Am. J. Respir. Crit. Care Med.,
Volume 160, Number 2, August 1999, 756-756
EXERCISE LIMITATION IN CHRONIC OBSTRUCTIVE
PULMONARY DISEASE (COPD)
To the Editor:
Oelberg and colleagues (1) advance the argument that cardiovascular factors may contribute to exercise intolerance in patients with COPD because helium-oxygen (He-O2) breathing,
although increasing maximal exercise ventilation, was not associated with improvements in maximal cardiac output and
O2 extraction. They outline in their introduction that He-O2
breathing is associated with a reduction in the work of breathing in patients with COPD during resting conditions (2) and
that in healthy older individuals (3) He-O2 breathing is associated with an increase in maximal exercise minute ventilation
(
E), presumably as a result of a reduction in the work of
breathing. The article they site (2) that describes a decrease in
the work of breathing with He-O2 breathing in patients with
COPD involves measurements made at rest where E did not increase above air-breathing levels. Babb (3) demonstrated that while He-O2 decreases resistance to air flow during heavy exercise the associated increase in E results in the same work of breathing, as compared with air breathing in healthy older subjects. Since Oelberg and colleagues (1) did not measure the
work of breathing in their patients, it is difficult to know if
overall ventilatory work was different between He-O2 and air breathing, given the observed increase in E with He-O2. It is possible that despite favorable changes in airway resistance
and expiratory flow that may have been induced by He-O2
breathing, the overall work of breathing remained abnormally
high (at levels similar to air-breathing) as compared with the
total external work performed during maximal exercise.
Given this possibility and the fact that the observed changes in
cardiac output and O2 extraction during maximal exercise are
not unlike what is observed (4) in untrained subjects, it seems
likely that pulmonary factors are primarily responsible for the
exercise intolerance noted by Oelberg and coworkers (1). Another issue not addressed in their paper relates to how an
acute unloading (assuming that unloading implies decreased
respiratory work) of the ventilatory pump might be expected
to improve exercise tolerance, cardiac output, and O2 extraction in patients who have been chronically deconditioned. Is
this a reasonable expectation (despite the possibility of the existence of a significant cardiac reserve) in such severely affected patients who did not take part in a conditioning program? Babb (3) suggests that He-O2 breathing in healthy
sedentary older subjects does not result in an increase in maximal exercise workload or heart rate, despite an increase in
maximal exercise E. Although cardiovascular factors limit
exercise in healthy individuals, the same cannot be said about
patients with COPD, particularly when the degree of pulmonary impairment is severe.
ANTHONY D. D'URZO
Primary Care Asthma Clinic
Toronto, Ontario, Canada
1.
Oelberg, D. A.,
R. M. Kacmarek,
P. P. Pappagianopoulos,
L. C. Ginns, and
D. M. Systrom.
1998.
Ventilatory and cardiovascular responses to
inspired He-O2 during exercise in chronic obstructive pulmonary disease.
Am. J. Respir. Crit. Care Med.
158:
1876-1882
[Abstract/Free Full Text].
2.
Swidwa, D. M.,
H. D. Montenegro,
M. D. Goldman,
K. R. Lutchen, and
G. M. Saidel.
1985.
Helium-oxygen breathing in severe chronic obstructive pulmonary disease.
Chest
87:
790-795
[Abstract/Free Full Text].
3.
Babb, T. G..
1997.
Ventilatory response to exercise in subjects breathing
CO2 or He-O2.
J. Appl. Physiol.
82:
746-754
[Abstract/Free Full Text].
4.
Fox, E. L., R. D. Bowers, and M. L. Foss. 1988. The Physiological Basis of
Physical Education and Athletics, 4th ed. Philadelphia, Saunders. 236-250.
From-the Authors:
Dr. D'Urzo's suggestion that in severe COPD, ventilatory work
is the same at high E when breathing He-O2 compared to
N2-O2 seems reasonable. The implication, however, that respiratory muscle function directly limits short-term incremental exercise performance in this population has little or no support in the literature (1). Moreover, the major finding of our
paper does not depend on any difference in peak exercise
work of breathing due to the inspired gas condition. He-O2
was simply used as a tool to mitigate, but not necessarily eliminate, the pulmonary mechanical limit to incremental exercise
in COPD and examine the resulting behavior of the Fick Principle variables. That the former was accomplished, we believe
is incontrovertible, given the observed increase in peak exercise E and relative hypocapnia during He-O2 breathing. As
previously stated, it was the failure of peak exercise cardiac output and systemic O2 extraction to increase proportionally
that was most interesting and suggestive of independent exercise limits. The abnormalities of blood flow and peripheral O2
utilization are far more severe than those expected in simple
deconditioning (2). Finally, the failure of (surrogate markers
of) cardiac output to increase during He-O2 in a (healthy sedentary older) population limited by cardiac output (3) sounds
frighteningly familiar and is exactly what was found!
DAVID A. OELBERG
DAVID M. SYSTROM
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts
1.
Gallagher, C. G..
1994.
Exercise limitation and clinical exercise testing in
chronic obstructive pulmonary disease.
Clin. Chest Med.
15:
305-326
[Medline].
2.
Saltin, B., G. Blomqvist, J. H. Mitchell, R. L. Johnson, K. Wildenthal, and
C. B. Chapmann. 1968. Response to exercise after bed rest and after
training. Circulation 38:VII 1-VII 78.
3.
Horvath, S. M., and
J. F. Borgia.
1984.
Cardiopulmonary gas transport
and aging.
Am. Rev. Respir. Dis.
129:
S68-S71
[Medline].
