(Circulation. 1995;91:1719-1724.)
© 1995 American Heart Association, Inc.
Articles |
Evaluation of Exercise Capacity Using Submaximal Exercise at a Constant Work Rate in Patients With Cardiovascular Disease
Presented in part at the annual meeting of Experimental Biology, Anaheim, Calif, April 1994.
From the Second Department of Internal Medicine (A.K., N.S., F.M., M.H.), Tokyo Medical and Dental University, Tokyo, Japan; Hokushin General Hospital (T.Y., H.K., K.S.), Nagano-ken, Japan; and Musashino Red Cross Hospital (H.A., A.N.), Tokyo, Japan.
Correspondence to Akira Koike, MD, Second Department of Internal Medicine, Tokyo Medical and Dental University, 5-45 Yushima 1-chome, Bunkyo-ku, Tokyo 113, Japan.
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Abstract |
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Background Symptom-limited incremental exercise tests are used to estimate the severity of cardiovascular disease and the patient's daily activity. However, there is a need for objective parameters for submaximal exercise. To test the hypothesis that a decrease in maximal exercise capacity can be estimated by oxygen uptake (
O2) kinetics, we measured
the time
constant of O2 both during
the onset of
constant work rate exercise at 50 W and during recovery from this
exercise and compared it with data obtained during maximal exercise in
patients with cardiovascular disease and in normal subjects.
Methods and Results A total of 34 patients with cardiovascular
disease and 14 normal subjects performed 6 minutes of 50-W constant
work rate exercise and an incremental exercise test to the
symptom-limited maximum on a cycle ergometer.
O2 was calculated from
respiratory gas
analysis on a breath-by-breath basis. The time constant of
O2 during the onset of 50-W
exercise was
61.4±15.2 seconds in patients with cardiovascular disease,
significantly longer (the kinetics of
O2
were slower) than that in normal subjects (48.8±10.4 seconds,
P=.008). The time constant of
O2 during the onset of
exercise was
significantly negatively correlated with peak
O2
(r=-.67) and maximal work
rate (r=-.66). The time constant during recovery, which
did
not differ significantly from that of exercise, was also prolonged in
patients with cardiovascular disease; it showed a negative correlation
with peak O2
(r=-.63) and
maximum work rate (r=-.54).
Conclusions The time constant of
O2 during and after
recovery from 50 W
of constant work rate exercise, which does not require the subject's
maximal effort, is a useful and objective measure of exercise capacity
in patients with mild to moderate cardiovascular disease.
Key Words: exercise • oxygen • cardiovascular diseases
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Symptom-limited incremental exercise tests have long been used to estimate the severity of cardiovascular disease and the patient's daily activity.1 2 3 4 Oxygen uptake (
O2) at maximal
exercise (peak
O2) is a noninvasive
parameter of
cardiac reserve. However, data obtained at maximal exercise may not be
reproducible5 because of factors such as the subject's
motivation and the criteria used by the physician to terminate the
exercise test. Thus, cardiologists are interested in obtaining
objective information based on submaximal rather than maximal
exercise.4 6
While at the onset of exercise the oxygen requirement of muscle
increases approximately exponentially, only a small amount of oxygen is
available from intracellular sources.7 Since the ability
to rapidly increase the delivery of oxygen is essential for cellular
homeostasis, the ability to match the
O2
to the cellular oxygen requirement depends on cardiac and circulatory
function. Thus, patients with cardiovascular disease may have a lower
uptake of oxygen (a slowing of
O2
kinetics) at the onset of exercise as compared with normal
subjects.
We hypothesized that a decrease in maximal exercise capacity can be
estimated from O2 kinetics
at the onset
of exercise. We therefore measured the time constant of
O2 during the onset of 50 W
of constant
work rate exercise and compared it with data obtained during maximal
exercise in incremental exercise testing conducted in patients with a
variety of cardiovascular diseases and in normal subjects. We also
compared the time constant of
O2 during
recovery from 50 W of constant work rate exercise with data on exercise
capacity in these subjects.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Subjects
Thirty-four consecutive patients with cardiovascular disease classified as New York Heart Association functional class I or II were studied between May 1992 and August 1993 (Table 1
).
Fourteen healthy subjects who were recruited from a medical screening
clinic during this period and determined to be free of any significant
disease on the basis of history, physical examination, chest
radiograph, 12-lead ECG, and other routine laboratory tests were also
studied (Table 1). These 14 subjects had a normal ECG response
on a
screening maximal ergometer exercise. Diagnoses of the patients
included previous myocardial infarction (13 patients), coronary artery
disease without myocardial infarction (7 patients), valvular heart
disease (6 patients), dilated cardiomyopathy (5 patients), hypertensive
heart disease (1 patient), and other heart disease (2 patients). We
excluded from the study those with pure mitral stenosis, aortic
stenosis, unstable angina, heart failure classified as functional class
III or IV, and documented lung disease. No patient had a myocardial
infarction within the month before enrollment in the study. All
patients were clinically stable at the time of the study. A ß-blocker
was withheld for 7 days. A slow-release nitrate or calcium antagonist
was withheld for 48 hours. All the other medications were withheld for
at least 24 hours before the study. The nature and purpose of the study
was explained to the subjects, and after being so informed, each
consented voluntarily to participate in the study.
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Exercise Protocol
An upright, electromagnetically braked
cycle ergometer
(Siemens-Elema 930, Siemens Elema AB) was used in the exercise test. On
the day of the study, each subject performed the 50-W constant work
rate test for 6 minutes starting from rest and then performed an
incremental exercise test to the symptom-limited maximum. The
incremental exercise test began with a 3-minute warm-up at 20 W and 60
rpm; the load then was increased incrementally by 1 W every 6 seconds.
The interval between the two tests was approximately 60 minutes. A
12-lead ECG was obtained every minute using a Case II Stress System
(Marquette Electronics). Cuff blood pressure was determined every
minute with an automatic indirect manometer (STBP-680F, Collin Denshi).
The end point of the incremental exercise test was chest pain in 3
patients who had coronary artery disease; it was leg fatigue or dyspnea
in the remaining subjects.
Measurements of O2
During
Exercise
O2 was
measured with the subject
at rest, seated on the ergometer, and throughout the exercise period,
using an Aeromonitor AE-280 (Minato Medical Science).8
This system consists of a microcomputer, a hot-wire flowmeter, and
oxygen and carbon dioxide gas analyzers (zirconium element–based
oxygen analyzer and infra-red carbon dioxide analyzer). Gas was sampled
at the rate of 220 mL/min through a filter by a suction pump through
the analyzers. The Aeromonitor AE-280 calculated the breath-by-breath
O2 based on the
mathematical
analysis described by Beaver et al.9 The system was
calibrated before each study.
Data Analysis
Resting
O2 was determined as the
average of 2 minutes with the subject sitting on the ergometer before
starting exercise. The O2
at 6 minutes
was determined as the average between 330 to 360 seconds during 50-W
exercise. Peak O2 was
defined as the
highest O2 that was
attained over a
10-second period during incremental exercise.
A five-point moving
average of the breath-by-breath data was used to
evaluate O2 kinetics during
the 50-W
constant work rate exercise. The time constant of
O2 kinetics was determined
by fitting a
monoexponential function to the
O2
response starting at exercise onset, assuming the resting value of
O2 as its
baseline.10 11
The time constant was derived by nonlinear regression by using
least-squares and iterative techniques10 11 with a
BMDP statistical software package.12 The time
constant of O2 during
recovery from the
50-W exercise was determined similarly in all subjects except for
subject 17 (Table 1
), whose respiratory gases could not be
obtained
during recovery.
Statistical Analysis
Data are reported as mean±SD.
Comparisons of variables between
normal subjects and patients with cardiovascular disease were made by
unpaired t tests. The comparison of the time constant of
O2 during exercise with
that of recovery
was made by paired t tests. Linear regression analysis
was used to correlate the time constant of
O2 and other variables.
Differences were
considered statistically significant at P<.05.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Table 2
shows the mean maximum work rate and the
peak O2 as determined in
the incremental
exercise tests in the cardiac patients and in the normal subjects.
Differences in both variables between the two groups were statistically
significant.
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Fig 1 shows the changes in
O2 during 50 W of constant
work rate
exercise and during recovery, along with the computer-derived line of
the best fit to a single exponential model of the
O2 response, for a
representative normal subject (subject 5 in Table 1). After the
onset of exercise, O2
increased
exponentially and reached a steady state within approximately 3 minutes
of exercise in the normal subject. The kinetics of
O2 during recovery from
exercise were
similar to that during exercise; the calculated time constants of
O2 during exercise and
recovery were
39.9 and 39.7 seconds, respectively.
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indicates time constant of
The time constant of O2
response during
50 W of exercise was determined in all subjects. The kinetics of
O2 during exercise tended
to be slower
in the patients with cardiovascular disease, showing a significantly
longer time constant as compared with the normal subjects (61.4±15.2
versus 48.8±10.4 seconds, P=.008). The mean time
constant
during recovery also was significantly longer in the patients with
cardiovascular disease than that of normal subjects (58.7±12.6 versus
49.4±11.7 seconds, P=.02).
The relation between the time constant of
O2 during 50-W exercise and
the
parameters for exercise capacity obtained during incremental exercise
testing appears for all subjects in Fig 2. The time
constant of O2 increased
with a decrease
in peak O2, with a
significant
negative correlation observed between the two variables
(r=-.67). There also was a significant negative
correlation
between the time constant of
O2 and the
maximum work rate (r=-.66). Similarly, the time constant
of
O2 during recovery showed a
significant
negative correlation with the peak
O2
(r=-.63) and the maximum work rate
(r=-.54) in
all subjects (Fig 3).
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Even in the patient population excluding normal subjects, the time
constant of O2 during 50-W
exercise
showed a significant negative correlation with peak
O2
(r=-.57) and the maximum
work rate (r=-.59). The time constant of
O2 during recovery from
50-W exercise
also showed a significant negative correlation with peak
O2
(r=-.56) and the maximum
work rate (r=-.40) in this population.
The time constant of O2
during
exercise at 50 W of constant work rate and that of recovery showed a
significant positive correlation (r=.53) (Fig
4). The difference between the time constant of
O2 during exercise and that
of recovery
was not significant by the paired t test.
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The time constant of O2
during exercise
became longer with age in normal subjects
(y=0.50x+26.8, r=.71); the time
constant of O2 during
recovery also
tended to be longer with age
(y=0.33x+34.8, r=.42).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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The
O2 response during
constant
work rate exercise is postulated to have three phases13 :
phase I, an immediate increase at the start of exercise lasting
approximately 20 seconds; phase II, a subsequent exponential increase
that lasts 2 to 3 minutes; and phase III, a steady-state level or slow
drift phase that starts at approximately 3 minutes. If the exercise at
a constant work rate is mild or moderate,
O2 usually reaches a steady
state within
3 minutes. However, at work rates associated with increased blood
lactate, O2 continues to
increase beyond
3 minutes. Although we did not measure the blood lactate concentration,
the time constant of O2 is
positively
correlated with blood lactate level during exercise.11
If the work rate is sufficiently high, the phase I increase in
O2 is relatively small. The
overall
increase in O2 during
constant work rate
exercise is determined mainly by increases in phase II and phase III.
However, if the work rate is very low (15 or 20 W), the total
O2 increase during 6
minutes of exercise
is determined mainly by the increase in phase I within the first 20
seconds.10 In this case, the increase in
O2 during phase II is
small, making it
difficult to estimate O2
kinetics during
this period. From our experience,14 most patients with
functional class I or II can comfortably sustain 50 W of constant work
rate exercise for 6 minutes. We therefore used a constant work rate
exercise of 50 W in all subjects studied. In some patients, 50 W may be
too high to be sustained for 6 minutes, especially those with severe
heart failure classified as functional class III or IV or severe
myocardial ischemia. However, the mean heart rate in our patients at 6
minutes at 50-W exercise was not very high (116±25 beats per minute;
Table 2). We therefore believe that this exercise can be
performed
safely by most patients with cardiovascular disease.
We used a single exponential equation to characterize the overall
kinetics of the increase in
O2. Although
the slowed O2 kinetics seen
in cardiac
patients may have been better fitted to a double exponential
equation,15 the methodology of this fitting would be too
complex to obtain a clinical parameter for exercise capacity. However,
a single exponential model is reported to characterize the increase in
O2 even during exercise
associated with
an increase in blood lactate.11 The
O2 during recovery from
exercise is also
known to decrease exponentially.16 Therefore, we used the
same exponential model for the decreasing
O2 kinetics during
recovery.
An oxygen deficit is defined as the difference between the predicted
amount of oxygen required to perform the exercise (steady-state
O2xduration of
exercise) and the actual
cumulative consumption of oxygen.17 Oxygen debt is the
difference between that consumed during recovery and the product of the
preexercise resting O2 and
the duration
of recovery.17 The oxygen deficit can be accounted for by
existing chemical energy stores in the muscle as well as in tissue and
blood, and, ultimately, the formation of ATP by the nonoxidative
metabolism of carbohydrate
substrates.7 10 18 The oxygen
deficit and oxygen debt will be equal if the duration of exercise is
long enough for the O2 to
reach a steady
state.19 The time constant of
O2 during exercise and
recovery can be
calculated from the following equations.20 21
 | (1) |
 | (2) |
Therefore, if the work rate is moderate and the duration of
exercise and recovery are long enough to reach a steady state, the time
constant of O2 during
recovery would
theoretically be identical to that of exercise, as we noted in this
study.
The time constants of O2
during exercise
and recovery were both significantly prolonged in patients with
cardiovascular disease as compared with normal subjects despite our
finding of no difference in hemodynamic variables either at rest or at
6 minutes of exercise (Table 2). Hughson and
Smyth22 and
Petersen et al23 reported that ß-blockade slows the
O2 increase during
submaximal exercise
in normal subjects. Sietsema et al24 demonstrated that
patients with cyanotic congenital heart disease exhibited prolonged
O2 response kinetics. The
O2 response also has been
slowed by
experimentally decreasing the blood oxygen content in normal
subjects.11 These previous findings are consistent with
our observations, although the normal subjects of the present study
were not age-matched with the patients, and the time constant of
O2 was found to be
influenced by
age.
Because the pulmonary O2
kinetics
closely reflect muscular O2
during the
onset of constant work rate exercise, the slowed pulmonary
O2 kinetics probably are
due to a
decrease in oxygen availability at the exercising muscles. Therefore,
the longer time constant of
O2 during
exercise seen in cardiac patients with decreased exercise capacity must
partly be related to their slower increase in cardiac output, as
recently reported.25 26 Although the mechanism
underlying
O2 kinetics during recovery
is not well
understood, the time course of cardiac output during recovery, which
probably is slower in patients with cardiovascular
disease,27 might have influenced recovery
O2 kinetics. However, the
O2 kinetics also are
related to
peripheral oxygen delivery and metabolic utilization at the exercising
muscles. Therefore, the abnormal
O2
kinetics may not be specific for cardiovascular disease.
Maximal O2, a plateau of
O2 despite further
increases in the work
rate, has been used as a useful parameter to evaluate maximal exercise
capacity. Although maximal
O2 is
generally determined by maximal cardiac output and the potential for
oxygen extraction by the exercising muscles,13 28
this
parameter is often difficult to obtain in patients with cardiovascular
disease because of limitations such as chest pain or leg discomfort
before attaining the target work rate. On the other hand, peak
O2, which is simply the
highest
O2 attained during the
incremental
exercise, is easily influenced by the patient's willingness to
exercise as well as the subjective evaluation of the physician who has
the responsibility to terminate the exercise test.
In patients with coronary artery disease, maximal exercise capacity may
be artificially limited due to onset of angina, which may not be
present at submaximal levels. Thus, there is a considerable amount
of interest in obtaining objective and submaximal measurements of
aerobic function. The time constant of
O2 during the initiation
and recovery
from the submaximal exercise is independent from maximal exercise
effort and may be a better reflection of exercise limitations at a
daily activity level compared with the maximal or peak
O2.
The present study used a Siemens Elema 930 ergometer, which
requires approximately 10 seconds to reach the established work rate
after the start of exercise. Therefore, the actual work rate was less
than 50 W in the first 10 seconds. The characteristics of the work rate
at the start of exercise may have influenced the phase I increase in
O2 and partly affected the
calculated
time constant of O2. This
influence
would be more marked at a very low work rate, in which the magnitude of
the increase in O2 during
the 6 minutes
of exercise is determined mainly during the first 20 seconds. However,
these characteristics did not affect the time constant of
O2 during recovery.
The time constants of O2
during both the
initiation of and the recovery from exercise showed significant
negative correlations with peak
O2 and
maximal work rate over a wide range of exercise capacity in our
subjects. Although the factors that determine
O2 kinetics, especially
during the
recovery from exercise, remain to be clarified, we believe that the
time constant of O2 both
during 50 W of
constant work rate exercise and during recovery from this exercise,
which does not require the subject's maximal effort, is a useful
parameter for objectively evaluating the exercise capacity of patients
with mild to moderate cardiovascular disease.
Received August 12, 1994; revision received September 22, 1994; accepted October 26, 1994.
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Y. Masaoka and I. Homma Expiratory time determined by individual anxiety levels in humans J Appl Physiol, April 1, 1999; 86(4): 1329 - 1336. [Abstract] [Full Text] [PDF]
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