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1 Dipartimento di Medicina Clinica, University of Rome "La Sapienza," and 2 Consiglio Nazionale delle Ricerche, 00185 Rome, Italy
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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To test the hypothesis that in chronic
obstructive pulmonary disease (COPD) patients the ventilatory and
metabolic requirements during cycling and walking exercise are
different, paralleling the level of breathlessness, we studied nine
patients with moderate to severe, stable COPD. Each subject underwent
two exercise protocols: a 1-min incremental cycle ergometer exercise
(C) and a "shuttle" walking test (W). Oxygen uptake
(
O2), CO2
output (CO2), minute ventilation (E), and heart rate (HR)
were measured with a portable telemetric system. Venous blood lactates
were monitored. Measurements of arterial blood gases and pH were
obtained in seven patients. Physiological dead space-tidal volume ratio
(VD/VT) was computed. At peak exercise, W vs. C
O2,
E, and HR values were similar, whereas
CO2 (848 ± 69 vs. 1,225 ± 45 ml/min; P < 0.001) and lactate (1.5 ± 0.2 vs. 4.1 ± 0.2 meq/l; P < 0.001) were lower, 
E/CO2
(35.7 ± 1.7 vs. 25.9 ± 1.3; P < 0.001) and
HR/O2 values (51 ± 3 vs. 40 ± 4; P < 0.05) were significantly
higher. Analyses of arterial blood gases at peak exercise revealed
higher VD/VT and lower arterial partial
pressure of oxygen values for W compared with C. In COPD, reduced
walking capacity is associated with an excessively high ventilatory
demand. Decreased pulmonary gas exchange efficiency and arterial
hypoxemia are likely to be responsible for the observed findings.
exercise; chronic obstructive pulmonary disease; pulmonary gas exchange; ventilatory demand
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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THE MECHANISMS OF REDUCED exercise tolerance in chronic
obstructive pulmonary disease (COPD) have been investigated in several laboratories, mostly by analysis of pulmonary gas exchange during cycle
ergometer testing. These studies have provided evidence that impairment
of muscle energetics, with early onset of anaerobic glycolysis and
consequent increase in ventilatory demands, is a major determinant in
reducing the ability of these patients to tolerate a physical effort
(3, 12). However, data obtained with this approach may not reflect
adequately the physiological and metabolic events that come into play
during routine daily activities. Patients with severe COPD often
exhibit intolerable dyspnea during walking, a light form of exercise
that involves both upper and lower extremities. It is likely that
during walking the metabolic and ventilatory responses differ from
those of cycling, primarily because of differences in recruitment of
muscle groups and/or in hemodynamic adaptations. Previous studies (4,
6, 13, 17) have compared ventilatory responses to treadmill and bicycle
exercise in COPD patients. To our knowledge, no data are available on
the ventilatory and metabolic [e.g., CO2 output
(CO2), lactate
production] adaptations to walking on flat ground in COPD. The
question that remains to be answered is whether, even during walking,
the ability of COPD patients to exercise is significantly influenced by
poor muscle aerobic capacity.
Data from literature suggest that a reduction in muscle oxidative capacity, not necessarily due to inactivity per se, is present in animals with lung emphysema (14) and in patients with COPD (12). Poor muscle oxidative capacity may contribute significantly to exercise limitation in COPD. Because of central respiratory limitation, however, the full oxidative potential of leg muscle is difficult to assess, particularly during exercise that involves large muscle mass such as cycle ergometry (15).
In a group of patients with moderate to severe COPD, we measured pulmonary gas exchange parameters, blood lactate, and arterial blood gases during maximal walking (W) and cycling (C) exercise. By examining the adaptations to these two types of physical effort, we tested the hypothesis that in COPD patients, in contrast to cycling, in which exercise capacity may be significantly affected by metabolic factors, W ability is likely to be influenced by ventilatory demand, dyspnea sensation, and lung gas exchange efficiency.
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MATERIALS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Nine male subjects with moderate to severe, stable chronic airway
obstruction and mild hypoxemia were studied. Admission criteria included clinical diagnosis of COPD, forced expiratory volume in 1 s
(FEV1) < 50% of predicted, and room air arterial partial pressure of oxygen (PaO2)
>55 and <75 Torr. The pertinent clinical and functional
characteristics of the subjects are summarized in Table
1. At the time of the study,
patients had no sacral or ankle edema and no evidence of cor pulmonale
or metabolic, renal, hepatic, or neuromuscular disorders. None of them
had received systemic steroids for at least 2 mo before the study. A
stable regimen of bronchodilators with oral theophylline, inhaled
2-stimulants, and inhaled steroids was maintained
throughout the study. The experimental protocol was approved by the
Committee for Protection of Human Subjects, University of Rome,
according to the Declaration of Helsinki; all subjects signed an
informed consent before initiation of the study.
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Equipment.
Spirometry and arterial blood gases were obtained before each bout of
exercise to confirm clinical stability. For C, each subject exercised
on an electromagnetically braked cycle ergometer (Bosch, ERG-551), and
pulmonary gas exchange indexes were determined breath by breath
(Cosmed, Quark b2, Rome, Italy). Patients breathed through
a face mask; ventilation was measured with a photoelectric turbine. Gas
was drawn from the distal part of the turbine by the use of a special
sample capillary of polymer Nafion (Perma Pure); O2 and
CO2 concentrations were determined by rapid response
analyzers (O2 zirconium, CO2 infrared).
Electrocardiogram was monitored continuously at 6 V by a cardioscope;
heart rate (HR) was derived from R-R intervals; and arterial
O2 saturation was monitored throughout the study by pulse
oximetry (Biox 3740, Ohmeda). Oxygen uptake
(O2, STPD), CO2 output
(CO2, STPD),
minute ventilation (E,
BTPS), and respiratory rate were measured for each
breath with the use of a computerized system. Corrections for the
transport delay from the mouthpiece to the sensors and for the rise
time of the analyzers were taken into account (1). Data were displayed
on-line and were also stored on disk for further analyses. During W, a
telemetric portable system (Cosmed, K4, Rome, Italy) was utilized for
O2, CO2,
E, and HR measurements. The K4 system
consisted of face mask, HR chest strip, battery and transmitting unit
(containing the O2 and CO2 gas analyzers), and
a receiving unit. The transmitting unit with battery pack and face mask
with tubing (total weight 0.8 kg) was attached to the individual with a
harness, and the receiving unit was connected to a personal computer
anywhere within 700 m of the transmitting unit. The face mask contained
a turbine for measurement of ventilation as well as a capillary gas
sampling port within the turbine's housing. The expired gas was
sampled at a rate proportional to ventilation, by way of a dynamic
sampling pump, through a special sample capillary of polymer Nafion
(Perma Pure) and into a microchamber containing the O2
(polarographic) and CO2 (infrared) electrodes.
O2 and CO2 analyzers were thermostated and
compensated for the variations of barometric pressure and humidity of
the environment. E (BTPS),
O2 (STPD), and
CO2 (STPD) were
calculated every 15 s. Calibration of the turbine by use of a 3-liter
syringe and a two-point calibration of the gas analyzers by use of gas
mixtures from tanks of standard gas were performed before each test.
O2,
CO2, and
E did not differ significantly between
K4 and breath-by-breath, either at peak or at submaximal level of exercise. The slopes of increments in
O2/W (10.4 ± 0.3 vs. 10.5 ± 0.4 ml · W
1 · min1)
and
E/CO2
(20.2 ± 0.6 vs. 19.7 ± 0.5) during the incremental test were also
similar. With the Bland-Altman test (2), the mean
O2 difference was
0.5
ml · kg1 · min1,
and the limits of agreement (means ± 2 SD) were +1.9 to 2.9 ml · min1 · kg1;
the biases in CO2 and
E were comparably small.
Exercise test. Before each test, a polyethylene venous catheter was inserted in a vein of the hand. For lactate measurements, venous blood samples, arterialized with the use of a warm pad, were obtained at rest and during the first 15 s of recovery from maximal W and C. Lactate was measured in duplicate immediately after sampling with an upgraded analyzer (2300, glucose-lactate analyzer, Yellow Springs Instruments, Yellow Springs, OH).
For W, after three practice sections performed within 10 days, a 1-min incremental modified "shuttle" walking test to volitional fatigue was performed. As originally described by Singh and co-workers (16), the modified shuttle test was performed in an enclosed corridor on a 10-m-long course identified by two cones inset 0.5 m from either end to avoid the need for abrupt changes in direction. The speed at which patients walked was dictated by an audiosignal played on a tape cassette originally generated from a microcomputer. The start of the test was indicated by a triple beep. Thereafter the tape emitted a single beep at regular intervals, at which point the subject attempted to be at the opposite end of the course, that is, by the time the patient heard the signal he should be turning round the cone to proceed back down the course. The initial walking speed was set at 0.50 m/s; subsequently the speed was increased each minute by 0.17 m/s. A change of speed to the next level was indicated by a triple beep. The operator sat alongside the course and gave no encouragement; the only verbal contact was the advice given each minute to increase the walking speed slowly. The test was stopped when the patient was not able to maintain the required speed. For C, a 1-min incremental exercise test was performed. After 3 min of rest and 2 min of unloaded pedaling, workload was increased (5 W/min) until exhaustion, i.e., the point when patients could no longer keep the pedaling frequency of 50 rpm. The interval between tests was 24-48 h and the order was randomized.E, HR, O2, and
CO2 were calculated every
15 s. Other variables obtained were respiratory exchange ratio (RER) = CO2/O2;
O2 pulse (in ml/beat) = O2/HR; HR reserve
(HRR, bpm) = (220 age) maximal HR; and breathing
reserve (BR, in l/min) = (FEV1 × 40) E max. At the end of the exercise,
patients were asked to estimate the degree of breathlessness and leg
fatigue by using a visual scale (10).
Seven of the nine patients agreed to be reevaluated with an identical
exercise protocol; W and C tests were performed in random order.
Spirometry and arterial blood gases were repeated before each bout of
exercise to confirm clinical stability. Pulmonary gas exchange
measurements were obtained by the telemetric system previously
described. Arterial samples for measurement of lactate, PaO2, arterial partial pressure of
CO2 (PaCO2),
and pH were obtained at rest and during the last 15 s of exercise.
Before each exercise test, a catheter was inserted into the brachial
artery of the nondominant arm. The catheter was flushed with a
heparinized saline solution. To avoid spurious dilution, 2 ml of blood
was discarded before collection of arterial samples. Lactate,
PaO2, and
PaCO2 were measured in duplicate
immediately after sampling with upgraded analyzers (2300 glucose-lactate analyzer, Yellow Springs Instruments; IL 1640, Lexington, MA). During the last 15 s of W, one investigator walked at
the patient's side; arterial sampling was obtained without interfering
with arm movements. The physiological dead space/tidal volume ratio
(VD/VT), an index of lung gas exchange
efficiency, was calculated by using the formula (19)
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Statistical analyses. Group data are presented as mean values ± SE. Differences among measured parameters were determined by paired t-test. Pearson's product-moment correlation coefficient (R) was used to detect correlations between criterion variables. The level of statistical significance was set at P < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Under the two experimental conditions, W and C, the duration of
exercise was comparable (6.1 ± 0.4 vs. 6.4 ± 0.3 min). The maximal
power output during C was 69 ± 3 W. During W, maximal speed achieved
was 1.3 ± 0.1 m/s. HRR and BR were similar. Maximal aerobic capacity
(Table 2) during W and C was uniformly
reduced as shown by the low
O2 peak values;
E, HR, and RER values were not
statistically different. By contrast, during W the following variables
were different vs. during C: 1) lactate,
CO2, and RER levels were
lower, suggesting a reduced contribution of nonaerobic metabolism
to energy generation, i.e., anaerobic glycolysis; 2) the slopes of
E/CO2
and HR/O2 were higher;
and 3) degree of breathlessness was greater, whereas
level of leg discomfort was smaller.
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Figure 1 shows the
E/CO2
and the HR/O2 responses
during exercise for a representative COPD patient. The rates of
increase of
E/CO2
and of HR/O2 were higher
during W than during C. The mean values of
E/CO2
and HR/O2 slopes, calculated
in each individual patient by linear regression analysis, were
significantly higher, W vs. C:
E/CO2,
y = 5 + 36x vs. y = 7 + 26x
(t = 4.72, P < 0.001);
HR/O2, y = 70 + 51x vs. y = 71 + 40x (t = 2.16, P < 0.05).
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E/CO2
values, arterial blood parameters, and VD/VT
values, obtained at peak exercise in seven patients, are presented in
Table 3. During W, higher
E/CO2
values were observed. In addition, VD/VT and pH
values were higher whereas PaO2 values were lower during W than during C. Mean
E,
O2,
CO2, and RER values, not
shown in the table, were not different from those observed in the
previous tests (Table 2).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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The most important finding of this study on COPD patients
is the more pronounced
E/CO2
response during W compared with C; this difference could not be
accounted for by a larger contribution of anaerobic glycolysis to
energy production (i.e., lactate levels were lower with W), whereas it
was associated with a worsening in lung gas exchange efficiency (i.e.,
higher VD/VT and lower PaO2 with W). During W, compared with
during C, despite a lower power output estimated from speed and weight
(52 ± 3 vs. 69 ± 3 W), lower
CO2, and a
much smaller lactate elevation, the E increment was similar. In addition, the
E/CO2
slope for W was steeper than the slope for C.
Two alternative explanations for the observed increased ventilatory response during W in COPD, individually or in combination (with or without a cause-effect interrelationship), are to be considered.
First, decreased lung gas exchange efficiency and hypoxemia lead to
increased ventilatory response; this in turn may be due to a larger
/
mismatch from differences in body
posture (gravitational effects on respiratory muscle, primarily the
diaphragm), functional residual capacity, and/or pulmonary
hemodynamics. Our findings of higher VD/VT and
lower PaO2 during W strongly support
this hypothesis. Ventilation during exercise depends on an interaction among CO2,
PaCO2, and
VD/VT. In COPD patients, because each of these
variables may change in a nonpredictable way during exercise, it is
important, in interpreting the level of ventilation, to know the
responses of its determinants. To reduce the number of variables that
complicate the interpretation of results, we preferred to analyze not
ventilation per se but rather the ventilatory equivalent for
CO2 (i.e.,
E/CO2)
(19). In the present study, the increased ventilatory demand observed
during W was related to a very low gas exchange efficiency, as
reflected by high VD/VT values. Even at rest
patients with COPD may show increased ventilation because of the
presence of / mismatching (18). An
above-normal level of ventilation is required to maintain normal
PaCO2 levels. At peak exercise our
patients experienced similar degrees of CO2 retention
during both W and C, indicating that the increase in ventilation was
not able to compensate for the /
mismatching; also, the lower
CO2 at peak W, in the
presence of a similar degree of CO2 retention and lower
lactate levels, is consistent with a smaller contribution of nonaerobic
CO2 production. What drives COPD patients to hyperventilate
during exercise is not clear. Several mechanisms may be hypothesized,
including the hypoxic ventilatory stimulus. In the present study, as
the result of high degree of /
mismatching and wasted ventilation, during W patients showed lower
PaO2 values that, in the presence of
high arterial PaCO2, may explain, at
least in part, the increased ventilatory demand. What can be reasonably
excluded is a significant contribution of lactic acidosis.
Another explanation for the increased ventilatory response during W
could be an increased neurogenic afferent to the respiratory centers,
pulmonary vagal mechanoreceptors from the extremities (5), and
hemodynamic stimuli (9). During W the arm muscles are active and may be
the source of reflex impulses to the respiratory centers; in about 50%
of the COPD patients studied by Celli et al. (4) and Delgado et al.
(6), breathing was dyssynchronous (i.e., contraction of accessory
muscles was not synchronous with diaphragmatic contraction) and dyspnea
was the major factor limiting the effort duration. By contrast, during
C the arms remain in a fixed position and are a less likely potential
source of ventilatory stimulation via neurogenic reflexes, and
limitation to effort is usually due to leg fatigue (10). In our study,
we have no data on intensity of neurogenic afferent; thus any comment
in this regard would be purely hypothetical. The only possible
speculation, suggested by the higher
HR/O2, is that during W
the component of neurogenic hyperpnea was larger.
The greater lactate and the higher
CO2 responses during C,
compared with W, are likely to be due to differences in the muscle mass
and types of fibers recruited during the two types of exercise. During
C the external work is performed by a smaller muscle mass; this implies
that each individual muscle fiber has to perform more work and that its
oxidative machinery is overwhelmed with greater lactate production.
Moreover, because contracting muscles may degrade lactate, it is also
possible that more lactate was removed during W. The fact that
O2 levels were similar at
peak W and C can be partially explained by the high O2 cost
of ventilation experienced by COPD patients (11); it is likely that
during W, because of the high ventilatory demand and greater
involvement of the trunk, the O2 cost of each liter of
ventilation was also increased.
Previous work on walking in patients with COPD is limited to simple
physiological measurements. In most instances, the investigators were
attempting to establish the optimal duration and type of ambulation,
with and without the observer's encouragement. After an initial wave
of enthusiasm for walking tests in assessing functional exercise
capacity, interest in this methodology declined because several
laboratories failed to establish significant correlations between
distance covered and resting routine physiological indexes. There are
few reports in the literature contrasting ventilatory and metabolic
adaptations to W vs. C in COPD patients. Swinburn and co-workers (17)
compared the cardiorespiratory responses to 12-min walking tests and to
cycle ergometer exercise in a group of patients with severe COPD.
Similarly to our study, they found no significant differences in peak
E and peak
O2 for the two types of
exercise. The device they used to measure pulmonary gas exchange,
however, did not allow them to measure
CO2 and RER. Errors in
O2 calculations may also have
been incurred because, with
CO2 not measured, the Haldane
correction could not be applied. Di Prampero and co-workers (7)
compared O2 responses and changes in blood lactate (lactate) in normal individuals during constant-load bouts of cycling exercise and square-wave stepping, which, to a slight extent, is similar to walking. With cycling, they
observed that lactate was greater than with stepping. The authors
postulated that the larger lactate was due to different specific
patterns of muscle fiber recruitment, static vs. dynamic components of
muscle contraction, and/or muscle perfusion. The relevance of these
findings to our investigation is limited because the subjects were
normal and walking was replaced by stepping. Guyatt and co-workers (8)
reported a correlation of low magnitude between walking-test scores and
data from maximal exercise on a cycle ergometer in patients with
chronic lung disease and heart failure; they implied that lack of a
close correlation should not be surprising because walking assesses a
patient's ability to undertake the activities of day-to-day life
whereas cycling is not a common physical effort. In a recent paper
(13), the effects of walking and cycling were investigated. The
response patterns of O2 peak
and blood lactate were similar to ours; valid comparisons between the
two reports cannot be made because that study contrasted cycling
exercise with graded constant speed treadmill exercise, a physical
effort that is functionally quite different from that of walking on
level ground.
In the first part of our study, a breath-by-breath apparatus for C and a telemetric system for W were used. This was done because we wanted to characterize pulmonary gas exchange responses precisely, and to this end the breath-by-breath approach is uniformly considered the gold standard. To eliminate the possible errors introduced by the use of two different techniques for measuring pulmonary gas exchange, a validation study was conducted. The validation experiments for the telemetric equipment demonstrated very small biases in gas exchange measurements. To minimize errors the following precautions were taken: the turbine was the same for the two sets of equipment, gas analyzers were calibrated with the same tanks before each test, and calibrations were verified at the end of each experiment. In the second part of experiments, when arterial blood measurements were obtained, only the telemetric system was used for both W and C.
In summary, our study showed that, in patients with moderate to severe COPD, maximal aerobic capacity is markedly reduced. More importantly, we were able to demonstrate that with W the ventilatory demand was greater than with C; this finding can be explained, at least in part, by a larger degree of lung gas exchange inefficiency (i.e., higher VD/VT) likely to be due to differences in body posture, functional residual capacity, and/or hemodynamics. By contrast, metabolic differences as reflected by blood lactate concentration did not explain the observed findings; during W, blood lactate levels were lower and pH values higher. The increased ventilatory demand during W may also be related to differences in muscle groups recruited and/or inequalities in neurogenic afferent from the lung or from the exercising limbs. Whatever the mechanisms of the increased ventilatory demand are, in COPD patients the ability to walk seems to be primarily affected by the ventilatory restraint. As a clinical corollary to our findings, it should be kept in mind that the information obtained in COPD patients during cycling may not reflect precisely their ventilatory and metabolic requirements for daily activities such as walking. Because the shuttle walking test evokes a maximal response in cardiopulmonary indexes, it also seems inappropriate for evaluating the level of daily activity in COPD patients.
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FOOTNOTES |
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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: P. Palange, Dipartimento di Medicina Clinica, Viale dell'Università 37, 00185 Rome, Italy (E-mail: palange{at}uniroma1.it).
Received 26 June 1998; accepted in final form 10 January 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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M. Poulain, F. Durand, B. Palomba, F. Ceugniet, J. Desplan, A. Varray, and C. Prefaut 6-Minute Walk Testing Is More Sensitive Than Maximal Incremental Cycle Testing for Detecting Oxygen Desaturation in Patients With COPD Chest, May 1, 2003; 123(5): 1401 - 1407. [Abstract] [Full Text] [PDF]
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) and cycling (C, 
) exercise tests in a
representative chronic obstructive pulmonary disease patient.