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J Appl Physiol 87: 1697-1704, 1999;
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Vol. 87, Issue 5, 1697-1704, November 1999

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

Riccardo Pellegrino, Carlo Villosio, Ugo Milanese, Giuseppe Garelli, Joseph R. Rodarte, and Vito Brusasco

Fisiopatologia Respiratoria e Cardiologia, Azienda Ospedaliera S. Croce e Carle, 12100 Cuneo, Italy; Servizio di Anestesia e Rianimazione, Ospedale Civile, 12037 Saluzzo, Italy; Pulmonary Section, Baylor College of Medicine, Houston, Texas 77030; and Cattedra di Fisiopatologia Respiratoria, Dipartimento di Scienze Motorie e Riabilitative, Università di Genova, 16132 Genova, Italy


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

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 ~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.

exercise hyperpnea; breathing pattern; functional residual capacity; airflow limitation


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

NORMAL RESPONSE TO EXERCISE in young subjects is initially to drop functional residual capacity (FRC), which may be sustained up to maximum loads (3-5, 10, 17, 26). In middle-aged people with the highest levels of exercise, FRC may return toward the control value (11), thus making ventilation more dependent on respiratory frequency. In contrast, in patients with airflow obstruction FRC drops less and may begin increasing at lower levels of ventilation (3, 5, 9, 12, 18, 19, 21, 23, 27) when tidal expiratory flow encroaches on maximal flow [expiratory flow limitation (EFL)] (3, 5, 12, 18, 21, 27). Even though increasing mean lung volume may be useful in avoiding the sensation of dyspnea associated with breathing in EFL (15, 16), it limits lung excursion [tidal volume (VT)], thus requiring an increase in breathing frequency (f) to maintain minute ventilation (VE) constant.

In the present study we explored the ventilatory pattern during exercise in subjects with mild-to-moderate airflow obstruction after a 2-mo strenuous physical training period during which tidal expiratory flow was limited. We hypothesized that one of two responses might occur: if EFL during training blunts the perception of the respiratory stimuli arising from the airways being dynamically compressed during tidal expiration, then for a given ventilation FRC would decrease during exercise after training, VT would increase, and f would decrease; if the perception of the EFL signal remains intact after training and inspiratory muscles become conditioned, then the subject would increase FRC during exercise to minimize EFL. Therefore, for a given VE, either VT would decrease and f increase compared with before training or VT would remain constant but occur at a higher lung volume.

These hypotheses were tested in a group of eight subjects, in whom a combination of a relatively young age, good physical performance, high motivation, and chronic airflow obstruction of only mild-to-moderate degree allowed them to attain very high levels of physical exercise and training. A group of six healthy individuals with similar anthropometric characteristics served as a control.


    METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Subjects. The study was conducted in eight male subjects with mild-to-moderate and fixed airflow obstruction. Forced expiratory volume in 1 s (FEV1) was 85 ± 14% of predicted, and the ratio of FEV1 to forced vital capacity (FVC) was 68 ± 5%. All individuals were smokers. None of these subjects suffered from respiratory exacerbation in the previous year. Six healthy men represented the control group. All individuals were physically active in recreational activities. The anthropometric and pulmonary function data are shown in Table 1.

                              
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  		Table 1.   Anthropometric and functional pulmonary data at control

Protocol. On the screening day the subjects attended the laboratory for the completion of a clinical history, a physical examination, an electrocardiogram, and spirometry before and 20 min after inhaling salbutamol (200 µg) through a spacer. Flow was measured at the mouth by a screen-type heated pneumotachograph linear up to 16 l/s, coupled to a differential pressure transducer (Jaeger, Würzburg, Germany). Volume was obtained by integrating the flow signal. FEV1 and FVC were measured in triplicate and calculated according to the recommendations of the American Thoracic Society (1). FRC was measured with the subjects sitting in a constant-volume body plethysmograph (Jaeger) and slowly panting against a closed shutter at end-tidal expiration. After the shutter was opened, expiratory reserve volume and inspiratory vital capacity were measured, thus allowing total lung capacity (TLC) to be calculated. Predicted values are from Quanjer et al. (20). Lack of reversibility to bronchodilators was defined as an increment of FEV1 and/or a FVC <12% of predicted (20). The subjects were taught to perform partial forced expiratory maneuvers initiated from end-tidal inspiration and practiced until reproducible results were obtained. All subjects gave informed consent.

On the first study day, the subjects attended the laboratory in the midafternoon after a light meal. Full forced expiratory flow-volume curves were recorded in triplicate through a mass flow sensor (Vmax, SensorMedics, Yorba Linda, CA). Maximum voluntary ventilation (MVV) was measured in duplicate with the same mass flow sensor by asking the subjects to breathe as much as they could for 12 s. Blood pressure and heart rate (HR) were measured. The subjects were familiarized with a modified Borg scale to rate respiratory sensation during exercise. Zero indicated no breathlessness, and 10 indicated intolerable dyspnea. A symptom-limited exercise test was performed on an electronically braked cycle ergometer (Marquette, Hellige, EC560, Milwaukee, WI), with the subject wearing a noseclip and breathing through the mass flow sensor (dead space 75 ml) connected to a saliva trap. A 12-lead electrocardiogram was continuously recorded (Marquette, Hellige, Max Personal). Oxygen uptake (VO2) and carbon dioxide output (VCO2) were measured breath by breath through rapid gas analyzers (Vmax, SensorMedics). Flow was continuously measured during inspiration and expiration and numerically integrated to determine volume. After a 3-min resting measurement and a 2-min warm-up, the workload was increased by 20 W every minute, with the subjects pedaling between 50 and 60 rpm until they could no longer sustain the imposed load.

Tidal and partial forced expiratory flow-volume loops were recorded at least three times at rest and once over the last 15 s of each step during exercise as follows. After four to six regular breaths, the subjects forcefully expired from end-tidal inspiration to near residual volume and then inhaled to TLC. This was necessary to locate tidal and partial flow-volume loops relative to TLC. Inspiratory capacity was defined as the difference between end-tidal expiratory lung volume and TLC and allowed FRC to be calculated at each step of exercise. Partial forced expiratory flows near control FRC were calculated at each step of the test to identify the potential changes in maximal flow during exercise. Special care was taken to maintain the position of the trunk fairly constant during the test. Breathlessness was recorded at control and at the end of each step of the exercise test by the subjects indicating a number on the Borg scale. In 11 individuals who had never attended the laboratory before, a practice exercise test was performed on a separate day. The results of the first test are not reported.

The training program was performed on an automatic cycle ergometer (Bikerace HC600, Technogym, Forlì, Italy), with sessions of 31 min each (including a 3-min warm-up and a 1-min cool-down), three times a week for 2 mo, and at an intensity that produced 80% of the maximum HR recorded during the initial exercise test. The load intensity was gradually adjusted over the first three to four training sessions to attain the desired HR. In the obstructed subjects, this intensity was associated with tidal expiratory flow encroaching on forced expiratory flow measured during a partial maneuver and was taken as an indication of breathing under EFL conditions during training. By contrast, in normal subjects tidal expiratory flow remained less than partial forced flow at control FRC. For all subjects, HR at the training level was well above the ventilatory anaerobic threshold (AT). As AT tends to increase during training, an additional exercise test was performed 1 mo after the beginning of the program to adjust the training intensity according to the new AT. All sessions were supervised by a chest physiotherapist.

All measurements except MVV were repeated at the end of the training period.

Data analysis. Only regular breaths recorded before the partial forced expiratory maneuver were used for analysis of breathing pattern. VT and inspiratory and expiratory times (TI and TE, respectively) were calculated breath by breath and averaged over several breaths. This allowed VE, f, mean inspiratory and expiratory flows [VT-to-TI and -TE ratio (VT/TI and VT/TE, respectively)], and the ratio of TI to total respiratory cycle duration (TT; TI/TT) to be computed. Partial forced expiratory flows were measured at the same absolute lung volume near control FRC before the initial exercise test. AT was determined from gas-exchange measurements (24) and expressed as percent VO2 max.

The relationship between lung hyperinflation and occurrence of EFL during exercise in the obstructed subjects was investigated by linear regression analysis of the changes in FRC (delta FRC) plotted against the differences between tidal and partial forced expiratory flows (delta flow) over five steps of the test for each individual both before and after physical training. Specifically, delta FRC was computed from the difference between FRC measured at the considered steps (40, 60, 80, and 100% VEmax) and its lowest value recorded at the beginning of exercise. Tidal expiratory flow was computed at the same five steps by averaging flow measured at 0.1, 0.5, and 1 liter above FRC over three breaths preceding the forced partial expiratory maneuver. Forced expiratory flow was computed by averaging flows recorded during the forced expiratory maneuver at the same steps and at a constant absolute lung volume corresponding to 0.1, 0.5, and 1 liter above the lowest FRC. Therefore, a positive delta FRC indicates the occurrence of lung hyperinflation during the steps, whereas a negative delta flow means that tidal flow would exceed partial flow if FRC remained constant, and thus indicates occurrence of EFL.

Statistics. Student's unpaired t-test and a chi 2 test with Yates's correction were used to analyze baseline differences between groups. A three-factor ANOVA for repeated measures was used to compare results between and within groups. A Newman-Keuls post hoc test was used for multiple comparisons. P < 0.05 was considered statistically significant. All values are expressed as means ± SD.


    RESULTS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Values for the ratio of FEV1 to FVC in the obstructed individuals were slightly but systematically less than the predicted values. Static lung volumes were similar between groups (Table 1).

Maximum exercise before physical training. Although still in the predicted range, the maximum workload, VO2, and HR were slightly but significantly less in the obstructed than in the normal individuals (Table 2). In general, hyperpnea in both groups was achieved by increasing VT at the beginning of exercise and f toward the end. In the normal subjects, FRC decreased soon after the beginning of exercise, whereas end-inspiratory lung volume (EILV) progressively increased. Figure 1B shows the decrease in FRC and increase in EILV at maximum load compared with control conditions. In two obstructed subjects, FRC increased early in exercise when tidal expiratory flow encroached on maximal flow recorded during the partial forced expiratory maneuver and tended to increase up to a maximum value at the end of exercise (Fig. 1A). In the other six obstructed individuals, FRC decreased and attained the lowest values soon after the beginning of exercise. Then, it slightly increased only when tidal expiratory flow exceeded maximum flow. The average intercept and slope of the linear regression between delta FRC and delta flow calculated for each subject were 0.15 ± 0.15 and -0.14 ± 0.10, respectively. In Fig. 2A, delta FRC is plotted against delta flow for each step of the test in all obstructed subjects. The significant negative correlation (r = -0.59, P < 0.001) shows that, as EFL becomes worse, FRC tends to increase. TI/TT tended to increase slightly more in the normal subjects than in the obstructed individuals. The VEmax-to- maximum VO2 (VO2 max) ratio was not significantly different between obstructed (33.2 ± 4.9) and normal subjects (31.2 ± 3.6), nor was the VEmax-to-maximum VCO2 (VCO2 max) ratio (VEmax/VCO2 max; 29.3 ± 3.3 and 28.7 ± 2.9, respectively). Breathlessness sensation was similar in both groups. Ventilatory AT was similar in both groups.

                              
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  		Table 2.   Respiratory and cardiovascular variables at maximum exercise workload before and after physical training



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  		Fig. 1.   Tidal and partial flow-volume curves at control (dashed lines) and at last step of exercise (solid lines) in an obstructed (A) and normal subject (B). Total lung capacity is at intersection of x- and y-axes. At control conditions, partial expiratory flow is greater than tidal flow in both subjects. During exercise, functional residual capacity (FRC) decreases in normal subject and tidal expiratory flow never attains partial flow. In contrast, FRC increases above control value in obstructed subject, and tidal expiratory flow exceeds maximum flow. Note increase in forced expiratory flow near control FRC at end of test.



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  		Fig. 2.   Relationship between absolute changes in FRC (delta FRC) above lowest value attained at beginning of exercise and absolute differences between tidal and partial expiratory flows measured over 5 steps of test in each of 8 obstructed subjects before (A) and after physical training (B). Symbols represent individual subjects. On both occasions, linear regression analysis showed significant correlation (r = -0.55 and -0.6, respectively; P < 0.001).

There was an increase in partial flow near control FRC during exercise that was close to significance and similar in both groups (Table 3), thus suggesting progressive bronchodilatation.

                              
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  		Table 3.   Isovolume partial forced expiratory flows at rest and maximum exercise performed before and after training

Maximum exercise after physical training. Exercise performance improved in both groups, as suggested by significant increments in maximum workload, VO2 max, and VEmax and no changes in HR. TI/TT tended to increase in the obstructed subjects while remaining constant in the normal subjects. Also, AT significantly increased in all subjects of both groups. VEmax/VO2 max was similar to before-training values in both obstructed (33.5 ± 4.9) and normal subjects (31.1 ± 3.6), and so was VEmax/VCO2 max (30.4 ± 3.8 and 29.2 ± 3.8, respectively). No significant relationship was found between the increase in VO2 max and control FEV1. Partial flow at the same pretraining lung volume increased in both groups by a magnitude similar to that before training (P < 0.05) (Table 3).

Breathing responses to exercise before and after training are presented in Table 4. In particular, opposite changes between groups occurred in FRC, VT, and f at similar levels of VE (Fig. 3). In the obstructed individuals, delta FRC was negatively correlated with delta EFL (r = -0.67, P < 0.001) (Fig. 2B). In addition, whereas the average intercept of the linear regressions computed for each subject was similar to that before training (0.16 ± 0.16), the average slope was significantly increased (-0.30 ± 0.16, P < 0.01). Taken together, these data suggest that lung hyperinflation is likely regulated by EFL and that experiencing the latter for a relatively long time may lead to prompter reaction to the stimuli arising from the airways undergoing EFL. EILV remained stable, so that VT decreased and f increased for any given VE. TI/TT, VT/TI, and VT/TE remained similar to values before training. In the normal individuals FRC tended to decrease after training from the beginning of the test. EILV remained stable; thus VT increased and f decreased for any given VE. The Borg score was unchanged for similar VE levels of exercise in both groups.

                              
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  		Table 4.   Respiratory and cardiovascular variables at similar control VE before and after training in obstructed and normal subjects



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  		Fig. 3.   Changes in tidal volume (VT; A), breathing frequency (f; B), and FRC (C) with physical training at rest and at 40, 60, 80, and 100% of pretraining maximal minute ventilation (VEmax) in obstructed (solid lines) and healthy subjects (dashed lines). Vertical bars, SD. Significant difference between groups: * P < 0.05, ** P < 0.01, *** P < 0.001.


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

The main results of this study are that after physical training in the obstructed individuals there was an increase in FRC, producing smaller VT and higher f when compared at the same VE. In contrast, normal subjects reduced FRC and f after training. As training in the obstructed subjects was conducted at an intensity at which tidal flow exceeded maximal flow at control FRC, these data would be consistent with the hypothesis that the respiratory system does not adapt to the stimuli arising downstream from the flow-limiting airways during exercise.

Technical aspects of the study. According to the classic criteria (7, 24), none of our obstructed individuals could be considered ventilatory limited during exercise as the VEmax-to-MVV ratio was well below 65-70%. However, all of them achieved maximal flows at submaximal workloads, and two had to increase FRC to generate more ventilation, which would suggest that the respiratory system somehow imposed an impediment to exercise (2-5, 9, 11, 12, 18, 19, 21, 23, 27). Comparing tidal with partial forced expiratory loops measured at the mouth, as we did in this study, may be useful in identifying the occurrence of EFL, but it is not devoid of pitfalls. For example, flow during a forced expiratory maneuver is underestimated at a given volume because of thoracic gas compression (22). Well aware of this problem, we avoided labeling as EFL the condition in which tidal and maximal flows were equal. However, we are confident that EFL conditions likely occurred in our patients during exercise when tidal expiratory flow exceeded maximal flow. Because of volume history (8) and time-dependence (14) effects on airway caliber, we measured flow during a forced expiratory maneuver initiated from end-tidal inspiration without any inspiratory pause. We found the maneuver fairly easy for the subjects to understand and perform. In addition, measuring expiratory flow at all workloads allowed bronchodilation to be revealed during exercise, as suggested by the progressive and significant increase in flow observed in both groups of subjects both before and after training. Had we applied a negative expiratory pressure during the various steps of the test, we could have been even more precise in detecting EFL and overcome all the aforementioned technical problems. However, even with the negative expiratory pressure technique we could have missed cases of EFL that were limited to some regions in the lung but nevertheless crucial with respect to the regulation of breathing. Finally, we tried to quantitate the changes in FRC during exercise by asking the subjects to take a deep breath to TLC soon after the partial expiratory maneuver, so that FRC and EILV could be computed from TLC. The validity of this method is based on the facts that TLC remains relatively constant during exercise (4, 26) and the inspiratory capacity well reflects the changes in FRC (4).

The intensity of the training sessions was consistently higher than control ventilatory AT and thus adequate to improve exercise performance in all subjects, as proved by the final increase in workload, VO2 max, VEmax, and AT during the exercise test after training. In the second month of the study, the intensity was adjusted according to the new AT measured during an additional exercise test.

Breathing pattern during control exercise. Although exercise performance in the obstructed subjects was slightly less than in the normal subjects, it was still within the normal range, and the breathing pattern during cycling was basically similar in the two groups. The increase in ventilation was mostly produced by an increase in VT at the beginning of exercise and by an increase in f toward the end of it in both obstructed and normal subjects. This was accomplished by both a decrease in FRC and a progressive increase in EILV. Once decreased, FRC remained low for the rest of the test and did not increase near maximum loads, as conversely reported in very fit young individuals when maximum flow is attained at maximum exercise (13). These data are in line with the general belief that FRC does not increase if EFL is not attained (see below). In contrast to normal subjects, all obstructed individuals achieved and exceeded maximal flow near FRC at some steps during exercise. When this occurred, FRC tended to increase, although this was more evident in a few subjects. Although we do not have an evident explanation for this variable behavior within the obstructed group, we speculate that increasing FRC under these conditions may be a matter of the amount of EFL and/or degree of dyspnea determined by the compressed airways. These findings are consistent with previous data reported by Babb and Rodarte (3).

Effects of physical training on exercise hyperpnea. In the normal subjects training was associated with a further increase in VT and decrease in FRC. Even though VE increased, tidal expiration never attained maximum flow, allowing FRC to remain low until the end of the test. Such a training-induced decrease in FRC and increase in VT during exercise in the normal subjects may be considered as the most economic choice that allows physical performance to improve. This assertion is also based on the assumption that decreasing FRC may help partition the work of breathing between inspiratory and expiratory muscles at high ventilation (10). Therefore, decreasing FRC and f seems to be part of a complex process, due to physical training, that tends to optimize breathing.

Paradoxically, in the obstructed subjects the improvement in physical performance and unchanged breathlessness sensation during exercise after training were associated with a higher rather than lower FRC and an increased f. We speculate that the more rapid breathing pattern after training originated in the premature interruption of expiration, which in turn caused FRC to increase and VT to decrease. Then, to maintain VE constant, f had to increase. Among the many causes that could explain the increment of FRC with training, we favor the one that links FRC to the minimum EFL. When maximal flow is achieved during tidal breathing, the airways downstream from the flow-limiting segments collapse and may cause dyspnea (3, 5, 6, 12, 15, 16, 18, 21). To avoid such a sensation, subjects tend to stop expiration prematurely at a volume at which EFL is absent or at a minimum. Some of the obstructed subjects showed this pattern before training. FRC initially dropped and then increased at high levels of ventilation. EILV increased and then plateaued. The final increments in VE were mostly from f. After training, the pattern was the same but more pronounced. At the same ventilation, FRC decreased less, mean lung volume increased more, and f was higher. All these findings raise the question of why a reflex response to impending EFL at the same ventilation mostly occurred after physical training. Although quite active in recreational activities, our obstructed subjects certainly did not experience EFL often and regularly in their daily life. With training regularly imposed for 30 min three times a week and for 2 mo at an intensity at which EFL could be sensed during each breath, the subjects could have had enough time to mature and refine a prompter response to EFL. Although we are aware of the difficulty of proving this interpretation, we believe that the significant increase in slope of the relationship between delta FRC and delta flow would suggest that repeated stimuli arising from the airways undergoing dynamic collapse may be perceived over time as unpleasant and generate prompter responses. On the other hand, the increase in FRC recorded at maximum load after training could be simply due to achieving higher VE and thus higher tidal expiratory flow. With partial forced expiratory flow at maximum load remaining unchanged after training (Table 3), an increase in tidal expiratory flow was necessarily associated with greater degree of EFL and, in turn, greater hyperinflation.

In a recent study, Babb et al. (2) reported an increase in FRC during exercise in healthy older individuals after physical training, which apparently seems to be in contrast to the response in our normal younger individuals. We do not have a clear explanation for this, but, as aged healthy people may easily attain maximum flow even below maximum workload (11), we speculate that during physical training they may experience EFL conditions and consequently behave like our patients with mild-to-moderate airflow obstruction.

It is a fact that two opposite responses of the respiratory system during exercise to long-standing physical training were associated with unmodified breathing sensation for the same ventilation but for greater workloads. In normal subjects, this was likely due to a balance between the sparing of some of the inspiratory work of breathing and greater activation of the expiratory muscles occurring after decreasing FRC. In contrast, the unmodified breathlessness in the obstructed subjects could have been due to the decrement in EFL, which weighted on the breathing sensation in a manner similar to the increase in elastic work of breathing at a higher lung volume.

Our study raises the question of how more rapid breathing at higher FRC during exercise could be tolerated after training. The cost of decreasing EFL by increasing mean lung volume and f is an increased load on inspiratory muscles. Although we do not have clear, direct evidence for this, we speculate that if exercise training conditioned the inspiratory muscles, the load of diminishing EFL would be smaller relative to inspiratory muscle capacity, and the subjects would adopt a pattern that decreased EFL.

In contrast to Yerg et al. (25), in neither group did we find a significant decrement in VE/VO2 at maximal or submaximal loads after physical training. We believe that this was likely due to the fact that all our subjects were quite physically active before the study. Had they been previously sedentary, physical training could have revealed greater and more substantial decrements in VEmax for any given VO2 max.

Conclusions. The results of this study are consistent with the hypothesis that experiencing EFL for a certain time still triggers strong signals during exercise, prompting specific reactions of the respiratory system during exercise. Although abnormal, such responses do not prevent exercise capacity from improving, so long as the intensity of physical training remains above the anaerobic threshold.


    ACKNOWLEDGEMENTS

The authors thank Prof. E. Uslenghi and technical staff members (S. Cagliero, O. Isaia, D. Dutto, and V. Marino) for invaluable cooperation; Dr. C. Biolé for data reduction; R. Perissin from SensorMedics Italia for technical assistance; and all the participants, without whose enthusiasm the study could not have been successfully carried out.


    FOOTNOTES

This study was supported in part by a grant from Ministero dell' Università e della Ricerca Scientifica e Tecnologica, Rome, Italy.

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

Address for reprint requests and other correspondence: V. Brusasco, Cattedra di Fisiopatologia Respiratoria, Dipartimento di Scienze Motorie e Riabilitative, Università di Genova, Largo R. Benzi 10, 16132 Genova, Italy (E-mail: brusasco{at}dism.unige.it).

Received 30 March 1999; accepted in final form 22 July 1999.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

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J APPL PHYSIOL 87(5):1697-1704
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