Variable airway function is a central feature of the asthmatic condition. Asthmatics thus exhibit daily and seasonal variation in airway inflammation, airways hyperresponsiveness (AHR), pulmonary function, and clinical symptoms (8,14,17). Exposure to a variety of immunological triggers such as pollens, pet dander, mold, and dust mites instigate airway inflammation, airway smooth muscle contraction, and worsened airway function. Several other nonimmunological triggers exist as well, including the inhalation of cold/dry air, exposure to environmental pollutants, and whole-body exercise. Importantly, AHR demonstrates seasonal variability and fluctuates with variations in environmental allergen concentrations, and in some asthmatics, AHR regularly varies during the course of 24 h (8,20). For all of these reasons, habitually active asthmatics are certain to exercise under conditions of variable airway (dys)function. The influences of this variable airway function on the responses to whole-body exercise are not known.
Regular exercise is a generally recommended therapeutic modality in patients with asthma (23,32,34). These recommendations are partially informed by studies demonstrating improved aerobic capacity with training and unchanged pulmonary function and exercise-induced bronchoconstriction (EIB) over time with training; pulmonary function and EIB neither worsen nor improve with training (34,40). Very few studies, however, have examined relationships between baseline airway function and exercise ventilation in the asthmatic. This is an important gap in the literature, as the variable airway function in asthma may interact with the exercise ventilatory response. This contrasts sharply with nonasthmatic persons, in which airway function is consistent on a day-to-day basis. Furthermore, most studies assessing responses to exercise in asthmatic subjects have not included comparisons with nonasthmatic control subjects. In general, the most meaningful insight into the physiological responses to exercise in a patient population can only be gleaned through comparisons with nondiseased control subjects. Improved understanding of the relationships between baseline airway function and exercise ventilation in the asthmatic (and compared with nonasthmatic counterparts) will help to inform exercise recommendations for this large clinical population.
It is reasonable to postulate a relationship between baseline airway function and exercise ventilation in the asthmatic. For example, preexercise bronchodilation might be expected to allow for increased exercise ventilation in the asthmatic. However, studies have consistently demonstrated an unchanged exercise ventilation after bronchodilation in asthmatic subjects (11,18,35,36). Conversely, a small number of investigations have experimentally worsened airway function before exercise in asthmatic subjects. In one experimental approach, exercise is preceded by the induction of airway narrowing via osmotic stress, including the inhalation of hypertonic saline (5) or voluntary eucapnic hyperpnea (6) or the inhalation of the bronchoconstrictor histamine (13). These studies, however, were not designed to carefully assess the effects of preexercise bronchoconstriction on ventilation during exercise, focusing instead on postexercise airway function in the asthmatic. Thus, the role of preexercise bronchoconstriction on ventilation during exercise in the asthmatic remains unknown.
The purpose of this study was to determine the effects of both improved and worsened preexercise airway mechanical function on the ventilatory responses to whole-body exercise in asthmatic adults as well as healthy controls. We hypothesized that exercise ventilation would be similar despite variable preexercise airway function in asthmatic subjects.
METHODS
Subject Selection
Adult male and female asthmatic and nonasthmatic subjects were recruited through advertisements in local newspapers and by flyers posted on the Johnson State College campus and within the local community. Before participation, subjects were fully informed of the procedures, risks, and benefits of the study, and written informed consent was obtained. The experiments described in this proposal were approved by the Johnson State College institutional review board for research involving human subjects.
All participants were between the ages of 18 and 45 yr, had a negative history for cardiovascular disease and other chronic illness (excepting asthma), were nonsmokers, and had an absence of respiratory infection during the 6 wk before participation. Asthmatic subjects were limited to those with mild disease that was controlled or partly controlled, as defined by the Global Initiative for Asthma (12). Asthmatic subjects currently taking inhaled or oral steroids were excluded from participation, as were those who had attended the emergency room for an asthma exacerbation during the previous 3 yr. All subjects completed two separate screening studies on different days to determine eligibility for participation as an asthmatic or nonasthmatic subject.
Screening Studies
Exercise-induced bronchospasm
All subjects completed an incremental exercise test to exhaustion. The inspirate consisted of dry air from a compressed gas tank (FIO2, 0.21, balance nitrogen). Pulmonary function was assessed before exercise and at 5, 10, 15, 20, and 30 min after exercise.
Bronchodilator reversibility
After baseline pulmonary function tests (PFT), subjects inhaled four actuations of a fast-acting β2-agonist. For each actuation, subjects exhaled to residual volume, depressed the actuator, inhaled slowly through a chamber (aerovent) to total lung capacity, and held their breath for 3–5 s before exhaling. Pulmonary function was assessed at several time points after β2-agonist inhalation.
Participants meeting at least one of the following two criteria were classified as asthmatic subjects: 1) ≥12% decrease in forced expiratory volume 1.0 s (FEV1.0) after the incremental exercise test to exhaustion and 2) ≥12% increase in FEV1.0 after the inhalation of the fast-acting β2-agonist.
Experimental design
All subjects completed four separate exercise studies with four different preexercise interventions. The interventions included 1) four actuations of a fast-acting β2-agonist to improve airway function, 2) a eucapnic voluntary hyperpnea challenge to worsen airway function, 3) a sham to the hyperpnea, and 4) a control trial. The order of experimental interventions for each subject was randomized, and intervention order was balanced among subjects within the control and the asthmatic groups. After each intervention, subjects completed an exercise bout on a magnetized cycle ergometer. Subjects were instructed to refrain from ingesting caffeine for 8 h before each study and inhaled β2-agonist for 12 h before each study.
Experimental interventions
All subjects completed four separate exercise challenges preceded by a different intervention, as follows.
B2-agonist [bronchodilation (BD)]
After baseline (BL) PFT, subjects inhaled four actuations of a fast-acting β2-agonist. Pulmonary function was assessed at 5 and 10 min after inhalation (postintervention [PI]). Exercise was commenced at 15 min after inhalation, corresponding closely with the time of maximal bronchodilation.
Eucapnic voluntary hyperpnea [bronchoconstriction (BC)]
The eucapnic voluntary hyperpnea (EVH) challenge was completed in accordance with the methods described by Anderson and Brannan (2). Briefly, subjects ventilated dry, compressed gas consisting of 21% O2 and 5% CO2 at a ventilation rate equal to FEV1.0 ×30. Pulmonary function was performed at 5 and 10 min after the challenge. Exercise was commenced 15 min after EVH, closely corresponding with the time of maximal airway narrowing.
Hyperpnea sham (SHAM)
A sham trial was used to control for subject expectation effects or behavioral responses to the EVH protocol. Using the same apparatus used for the EVH challenge, subjects were instructed to breathe in a normal, relaxed manner. Subjects inhaled room air during this trial; however, they were told that they were breathing air from the tank of compressed gas. The Douglas bag was filled with gas before the study, and laboratory personnel mimicked adjustment of a three-way valve and briefly opened the nozzle on the tank occasionally during the experiment. Pulmonary function was assessed at 5 and 10 min after the protocol, after which time exercise was commenced.
Control (CON)
After baseline PFT, subjects rested in a comfortable, seated position for 10 min. Pulmonary function was reassessed and followed immediately by the exercise test.
Pulmonary function
PFTs were completed with a Medgraphics automated spirometer. All PFTs were completed in the seated, upright position according to recommendations by the American Thoracic Society and European Respiratory Society (29). During each measurement, subjects completed maximal volitional flow-volume maneuvers for the determination of peak expiratory flow, forced vital capacity (FVC), forced expiratory volume 1.0 s (FEV1.0), and forced expiratory flow at 50% of FVC (FEF50%). Slow vital capacities were performed for the determination of inspiratory capacity (IC). Predicted values are from Quanjer et al. (33).
Exercise apparatus
All exercise was completed on a magnetically braked cycle ergometer (Velotron, Seattle, WA). Subjects breathed through a two-way, nonrebreathing valve (Hans-Rudolph) with noseclips in place. Compressed gas (21% O2, balance nitrogen) was used as the inspirate for all exercise studies in both asthmatic and nonasthmatic subjects. Separate pneumotachographs (Hans Rudolph; Shawnee, KS) were used to determine inspiratory and expiratory flow rates. Separate oxygen and carbon dioxide gas analyzers (AEI Technologies; Columbus, IN) were used to analyze expired gases. A Powerlab 16-channel data acquisition system (ADInstruments; Dunedin, New Zealand) interfaced with a laptop computer was used to collect resting and exercise data.
Exercise protocol
Before exercise, subjects performed multiple IC maneuvers and several maximal volitional flow-volume loops. After resting data collection, subjects completed 3 min of exercise at a workload equal to 70% of the peak workload achieved during the maximal exercise test (WU). Exercise workload was then increased to 85% of peak workload and was continued to volitional exhaustion (prolonged). ICs were performed during WU and at regular intervals during prolonged exercise.
Exercise measurements
Inspired and expired airflow rates and expired gases were used to calculate oxygen consumption (V˙O2) and carbon dioxide production (V˙CO2), minute ventilation (V˙E), tidal volume (VT), breathing frequency (fb), and IC. A Polar heart rate monitor (Polar Electro, Lake Success, NY) was used to record heart rate during exercise. A modified Borg scale (0–10) was used to rate perceived exertion for both breathing and leg discomfort.
Statistical analysis
A three-factor [group (asthma vs nonasthma) × trial (control, β2-agonist, hyperpnea, and sham) × time (exercise time)] repeated-measures ANOVA was used to analyze the exercise responses. When significant main effects were found, Bonferroni-corrected multiple pairwise comparisons were used for post hoc analysis. Linear regression was used to analyze relationships between selected variables. Tabular data are presented as mean ± SD. Data in figures are presented as mean ± SEM. Significance was set at α < 0.05. The statistical software program SYSTAT was used to analyze all data (SYSTAT 12 San Jose, CA).
RESULTS
Group characteristics
Group descriptive characteristics and results from the screening studies are shown in Table 1. There were no differences in age, height, weight, V˙O2peak, or exercise peak power output between control and asthmatic subjects. The baseline pulmonary function and the change in FEV1.0 after both bronchodilator and incremental exercise were significantly different between asthmatic and control subjects. Thus, the two groups were well matched for anthropometric characteristics and exercise capacity, but AHR was only present in asthmatic subjects. Of the eight asthmatic subjects, six were prescribed an inhaled β-agonist on an as needed basis.
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TABLE 1: Descriptive characteristics for control and asthmatic subjects.
Pulmonary function
Group mean results for FEV1.0 and FEF50% at baseline (i.e., upon arrival to lab) and after each intervention (PI) in control and asthmatic subjects are shown in Figure 1. Overall, FEV1.0 and FEF50% were lower in asthmatic compared with control subjects. In asthmatic subjects, EVH caused a decrease of 1.0 ± 0.6 (−27% ± 15%) and 1.7 ± 0.8 (−43% ± 13%) L in FEV1.0 and FEF50%, respectively. Moreover, PI values for FEV1.0 and FEF50% were 1.3 ± 0.8 L (+57% ± 47%) and 2.3 ± 0.8 L (+209% ± 237%) higher during BD compared with BC in asthmatic subjects. These differences were not seen in control subjects. Results for peak expiratory flow were very similar to FEV1.0 and FEF50% (data not shown). However, there were no significant differences in FVC between the control and the asthmatic groups or within either group (data not shown). Thus, airway function was markedly different upon exercise commencement among the four experimental trials in asthmatic subjects.
FIGURE 1: Forced expiratory volume 1.0 s (FEV1.0) and forced expiratory flow at 50% forced vital capacity (FEF50%) in control and asthmatic subjects at baseline and after an intervention during four experimental trials: control, bronchodilation (BD), sham (SHAM), and bronchoconstriction (BC). A, FEV1.0 at baseline and after each of four interventions in control subjects. B, FEV1.0 at baseline and after each of four interventions in asthmatic subjects. C, FEF50% at baseline and after each of four interventions in control subjects. D, FEF50% at baseline and after each of four interventions in asthmatic subjects. Note that FEV1.0 and FEF50% were lower in asthmatic subjects compared with control subjects. Also, note the marked changes in FEV1.0 and FEF50% after BD and BC in asthmatic subjects. *P < 0.05 vs control group; †P < 0.05 vs baseline; aP < 0.05 vs CON trial; bP < 0.05 vs BD trial; cP < 0.05 vs SHAM trial.
Exercise workload and time
All subjects in both groups exercised at 70% (WU) and 85% (prolonged) of their individual peak workload attained during a maximal incremental exercise test. Workload during WU (control group = 177 ± 34 W, asthma group = 180 ± 39 W) and prolonged exercise (control group = 220 ± 42 W, asthma group = 225 ± 46 W) was not different between control and asthmatic subjects. In control subjects, exercise time to exhaustion was 8.0 ± 2.9, 7.4 ± 2.7, 7.7 ± 2.0, and 8.3 ± 2.9 min during CON, BD, SHAM, and BC trials, respectively (P > 0.05). In asthmatic subjects, time to exhaustion was 5.6 ± 1.3, 6.0 ± 2.3, 5.4 ± 1.4, and 5.5 ± 2.5 min during CON, BD, SHAM, and BC, respectively (P > 0.05). Group mean exercise time was not different between control and asthmatic subjects among any of the four trials (Bonferroni adjusted P values: control trial, P = 0.177; BD trial, P = 1.0; SHAM trial, P = 0.214; BC trial, P = 0.073).
Exercise ventilation
Results for V˙E, VT, fb, and the ventilatory equivalent for CO2 production (V˙E/V˙CO2) are shown in Figure 2. Within both control and asthmatic subjects, there were no differences among trials for any of the ventilatory variables. Moreover, there were no differences between control and asthmatic subjects for any of the variables among the four experimental trials. Figure 3 depicts the relationship between PI FEV1.0 and exercise V˙E/V˙CO2 in control and asthmatic subjects. In both control and asthmatic subjects, there was no relationship between PI FEV1.0 and exercise V˙E/V˙CO2. These results highlight the dissociation between baseline airway function and exercise ventilation in control and asthmatic subjects.
FIGURE 2: Ventilatory variables at rest, during warm-up exercise (WU), during exercise to exhaustion (1 min, 3 min, and end exercise) and 3 min after exercise (Rec) in control and asthmatic subjects during four experimental trials. Control group results are shown in A, C, E, and G. Asthma group results are shown in B, D, F, and H. There were no significant differences for any variable within either the control or the asthmatic group. Moreover, there were no significant differences between control and asthmatic subjects for any of the variables.
FIGURE 3: Correlations between postintervention forced expiratory volume 1.0 s (FEV1.0) and exercise ventilatory equivalent for CO2 production (V˙E/V˙CO2) in control (dark symbols) and asthmatic (open symbols) subjects. There was no relationship between postintervention FEV1.0 and V˙E/V˙CO2 in either control or asthmatic subjects. Circles, control trial; squares, bronchodilation trial; diamonds, sham trial; triangles, bronchoconstriction trial.
Exercise lung volumes
Results for IC and VT/IC are shown in Figure 4. There were no significant differences in IC or VT/IC either within or between control and asthmatic subjects. In control subjects, IC exhibited the usual intensity- and time-dependent increase during exercise and exhibited a plateau at the end of exercise. In asthmatic subjects, a significant main effect of exercise trial was found, but Bonferroni-corrected pairwise comparisons were not significant. In asthmatic subjects, results for IC were similar during CON, BD, and SHAM, during which IC increased during WU but, thereafter, demonstrated a decreasing trend throughout prolonged exercise to approach resting values by end exercise. During BC, the IC after intervention was, on average, 0.6 ± 0.3 L lower than the other three trials (P > 0.05). During exercise, however, IC increased so that it equaled the other three trials by the end of exercise.
FIGURE 4: Inspiratory capacity (IC) and ratio of tidal volume to IC (V T/IC) at rest, during warm-up exercise (WU), and during exercise to exhaustion (1 min, 3 min, and end) during four experimental trials in control (A and C) and asthmatic (B and D) subjects. In control subjects, IC and V T/IC exhibited a similar pattern during all four trials. In asthmatic subjects, note the lower IC at rest and early during exercise during the bronchoconstriction trial compared with the other three trials. Also, note that IC decreased during exercise in asthmatic but not in control subjects. There were no significant differences.
Other exercise responses
In Table 2, group mean values for V˙O2, V˙E/V˙O2, HR, RPE-breath, and RPE-leg are shown for control and asthmatic subjects. In general, values for these variables were not different among the four trials within either subject group. Moreover, there were no significant differences between control and asthmatic subjects for any of the variables at any time point among the four exercise trials.
TABLE 2: Physiological variables measured at baseline, during warm-up exercise, and during exercise to exhaustion in control and asthmatic subjects.
DISCUSSION
We sought to determine the effects of variable preexercise airway function on the ventilatory responses to whole-body exercise in asthmatic adults. Moreover, all studies were completed by a control group of nonasthmatic subjects. We hypothesized that exercise ventilation would be similar despite variable preexercise airway function in asthmatic subjects. Indeed, despite markedly different preexercise pulmonary function in asthmatic subjects, exercise ventilation was nearly identical among the four trials. Furthermore, there were no differences in exercise ventilation between control and asthmatic subjects among any of the four trials. These results demonstrate a robust pulmonary system in the mild asthmatic, one that is apparently capable of adequately responding to the acute demand for increased airflow necessitated by high-intensity aerobic exercise. From a clinical standpoint, these findings support the idea that regular exercise may be beneficial for the asthmatic (24,28).
Exercise workload
The exercise intensity was set at 85% of the peak workrate achieved during an incremental exercise test to exhaustion. This demanding exercise workload was both high enough to challenge the capacity of the pulmonary system for generating airflow—reflecting the contractile properties of the respiratory muscles and the airway structural and parenchymal determinants of airflow—but also low enough so that subjects were able to exercise for a duration sufficient to address the purpose of this study. A workload either higher or lower than this would not have met these criteria. In addition, the exercise workload in this study is very similar to the workload generally used in studies evaluating EIB.
Preexercise pulmonary function
In the current study, pulmonary function was used as an indication of the overall state of airway function before exercise. To this end, the decreased forced expiratory flow rates before exercise during BC and the increased flow rates during BD indicate markedly different states of airway function before the exercise in asthmatic subjects (Figs. 1B and 1D). Thus, at the onset of exercise during BC, the capacity for generating airflow was severely compromised. Nonetheless, this markedly disparate preexercise airflow generating capacity had no effect on the exercise ventilatory response.
In control subjects, pulmonary function increased slightly after bronchodilator and decreased slightly after EVH. In both cases, the changes from BL were statistically significant. Interestingly, pulmonary function also decreased slightly but significantly between BL and PI during both CON and SHAM trials. Thus, the tendency for pulmonary function to decrease with multiple efforts in asthmatics (i.e., spirometry-induced bronchospasm) may also be the case for nonasthmatic subjects (16). We also note that although the magnitude of decrease in pulmonary function during CON and SHAM was less in nonasthmatics, the greater uniformity of response actually resulted in more statistical significance. These findings exemplify the conundrum of distinguishing between statistical versus physiological significance in human biology. These findings also highlight the fact that both between- and within-subject variability in pulmonary function—and likely other measures of physiologic functioning—will always be greater in a group of asthmatics compared with nonasthmatic counterparts. Given the variability in airway inflammation, AHR, and lung function in the asthmatic, this is not surprising.
Exercise ventilation
To the best of our knowledge, only one previous study has assessed exercise ventilation after both improved (via metaproterenol) and worsened (via methacholine) airway mechanical function in asthmatic subjects (26). Mahler et al. reported reduced VT and V˙E at peak exercise after methacholine challenge compared with a control trial and preexercise bronchodilation in adults with reversible obstructive airway disease. In the current study, exercise ventilation was not affected by variable preexercise airway mechanical function. There are several differences between the current study and the study by Mahler et al. Most notably, subjects in the study by Mahler were both older and had more severe airways obstruction than our subjects. Second, the methods for inducing bronchoconstriction are very different between the two studies. In one case, a direct-acting bronchiolar smooth muscle agonist was used (i.e., cholinergic agonist, methacholine), whereas in the current study airway narrowing was induced by the indirect inflammatory effects of dry gas hyperpnea.
Although airway resistance is determined by interactions among several variables, it is most sensitive to changes in airway radius (9). Considering this importance of airway diameter in determining airflow, it is reasonable to posit a relationship between baseline airway function and exercise ventilation. Evidence that supports this hypothesis, however, is limited. Previous investigations have assessed the effects of preexercise bronchodilation on exercise ventilation and exercise capacity in asthmatic adults (11,18,35–37). In all of these studies, preexercise bronchodilation had no effect on exercise ventilation as compared with control and placebo conditions. In fact, the airways of asthmatic subjects undergo an initial bronchodilation during whole-body exercise (4,10,15,38). Thus, the natural bronchodilation with exercise may obviate the potential for altered airway function—whether improved or impaired—to influence exercise ventilation. An interesting experiment would be to prevent bronchodilation during exercise in asthmatic subjects. Presumably, this would be difficult, however, as exercise bronchodilation still occurs when the bronchoconstrictors histamine and methacholine are inhaled during exercise in the asthmatic (19,38). A gradual bronchoconstriction can occur over time during moderate intensity exercise lasting longer than ∼10 min (4,21), but the effects of this gradual bronchoconstriction on exercise ventilation and performance have not been studied.
In this study, subjects exercised after 6 min of voluntary eucapnic hyperpnea. Voluntary hyperpnea stimulates the release of inflammatory mediators from resident (i.e., epithelial) and nonresident (i.e., mast cells) airway cells (1,22). In the asthmatic, this nonspecific stimulus causes bronchiolar smooth muscle contraction, plasma exudation, airway wall edema, and mucus secretion into the airways. The stimulus for this inflammatory-based airway narrowing with voluntary hyperpnea is thought to be identical to the osmotically based stimulus for airway narrowing after whole-body exercise. In this study, subjects began exercise within 15 min after the EVH challenge, well before airway narrowing and inflammation had resolved.
A major finding of this study is that exercise ventilation was not affected by the poor airway function before exercise. In previous studies, asthmatic subjects have exercised after a variety of procedures that cause airway narrowing, including inhaled histamine, aerosolized hypertonic saline, methacholine, and EVH (5,6,13,25). The purpose of these investigations, however, was to study bronchoconstriction after exercise, and analyses of exercise ventilation were minimal. Moreover, exercise was not commenced until pulmonary function had returned, or nearly returned, to baseline values; exercise began between 30 min and 6 h after the preexercise challenge. In the current study, exercise was commenced within 10–15 min of the EVH challenge, when FEV1.0 was still significantly reduced by the challenge.
In one previous study, asthmatic subjects completed an exercise challenge during the midst of a spontaneous asthma attack and also during a late asthmatic reaction to inhaled allergen (10). Exercise ventilation and V˙O2peak were preserved during both exercise conditions. In a different study, exercise ventilation was compared between two exercise bouts in which pulmonary function preceding the second bout was decreased compared with the first (15). Exercise ventilation during the second bout was identical with the first bout. The current findings support and extend these observations.
Exercise lung volumes
There were no statistically significant differences in operating lung volumes in either control or asthmatic subjects. In asthmatic subjects, the average 0.6-L difference in preexercise IC between BC and the other three trials, although not statistically significant, is certainly of some physiological significance. This finding is in agreement with other studies demonstrating a decreased IC with bronchoconstriction in asthmatic subjects (31,39). An increased end-expiratory lung volume (i.e., dynamic hyperinflation) with bronchoconstriction likely represents a compensatory response to increase airway diameter or reduce airway closure due to interdependence between the airways and lung parenchyma (7). Importantly, the decreased preexercise IC during BC was not maintained during exercise, as exercise IC increased progressively to equal the values seen during the other three trials by end exercise. The slight differences in resting VT/IC between BC and the other trials also disappeared during exercise. Collectively, these results demonstrate a robustly “agile” pulmonary system in the asthmatic, with a wonderful ability to respond to the requirement for increased airflow during exercise.
Perceptual responses during exercise
Despite the differences in preexercise airway function among trials in asthmatic subjects, both breathing and leg discomfort were the same during all four exercise trials. Perhaps most interesting is the unchanged RPE-breath after EVH. Intuitively, breathing discomfort would be expected to increase after bronchoconstriction. In asthmatic subjects at rest, however, the relationships between airway function and perception of breathlessness are unclear (30). In one study, preexercise bronchoconstriction via methacholine did cause an increased intercept for the relationship between exercise workrate and RPE-breath (26). In the same study, however, there were no changes in slope or intercept between RPE-breath and all other exercise variables, including flow rate, mouth pressure, breathing frequency, or tidal volume. Perceptual responses to exercise result from a complicated amalgamation of multiple ascending and descending neurohumerol inputs (27). Further investigation is needed to improve our understanding of the determinants of effort perception during exercise and how perception of these determinants may be altered in disorders of the pulmonary system.
Generalizability of findings
The findings in this study are limited to asthmatic adults with primarily mild disease. Subjects were able to increase ventilation during exercise no matter how compromised airway function was before exercise. In asthmatics with more severely inflamed airways or greater degrees of airflow limitation, the ability to increase ventilation during exercise will likely be more limited.
In the current study, exercise consisted of 3 min at 70% peak power output followed by exercise to exhaustion at 85% peak power output. The current findings are thus confined to the high intensity, relatively short duration exercise completed by subjects in this study. There are a variety of bronchodilatory and bronchconstricting factors that interact to determine airway caliber during exercise in the asthmatic (3), and the balance of these factors will vary depending on exercise duration and intensity. For example, bronchoconstriction can occur during submaximal exercise lasting 10 min or longer and also during variable intensity exercise when exercise workload is decreased (4,21). The current findings of unchanged exercise ventilation despite altered preexercise airway function should not be generalized to all intensities and durations of aerobic exercise. Further studies will be necessary to determine the relationships among airway function, exercise ventilation, and exercise workload and duration in asthmatic subjects.
CONCLUSIONS
We evaluated the effects of both improved and worsened airway function on exercise ventilation in asthmatic adults and compared the results with nonasthmatic control subjects. In a group of mild asthmatics, exercise ventilation was not affected by significant alterations in preexercise airway function. Notably, exercise ventilation was nearly indistinguishable between the asthmatic and control subjects. These findings corroborate previous studies demonstrating unchanged exercise ventilation and capacity after preexercise bronchodilation in the asthmatic. Moreover, these results demonstrate a remarkable dissociation between preexercise airway function and the exercise ventilatory response in the mildly asthmatic adult. These findings also contrast with the general notion that baseline airway function influences exercise ventilation in the asthmatic.
This study was supported by the Vermont Genetics Network (grant no. 8P20GM103449) from the INBRE Program of the National Institute of General Medical Sciences (NIGMS) and the National Center for Research Resources (NCRR), components of the National Institutes of Health (NIH). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of NIGMS or NIH.
The authors declare no conflict of interest.
The results of this manuscript do not constitute endorsement by the American College of Sports Medicine.
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