL and CHF), MVV increased during submaximal exercise only in normal subjects but not in patients with CHF (+ 11% vs +0%, P &lt; 0.05). The exercise-induced increase in MW in normal subjects may represent an adaptive response to exercise related to exercise-induced bronchodilation or sympathetic stimulation of the diaphragm. These mechanisms may be attenuated in CHF secondary to bronchial edema from high left ventricular filling pressures, or due to intrinsic diaphragmatic muscle abnormalities. The absence of normal ventilatory adaptations to exercise may contribute to exercise intolerance in patients with CHF

Exercise-induced Bronchodilation in Asthma

Of 34 symptomatic adult asthmatic patients (23 men) aged 51 +/- 13 years (mean +/- 1 SD) with moderately severe airways obstruction who underwent maximal exercise testing at room temperature (22 degrees C) and humidity (44 percent RH) using a bicycle ergometer, we identified seven male patients aged 56 +/- 9 years in whom forced expired volume in one second (FEV1) increased greater than or equal to 20 percent over the baseline pre-exercise value (exercise-induced bronchodilation). At maximal exercise, these patients achieved an O2 consumption of 1.4 +/- 0.4 L/min and a minute ventilation of 56 +/- 9 L/min. Baseline FEV1 was 1.3 +/- 0.5 L (SD) (43 +/- 12 percent predicted) and increased to 2.1 +/- 0.5 L at five minutes after exercise and persisted at least 20 minutes. Exercise was repeated in all seven patients on a separate day one to six months later, and results were similar in six. In these seven patients, three minutes of voluntary isocapnic hyperventilation achieving a minute ventilation comparable to that during maximal exercise led to an increase in FEV1 of 20 +/- 18 percent (range 0 to 54 percent). The Vmax50 was 22 +/- 30 percent before, and 10 +/- 21 percent after maximal exercise and 25 +/- 37 percent before, and 11 +/- 22 percent after isocapnic hyperventilation. Pre-treatment with acetylsalicylic acid (mean serum concentration 120 +/- 64 micrograms/ml) in the six patients with reproducible bronchodilation completely blocked exercise bronchodilation in one patient and blunted it in four others. Findings suggest that a subset of adult patients with symptomatic asthma may develop bronchodilation after six to eight minutes of exercise, that exercise-induced bronchodilation may in part be reproduced with isocapnic hyperventilation, and that it may be blocked completely or partially by acetylsalicylic acid, implying mediation by prostaglandins.

Airway response in asthmatic children during and after exercise.

This study investigated the effect of moderate treadmill exercise on the airways of normal and asthmatic children using an effort-independent method (total respiratory resistance) as well as conventional pulmonary functions. Changes in total respiratory resistance (Rrs) were measured during and after exercise using a forced oscillation technique. Conventional spirometric (PEFR, FEV1 and MMEF) and body plethysmographic measurements (Raw, Vtg) were also determined before and after exercise. A rapid, signigicant decrease in Rrs, suggesting bronchodilation during exercise, was observed in both groups tested, but this decrease was greater in normal children than in asthmatic patients. The bronchodilation persisted throughout the exercise period in both the asthmatic and the normal children. Increasing the length of the exercise from 10 to 20 min did not alter the degree or the duration of exercise-induced bronchodilation. In both normal children and patients with bronchial asthma, during moderate treadmill exercice, a significant, persistent bronchodilation can be detected. At the end of exercise, bronchoconstriction developed in asthmatic patients, while the values in normal subjects returned to their preexercise levels.