Effect of mild-to-moderate airflow limitation on exercise capacity.

Effect of mild-to-moderate airflow limitation on exercise capacity T. G. BABB, R. VIGGIANO, B. HURLEY, B. STAATS, AND Jo R. RODARTE The Methodist Hospital, Baylor College of Medicine, Houston, Texas 77030; Thwacic Diseases Research Unit, Mayo Clinic and Fuundation, Rochester, Mimesota 55905; and Central Plains Clinic, Sioux Falls, South Dakota 57105

increasing EELV during exercise is a response that is in contrast to that observed in normal subjects (11,18,31) and places the respiratory muscles at a mechanical distermine the effect of mild-to-moderate airflow limitation on advantage (17). Typically, patients who have a reduced exercise tolerance and end-expiratory lung volume (EELV), exercise capacity, a reduced ventilatory reserve [VE,,,/ we studied 9 control subjectswith normal pulmonary function MVV > 70% maximal voluntary ventilation (MVV)], [forced expired volume in 1 s (FEV,) 105% pred; % of forced and/or hypercapnia and do not attain maximal heart vital capacity expired in I s (FEV,/FVC% ) 811and 12 patients rate (HR) are considered to have ventilatory limitation with mild-to-moderate airflow limitation (FEV, 72% pred; to exercise (7,29,30). Even in patients who do not meet FEV,/FVC % 58) during progressive cycle ergometry. Maxiventilamal exercise capacity. was reduced in patients [69% of pred the usually accepted criteria for determining maximal 0, uptake (Vo,,,)] compared with controls (104% tory limitation to exercise, the airflow limitation and Pred v”, max t P < 0.01);however, maximal expired minute ven- altered mechanics could contribute to a reduced exercise tilation-to-maximum voluntary ventilation ratio and maxi- capacity. mal heart rate were not significantly different between conTo determine the effects of mild-to-moderate CAL on trols and patients. Overall, there was a closerelationship be- exercise tolerance we measured maximal exercise capactween vozmax and FEV, (r2 = 0.62). Resting EELV was similar ity and ventilatory pattern during cycle ergometry in between controls and patients [53% of total lung capacity patients with mild-to-moderate CAL. We hypothesized (TLC)], but at maximal exercise the controls decreasedEELV CAL could affect the ventilatory to 45% of TLC (P c O.Ol), whereas the patients increased that mild-to-moderate the patients may not EELV to 58% of TLC (P -c 0.05). Overall, EELV was signifi- response to exercise, although ventilatory limicantly correlated to both Vogmax(r = -0.71, P -K 0.001) and meet the usual criteria for determining FEV, (r = -0.68, P < 0.001).This relationship suggestsa ventitation to maximal exercise. BABB, T. G., R.VIGGIANO, B. HUXLEY, B. STAATS, AND J. R. RODARTE. Effect of mild-to-moderate air&w limitation on exercisecapacity. J. Appl. Physiol. 70(l): 223-230, 1991.--To de-

latory influence on exercise capacity; however, the increased EELV and associatedpleural pressurescould influence cardio- METHODS vascular function during exercise. We suggest that the inSubjects. Nine men with normal pulmonary function crease in EELV should be considereda responsereflective of to participate in the study as control subthe effect of airflow limitation on the ventilatory responseto volunteered jects. Resting pulmonary function studies included exexercise. maximal ventilation; breathing pattern; lung volume; chronic obstructive pulmonary disease

SEVERE chronic airflow limitation (CAL) has been shown to limit exercise tolerance (14), the effect of mild-to-moderate CAL on exercise tolerance has not been studied. Patients with severe CAL increase end-expiratory lung volume (EELV) during exercise to achieve higher maximal expiratory flows (8, 10, 16, 24, 28). Although this increase in EELV allows the patients to achieve a greater ventilatory capacity, ventilatory limitation is still a major factor limiting exercise. Patients with mild-to-moderate CAL may also increase EELV to meet the increased ventilatory demand of exercise. Unlike patients with severe CAL, increasing EELV may allow patients with mild-to-moderate CAL to preserve ventilatory capacity despite airflow limitation and altered ventilatory mechanics. Nevertheless,

ALTHOUGH

piratory spirometry, lung volume determinations by open-circuit N,-washout technique (25), and diffusing capacity for carbon monoxide (DL& by steady-state method (3). MVV was determined from the maximal ventilation obtained in five successive breaths and extrapolated to 1 min. The pulmonary function technician observed an analog display proportional to ventilation and coached subjects to achieve maximal values. Although this technique for calculating MVV gives a slightly greater value than the 12-s test, patients and controls would be affected equally. The patients were recruited from those undergoing routine pulmonary function testing for clinical reasons. Twelve patients who fulfilled the following criteria volunteered for participation in the study: 1) 50% K forced vital capacity expired in 1 s (FEVJFVC) < 65% ; 2) total lung capacity (TLC) > 90% of predicted; 3) DL~* > 50% predicted; 4) forced expired volume in I s (FE&) after bronchodilator < 120% FEV, before bronchodilator; and 5) no history of asthma, cardiac, or orthopedic problems. Controls were recruited by solicitation and screened for normal pulmo-

0161-7567/91 $1.50 Copyright 0 1991 the AmericanPhysiological

Society

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224

AIRFLOW

1. Subject physical

TABLE

pulmonary

characteristics

LIMITATION

AND

and

function

Age, yr

EIt, cm w kg VC, liters

Controls

Patients

48.8t5.4 173.2t7.4 81.1t8.0 4.87M.63

54.2t8.3 1’76.7t6.6 84.6k9.0 4.6WO.75

TLC

liters %Pred RV/TLC, FE&

%

liters %Pred

6.79t0.88 105tlO 29.5t3.9

7.371tO.96 109t9

40.1*5.4*

3.8620.53 105t12

2.71t0.45”

FE&/FEV %

8l.lt5.4

%Pred MVV, liters

lOlt7 177~123

58.3&6.2* 74t8

ho

ml min-l 9Torr-’ l

%Pred

Sa,, %

32.1t4.3 112218 97.2t0.8

72tlO

117t19*

24.4+6.1? 80t18 95.2&l .5-f

Values are means t SD. Arterial O2 saturation (Sao,) was measured by ear oximetry at rest. See text for abbreviations. * P c 0.001. ‘t P < 0.01.

nary function. None of the control subjects or patients participated in regular strenuous physical activity, and none reported more than mild symptoms of dyspnea during their normal daily activities. The protocol was approved by the Institutional Review Board, and informed consent was obtained from all controls and patients. Physical characteristics and pulmonary function data for the controls and patients are presented in Table 1. The patients were not significantly older than the controls. Five of the control subjects were current smokers, three had never smoked, and one had only a minimal smoking history. Eight of the patients were current smokers, two had quit before the study, and two had never smoked. The patients had significantly lower expiratory flow, MVV, diffusing capacity, and resting arterial saturation. Except for residual volume (RV), static lung volumes were not significantly different. The controls had normal pulmonary function. 2Maximat exercise test. Graded cycle ergometry was performed using 2-min increments in work rate on a calibrated cycle ergometer (Siemens 380B). Gas exchange measurements were made during the last 30 s of each increment. At maximal exercise, the gas exchange measurements were made over the last 30 s just before the measurement of dynamic flow-volume curves and inspiratory capacity (IC). The work rate increment was individually determined and was 20, 25, or 30 W. Exercise continued until volitional terAmination of the test. All subjects were urged to continue for as long as possible. Measurements of minute ventilation (by), tidal volume (VT), breathing frequency (f), 0, uptake (%J, and CO, output (ho,) were made using an on-line breathby-breath system (Medical Graphics System). System quality control was performed weekly by comparing (within 5% agreement) average breath-by-breath mea-

EXERCISE

CAPACITY

surements with simultaneous measurements made from bag collections of expired gases (22). Volume was determined from the digital integration of flow over time (Fleisch no. 3 pneumotachograph and Validyne MP 45). Expired gas concentrations were continuously sampled at the mouth and analyzed using a Perkin-Elmer mass spectrometer (MGA 1100). Calibration of the analyzer was performed using reference gases before each test. Electrocardiogram and blood pressure by auscultation were monitored at rest and at each work rate. Arterial 0, saturation was estimated using a Hewlett-Packard ear oximeter (model 47201A). MaximaL and tidaljbw-volume loops. Maximal and tidal flow-volume loops were determined at rest, and tidal flow-volume loops were determined during exercise. At rest and during exercise the controls and patients breathed through a Hans Rudolph three-way rebreathing valve (2870A, dead space -90 ml). For the measurement of maximal flow-volume loops and tidal flow-volume loops, the valve was turned to allow rebreathing from a wedge spirometer (MedSci 270). The flow and volume signals were measured from the spirometer and recorded on FM tape. Maximal flow-volume loops were obtained with the subjects seated on the cycle ergometer. To eliminate the effect of gas compression on maximal expiratory flow, multiple expiratory vital capacities were performed with graded efforts (24), An outer perimeter curve was drawn by eye to estimate the composite of the graded efforts. This composite curve was used to represent maximal expiratory flow corrected for gas compression artifact (4). In some subjects we compared the composite curve with that determined in an integrated-flow body plethysmograph and found good agreement. Although changes in maximal expiratory flow may occur during exercise from bronchodilation, we did not attempt to measure maximal expiratory flow during exercise because we could not correct for the gas compression artifact. It is impossible for subjects to perform repeated forced vital capacities during exercise. Furthermore, we did not have the subjects perform maximal flow-volume loops immediately after exercise. We cannot exclude the possibility that some of our subjects had bronchodilation during exercise. Rest and maximal exercise tidal flow-volume loops were determined just before measurement of IC. Rest and exercise EELS: EELV was estimated by having the subjects rebreathe from the wedge spirometer for approximately four breaths and then inhale to TLC twice to confirm the maximal IC. Also, for selected subjects, maximal inspiration was confirmed by measurements of minimal pleural pressure estimated from an esophageal balloon. The average end-expiratory position was determined before the maximal inspiratory efforts. EELV was then determined relative to TLC by subtracting the IC from the previously determined TLC and is reported as a percentage of TLC. TLC was measured while the subject was in the seated position. All EELV measurements at rest and during maximal exercise were made with the subjects seated on the cycle ergometer. At selected work increments and at maximum, the subjects briefly rebreathed from the wedge


AIRFLOW

LIMITATION

AND

EXERCISE

spirometer and inhaled to TLC as described above. Later the FM tape was played back at reduced speed on an X-Y recorder to generate the flow-volume loops. Exercise data were obtained from the last 30 s of the exercise increment. We assumed that TLC does not change significantly during exercise in controls or patients (27, 28, 31). IC has been used as an indicator of EELV in many prior studies (1,5,9,10,13,18,23,24,31). The subjects in our study were able to perform the procedure without difficulty. Data analysis. The two groups, control subjects and patients, were compared using a nonpaired t test. A paired t test was performed to compare resting and maximal exercise values within the same group. To test the relationship of variables a Pearson product-moment correlation coefficient was calculated. Unless stated otherwise, P < 0.05 was considered significant.

225

CAPACITY

4

c

l -

3

E 2

1

2

4

CONTROLS

cl

PATIENTS

3

4

5

FEW, L I. Relationship between FEV, and vozrnax for 9 subjects with normal lung function and 12 patients with mild-to-moderate airflow limitation. Y = 0.343 + 0.540X, r2 = 0.62, P < 0.001. FIG.

RESULTS

Curdiorespiratory responses to maximal exercise. Maximal cardiorespiratory responses to graded cycle ergometry are presented in Table 2. Five of the 9 control subjects and 5 of the 12 patients had a plateau of VO, at the highest work rate. The patients had a significantly lower exercise capacity than the controls, who had a normal exercise capacity. Maximal HR was 89 t 9 and 92 t 9% of age-predicted maximal HR in the controls and the patients, respectively. *The patients had higher HRs at work loads requiring VO, values of 1.0 and 1.5 l/min and thus reached approximately the same maximal HR at a lower maximal VO, (%,,,,). The maximal 0, pulse (VoJHR) was lower in the patients than in the controls. Maximal mivute ventilation (VE,,) was lower in the patients, but VE,, /MVV was not significantly different. VT as a percentage of FVC was significantly (P c 0.05) lower in the patients. The inspiratory duty cycle (TI/TT) at maximal exercise was similar between

2. Maxima2 to graded exercise

TABLE

curdiorespiratory

Variable

Load, W

responses

Controls

Patients

226.3242.5

170&22.3*

90,

Vmin %Pred v02 lIlaX*

2.52t0.39 ml O2 kg” 4min-f l

HR beats/min %Pred ~o$HR, ml &/beat VE, l/min f, breaths/min VT,

liters

VT/FVC b/MVV,

5%

TI/TT Sa,, %

1.74t0.29”

104t26

69t13

30.7t6.5

20.3+3.5*

157.0-t-15.0 8929 15.8t2.9 109.9t13.6 39.lt7.0 2.81tO.60 57.4t7.4

155.9t16.6 92tlO 11.0+1.8*

79.9+9.7? 36.4t9.6 2.34t0.65 49.7&3.7t

61.7k13.4

70.2t16.3

0.46t96.4 96.4kl.l

0.44t0.03 94.2t2.0”

Values are means * SD. Sa,,, arterial O2 saturation. See text for other abbreviations. Significantly different between groups: * P -C 0.01; t P < 0.05; $ P < 0.001.

the two groups. There was a slight but significant difference in arterial 0, saturation at maximal exercise. The patients’ vo2 max and 9~~~~ were 69 and 73% of those of the controls. The reduction in vo2max and VE,,, in the patients was similar to that observed for FEV, (70%) (Fig. I). The correlation coefficients for FEV, and vo 2 max (r = 0.78) and FEV, and VE,,, (r = 0.71) were significantly different from zero (P < 0.001). Flow-volume loops. None of the control subjects were breathing on their maximal flow-volume loop at rest; however, six of the nine controls ((72, J-6, 7, and 9) had some portion of their maximal exercise tidal expiratory flow-volume curve impinging on maximal expiratory flow (Fig. 2). Three of the six (C2, 6, and 9) had flow impingement only in the latter part of the VT, whereas the other three controls (Ch, 5, and 7) had flow impingement over a large percentage of the VT. The remaining three controls (Cl, 3, and 8) could have sustained the flow near end expiration for ~0.5 liter before hitting their maximal expiratory flow-volume curve.’ Seven of the 12 patients (PI-~, 5, T-8, and 11) were breathing on some part of their maximal expiratory flow-volume curve at rest (Fig. 3). At maximal exercise all but one of the patients (PZ) had tidal expiratory flows that equaled or exceeded some portion of their maximal expiratory flow-volume curve obtained at rest. Some control subjects (G, ?‘, and 9) had flows that exceeded their maximal expiratory flows determined by their preexercise maximal flow-volume Curves (Fig. 2'). This was more pronounced in the patients (Fig. 3). We did not want to disrupt the subjects’ normal exercise response by attempting multiple forced expiratory vital ’ In some subjects exercise tidal expiratory flow exceeded maximal expiratory flow measured at rest. Expiratory flow exceeding the maximal expiratory flow-volume envelope (Figs. 2 and 3) has been previously described and is thought to result from parallel inhomogeneity of airflow in diseased lungs (21), gas compression artifact (15), and/or bronchodilation during exercise (13). In our control subjects, we assume that bronchodilation would be the most likely explanation.


226

AIRFLOW

LIMITATION

AND

Cl

EXERCISE

CAPACITY

c2

12

Expiration

10 8

-2 -4 J

I

I

J

J

J

1

1

J

J

I

I

I

1

4

5

6

7

C6

12 10 8

u !i 3 s2 0 ii

6 4

0 -2 -4 -6

T

I

J

J

J

I

I

I

c9

C8

c7 12 10 8

0

12

3

Volume,

4

5

L

6

7

0

1

2

3

Volume,

4

5

L

6

7

0

12

3

Volume,

L

2. Resting maximal flow-volume loop (bold line), composite maximal flow-volume loop from graded efforts (dashed I’me ) , resting tidal flow-volume loop (small dashed loop), and maximal exercise tidal flow-volume loop (thin line) for each control subject (WCS). FIG.


AIRFLOW

LIMITATION

AND EXERCISE

CAPACITY

227

PI

P4 Expiration

P5

P6

7

P?

P8

1

6

P9

PI0

PI2

10

6 8 cn 3

4

$2 ii

0

I

2

3

4

5

0

f

12

f

I

I

I

f

I

3

4

5

6

7

0

12

3

4

5

6

7

0

Volume, L Volume, L Volume, L FIG. 3. Resting maximal flow-volume loop (bold line), composite maximal flow-volume loop from graded efforts (dashed line), resting tidal flow-volume loop (small dashed loop), and maximal exercise tidal flow-volume loop (thin line) for each patient (PI-f~).

capacities during exercise. It is unfortunate that we did not systematically perform them after exercise to assess bronchodilation. However, when the exercise tidal flow-volume curve exceeded the control flow-volume curve and had an expiratory slope roughly parallel to the preexercise maximal flow-volume curve, we considered this subject to be flow limited. EELV. At rest there was no difference in EELV (STLC) between the control subjects and patients (Fig.

4). At maximal exercise the controls’ EELV decreased to 45% of TLC (P < 0.01). In contrast, the patients increased their EELV during maximal exercise to 58% of TLC (P c 0.05). EELV was significantly different be-

12

3

4

5

6?

Volume, L

tween the controls and patients during maximal exercise (P < 0.001). ThFre were significant correlations between EELV and V02max (r = -0.71, P = 0.0003) and EELV and FEV, (r = -0.68, P = 0.0007) (Fig. 5). Eight of the nine control subjects (Cl-5 and T-9) decreased their EELV during exercise (Fig. 2). Seven of the 12 patients (PI, 2, 5, 7-8, IO, and 11) increased their EELV, 3 (P3-4 and 9) had little or no change, and 2 (P6 and 12) reduced their EELV slightly during maximal exercise (Fig. 3). Patients 6 and 12, who decreased their EELV during maximal exercise, also had flows in excess of their control maximal flow-volume curve consistent with exercise-induced bronchodilation (see below). End-


228

AIRFLOW

LIMITATION

AND

60

20 REST

MAXIMAL

EXERCISE

4. EELV at rest and during maximal exercise for controls (n = 9) and patients (n = 12). Values are means +_ SD. Groups were significantly different during maximal exercise (* P -c 0.001). There was a significant (P < 0.01) decrease in EELV in control subjects and a significant (P < 0.05) increase in EELV in patients. FIG.

inspiratory lung volume (EILV) was similar for the controls and patients at rest (68 and 64% TLC, respectively) and during maximal exercise (86 and 89% TLC, respectively).

EXERCISE

CAPACITY

reserve (VE ,,,/MVV > 70% MVV), and/or hypercapnia without limitation by nonventilatory factors such as maximal cardiac frequency are considered to have ventilatory limitation to exercise (7, 29, 30). We cannot exclude the possibility that it is by coincidence that VO 2max and FEV, were reduced by the same proportion (69 and 70%) in the patients. The relationship between FEV, and Vo2,,, (Fig. 1) has been observed in patients with severe disease (14, 19) but has not previously been reported in patients with such mild disease. This relationship is not explained by differences in body size between patients and control subjects who were similar. A similar correlation occurred between V0 2max in milliliters of 0, per kilogram per minute and percent predicted FEV, (data not shown). The hypothesis that the patients’ lung disease contributes to their reduced exercise capacity warrants consideration. A qualitative difference between patients and controls is the change in EELV at maximal exercise. The normal subjects reduced their EELV with exercise, a finding consistent with previously reported data (11,18, 26,31). An EELV lower than functional residual capacity (FRC) places the diaphragm on a more optimal part of its length-tension curve, improves the mechanical advantage of the inspiratory muscles, and reduces the elastic work of the inspiratory muscles (20). Our control subjects were impinging on their maximal expiratory flow-volume curve near end expiration, consistent with the study of Olafsson and Hyatt (23) in older subjects

DISCUSSION

A reduced exercise capacity has not been previously documented for patients with mild-to-moderate CAL. Despite a lower maximal exercise capacity, the patients’ ventilation was not limited on the basis of the usually accepted criteria for determining ventilatory limitation to exercise. The usually accepted criteria for establishing cardiovascular. rather than ventilatory limitation are 1) an exercise VE that is considerably less than the MVV (40%), 2) a maximal HR that is within two standard deviations of the predicted maximal HR, and 3) an arterial 0, saturation >90% (7,29,30). In elite athletes a decrease in arterial 0, saturation may occur at maximal exercise, but this does not normally occur in fit individuals (6). According to VE ,,,/MVV (‘?O.Z%), our patients had a minimally reduced ventilatory reserve at the termination of exercise but were not significantly different from the control subjects. Had we used the more conventional 12-s MVV, we would have obtained slightly lower values but the ventilatory reserve computed for both the controls and patients would have been affected equally. The patients obtained 92% of their maximal predicted HR, indicating that as a group there was little or no cardiac reserve at the end of exercise. Although there was a slight but significant difference in arterial 0, saturation at maximal exercise, the patients’ arterial 0, saturation was >90%. Our patients do not meet the conventional criteria for ventilatory limitation to exercise; therefore, by these criteria, the cardiovascular system would seem to be the major factor limiting exercise in

both patients and controls. Typically, only patients who have a reduced exercise caDacitv. a reduced ventilatorv

mJ r^

W L l Cl

0

CONTROLS PATIENTS

I 40

1 50

r 60

I 70

1 80

I 50

I 60

I 70

I 80

l

l-

.

CONTROLS

Cl

PATIENTS

1 40

EELV, OhTLC 5. Relationships between EELV at maxima! exercise and FE& (top: Y = 6.20 - 0.057X, r2 = 0.46, P < 0.001) and VO, max(bottm: Y= 4.21 - o.o4lx, r2 = 0.50, P K 0.001) for 9 controls and 12 patients with mild-to-moderate airflow limitation. FIG.


AIRFLOW

LIMITATION

AND EXERCISE

and with younger subjects at higher levels of ventilation (9,12). However, EELV was still less than resting FRC. In contrast, the patients’ EELV at maximal exercise was considerably higher than control FRC. At rest, over half of our patients were at maximal expiratory flow near FRC. The remainder had very little expiratory flow reserve. Although resting FRC as a fraction of TLC was not different from that of the controls (Fig. 4) because of the increased RV/TLC in the patients, expiratory reserve volume was reduced. Below FRC, the patients’ maximal expiratory flow was very low. If the patients had reduced EELV, even utilizing maximal expiratory flow, their mean expiratory flow rate would be less than during tidal breathing at rest. Once expiratory flow follows the maximal expiratory flow-volume curve, for a given VT and EELV, expiratory time and thus mean expiratory flow are fixed (2). With a fixed VT and EELV, ventilation can be increased only by increasing mean inspiratory flow rate and decreasing inspiratory time as a fraction of total cycle time. Although our subjects’ inspiratory flow at rest was much less than maximal, Tu'TT stayed relatively constant with graded exercise in both patient and control groups. If EELV and TI/TT are held constant, subjects could increase ventilation by increasing VT, but this would require an increase in expiratory time and thus a decreased f. We did not observe this pattern in our subjects. Increasing EELV to a volume where maximal expiratory flow is higher increases mean expiratory flow rate and thus ventilatory capacity. At maximal exercise the patients had increased their EELV to 58% of TLC. The patients’ EILV at that time was 89% of TLC. It is likely that the elastic work of breathing is prohibitive when EILV is >90% TLC (17, 31). Except for patient 2, who had a dramatic increase in EELV, the patients were all utilizing maximal expiratory flow over most of their VT'S. In fact it would appear from Fig. 3 that these patients could not ventilate more; yet their maximum exercise ventilation was only 70% of their MVV. This is because patients perform their MVV at very high lung volumes with high frequencies, small VT's, and excessive expiratory effort, a pattern we have never observed during exercise-stimulated ventilation. For these reasons, the MVV is a nonphysiological estimator of VE,,, and a VE,,/MVV >70% may not always accurately reflect ventilatory limits to exercise. In contrast, even though all the controls were impinging on maximal flow at least near end expiration, most of them could have increased their ventilation significantly by increasing EELV. It is doubtful whether the patients could have increased EELV further, considering that their EILV was approaching 90% of TLC. Furthermore, among all subjects, there was a significant. correlation between EELV at maximal exercise and VoZmax. There was no correlation between these variables at rest (data not shown). This finding has not been previously reported. The relationship also holds when VOW,, and FEV, are expressed as percent predicted (data not shown). The relationship between EELV and VO, maxraises the possibility that hyperinflation and the associated reduced mean pleural pressures could limit cardiovascular function and, thus, exercise capacity (24). However, we sug-

229

CAPACITY

gest that VE m8X/MVV and percent maximal predicted HR may not be the most appropriate variables for determining whether ventilatory limitation is responsible for the reduced exercise capacity observed in our patients. We therefore conclude that in our control subjects a normal exercise capacity was determined by cardiovascular factors as judged by demonstration of a plateau in VoZ in over half the controls and a maximal HR in the presence of ventilatory reserve. Although flow limited at end expiration during maximal exercise, these older normal subjects were able to achieve maximal predicted HR with an EELV at or below control EELV. In contrast, our patients were at or near flow limitation at rest and responded to the ventilatory demands of exercise by increasing EELV. It is difficult to conceive that our patients could increase their ventilation sufficiently to achieve a 30% increase in VO, maxrequired to match that of the control subjects. Nevertheless, by conventional criteria, we have not demonstrated a ventilatory limitation to exercise. Although the patients’ arterial 0, saturation decreased slightly at maximal exercise, it exceeded 90%. The increased HR at comparable Vo, values and the reduced Vozmaxat maximal HR in the patients are typical of deconditioning. We suggest that the abnormal ventilatory response produced by the patients’ limited expiratory flow reserve may have caused them to reduce the intensity of their daily activities, thereby producing deconditioning. Therefore the abnormal ventilatory mechanics may have been responsible for deconditioning so that their maximal exercise capacity was reduced in proportion to the severity of their lung disease as judged by FEV, and maximal EELV. Alternatively, breathing at high lung volumes may have reduced maximal cardiac output in these patients. The authors are grateful to the many technical staff members who helped on this project. This study was supported in part by National Heart, Lung, and Blood Institute Research Grants HL-21584 and HL-07222. Address for reprint requests: T. G. Babb, 520B, Dept. of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. Received 1 May 1989; accepted in final form 6 September 1990. REFERENCES 1. BABB, T. G., E. R. BUSKIRK, AND J. L. HODGSON. Exercise end-expiratory lung volumes in lean and moderately obese women. Int. J. Obesity 13: 11-19, 1989. 2. BABB, T. G., J. R. RODARTE, AND J. YOUNG. Maximal ventilation, breathing pattern, and EELV (Abstract). PhysioZo&st 31: Al57, 1988. 3. BECK, K. C., R. E. HYATT, B. A. STAATS, P. L. ENRIGHT, AND J. R. RODARTE. Carbon monoxide diffusing capacity of the lungs determined by single-breath and steady-state exercise methods. Mayo Clin. Proc. 64: 51-59, 1989. 4. BOUHUYS, A., AND B. JONSON. Alveolar pressure, airflow rate, and lung inflation in man. J. AppZ. Physiol. 22: 1086-1100,1967. 5. CHA, E. J., D. SEDLOCK, AND S. M. YAMASHIRO. Changes in lung volume and breathing pattern during exercise and CO, inhalation in humans. J. AppZ. PhysioZ. 62: 1544-1550,1987. 6. DEMPSEY, J. A., P, G. HANSON, AND K. S. HENDERSON. Exercise-induced arterial hypoxaemia in healthy human subjects at sea level. J. PhysioZ, Lmd. 355: 161-175, 1984. 7. DILLARD, T. A. Ventilatory limitation of COPD. Chest 92: 195-196,1987. 8. GRIMBY, G., B. ELGEFORS, AND H. OXHOJ.

exercise: prediction Ventilatory

in

levels and


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chest wall mechanics during exercise in obstructive lung disease. Scam-Z.J Respir. LG. 54: 45-52, 1973. 9. GRIMBY, G., B. SALTIN, L. WILHELMSEN. Pulmonary flow-volume and pressure-volume relationship during submaximal and maximal exercise in young well-trained men. B&h Physio-Pathol, Re-

AppZ. Physiob 64: 135-146, 1988. 12. HESSER, C. M., D. LINNARSSON, AND

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Exercise capacity and ventilatory, circulatory, and symptom limitation in patients with chronic airflow limitation.

Effect of chronic airflow limitation on resting oxygen consumption.

Mechanism of bronchodilator effect in chronic airflow limitation.

Effect of airflow limitation on acute exacerbations in patients with destroyed lungs by tuberculosis.

Randomised controlled trial of weightlifting exercise in patients with chronic airflow limitation.

Impact of airflow limitation in chronic heart failure.

Effect of chromosome substitution on intrinsic exercise capacity in mice.

Effect of inspiration on airway dimensions measured in maximal inspiration CT images of subjects without airflow limitation.

Upper airway anesthesia induces airflow limitation in awake humans.

Breathlessness in patients with severe chronic airflow limitation. Physiologic correlations.

Controlled trial of respiratory muscle training in chronic airflow limitation.

The epidemiology and therapy of airflow limitation in the elderly.

Chronic airflow limitation in South African gold miners.

Ventilation heterogeneity in ex-smokers without airflow limitation.

Impact of airflow limitation on carotid atherosclerosis in coronary artery disease patients.

The impact of smoking on airflow limitation in subjects with history of asthma and inactive tuberculosis.

Asthma, airflow limitation and mortality risk in the general population.

Respiratory muscle training in chronic airflow limitation: a meta-analysis.

Effect of airway blood flow on airflow.

Flow limitation and regulation of functional residual capacity during exercise in a physically active aging population.

How Common Is Airflow Limitation in Patients With Emphysema on CT Scan of the Chest?

Mechanisms of exercise limitation in hypertrophic cardiomyopathy.

The paroxetine effect on exercise performance depends on the aerobic capacity of exercising individuals.

A comprehensive analysis of association of medical history with airflow limitation: a cross-sectional study.