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(Circulation. 1999;100:503-508.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Respiratory Muscles Performance Is Related to Oxygen Kinetics During Maximal Exercise and Early Recovery in Patients With Congestive Heart Failure
From the Departments of Pulmonary and Critical Care Medicine (S.N., C.K., A.S., C.R.) and Clinical Therapeutics (J.N., G.A., J.K., E.T.), National and Kapodestrian University, Athens, Hellas, Greece.
Correspondence to Serafim Nanas, MD, Pulmonary and Critical Care Department, Evgenidio Hospital, Papadiamantopoulou 20, Athens 11528, Hellas, Greece.
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Abstract |
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 Top Abstract IntroductionPatients and MethodsResultsDiscussionReferences |
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Background—Dyspnea and fatigue are the main causes of exercise limitation in chronic heart failure (CHF) patients, whose peak inspiratory (Pimax) and expiratory pressures (Pemax) are often reduced. The aim of this study was to examine the relationship between respiratory muscle performance and oxygen kinetics.
Methods and Results—A total of 55 patients (NYHA class I
to III) and 11 healthy subjects underwent cardiopulmonary
exercise tests (CPET) on a treadmill. In 45 of the 55 patients (group
I) and in healthy subjects (group II), pulmonary function
tests, Pimax, and Pemax were measured before
and 10 minutes after exercise, and oxygen kinetics were monitored
throughout and during early recovery from CPET. The first degree slope
of oxygen consumption (
O2) decline
during early recovery (O2/t-slope) and
O2 half-time (T1/2)
were calculated. In 10 of the 55 CHF patients (group III), the
measurements of Pimax were repeated 2, 5, and 10 minutes
after CPET. A >10% reduction in Pimax after CPET
(subgroup IA) was measured in 11 of 45 patients. In contrast, 34 of 45
CHF patients (subgroup IB) and all control subjects (group II) had
Pimax>90% of baseline value after CPET. Subgroup IA
patients had significantly lower peak O2
(13.5±2.1 versus 17.8±5.6 mL · kg-1 ·
min-1; P<0.001), lower
anaerobic thresholds (10.1±2.4 versus 13.6±4.6 mL
· kg-1 · min-1;
P=0.003) and lower
O2/t-slopes (0.365±0.126 versus
0.519±0.227 L · min-1 · min-1;
P=0.008) than subgroup IB patients.
Conclusions—The reduction of Pimax after exercise is associated with prolonged early recovery of oxygen kinetics, which may explain, in part, the role played by respiratory muscles in exercise intolerance in CHF patients.
Key Words: respiratory muscles • heart failure • oxygen • exercise test
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Introduction |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences |
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It has been suggested that respiratory muscle fatigue may limit the exercise capacity of even normal subjects.1 2 3 4 Dyspnea and fatigue are the main causes of exercise limitation, which negatively affects the quality of life of patients with chronic heart failure (CHF).5 6 7 Respiratory muscle dysfunction may play a role, although this has not been investigated in depth. It has been proposed that dyspnea is influenced by the central nervous system's perception of inspiratory motor output, a signal that increases with a reduction in respiratory muscle strength.8 Respiratory muscle strength depends, among others, on age, sex, nutritional status, smoking, and fitness level.9 10 11 12 13 14 Clinical studies have shown that peak inspiratory (Pimax) and expiratory pressures (Pemax),15 16 17 18 as well as respiratory muscle endurance,19 are reduced in patients suffering from CHF compared with age-matched normal subjects. This reduction correlates with the degree of dyspnea.20 The cause of this respiratory muscle dysfunction remains speculative.
Recent data support the view that the rate of decline in oxygen
consumption (O2) during early
recovery from exercise correlates well with exercise tolerance in
patients with CHF.21 22 The half-time of
O2 decline in early recovery
from exercise is prolonged in these patients compared with normal
volunteers, and nuclear magnetic resonance spectroscopy shows
that a slower recovery of limb-muscle energy stores partly accounts for
this phenomenon.22 These findings agree with the results
of experiments in isolated perfused canine muscles, which showed that
the recovery of O2 follows the
same time course as the recovery of high-energy
phosphates.23
Because the time course of energy-store resynthesis resembles the recovery of maximum strength after exhaustive exercise in humans,24 25 we hypothesized that the recovery of muscle energy stores, as expressed by early exercise recovery in oxygen kinetics, is associated with respiratory muscle performance. The objective of this study was to examine the relationship between maximal respiratory mouth pressures, before and after exercise, and early recovery oxygen kinetics.
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Patients and Methods |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences |
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A total of 55 patients (49 men and 6 women) with CHF and 11 healthy volunteers were studied. The study was reviewed and approved by the Human Study Committee of our Institution, and informed consent was formally obtained from each participant. All subjects performed tests of maximal respiratory pressures before and after cardiopulmonary exercise tests (CPET). In 45 of the 55 patients (41 men and 4 women) with CHF (group I) and in the 11 healthy volunteers (group II), the measurements of maximal respiratory pressures were performed before and 10 minutes after the end of CPET. In the remaining 10 of the 55 patients with CHF (group III), the measurements of maximal respiratory pressures were performed before the beginning of CPET and were repeated 2, 5, and 10 minutes after the end of CPET. Table 1
lists selected
characteristics pertaining to each group. All patients were clinically
stable and optimally treated at the time of study. Those with recent
myocardial infarction, respiratory insufficiency, or other conditions
affecting exercise capacity were excluded from the study.
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Pulmonary Function Tests
Each study participant had forced vital capacity (FVC) and forced
expiratory volume in 1 second (FEV-1) measured in the sitting position
before exercise.
Maximal Respiratory Pressures
The measurements of maximal respiratory pressures were performed
using the Vmax 229 system of pulmonary and
metabolic tests (Sensormedics). The method used was
similar to that described by Black and Hyatt.10 Patients
were seated and breathed through a scuba-type mouthpiece attached to a
3-way valve with a small leak incorporated in the
airway.26 For the measurement of
Pimax, each patient was instructed to exhale to
the residual volume followed by a maximal inspiratory effort through
the mouthpiece. The maneuver was repeated until 3 reproducible
measurements with a <5% variability had been obtained; the highest
pressure measured was used for analysis. For the measurement of
Pemax, each patient was instructed to inhale to
total lung capacity followed by a maximal expiratory effort through the
mouthpiece. During expiratory maneuvers, light pressure was applied to
the cheeks to minimize the contribution of facial
muscles.26
Pulmonary function tests and respiratory pressure measurements were repeated 10 minutes after the end of CPET for all study participants. However, in group III, additional respiratory pressure measurements were obtained 2 and 5 minutes after the end of CPET. Differences in maximal respiratory pressures measured before and after the exercise test were considered an index of respiratory-muscle endurance. A reduction of 10% in maximal pressures after CPET was chosen to separate 2 subgroups of patients included in group I. This arbitrary percentage was chosen because it represents twice the generally accepted intraindividual variation in measured maximal respiratory pressures. Subgroup IA includes the patients who had a reduction in Pimax>10% between baseline value and exercise, and subgroup IB included the patients who had a Pimax>90% of baseline value after exercise.
Cardiopulmonary Exercise Testing
CPET was performed on a treadmill. The protocol (modified
Bruce or modified Naughton)27 was chosen to avoid an
exercise duration longer than 15 minutes. Blood pressure measurements
were obtained every 2 minutes using a standard-cuff mercury
sphygmomanometer. ECG and peripheral blood
O2 saturation were monitored throughout the test.
Patients and normal volunteers self-graded their degree of dyspnea
during CPET using the Borg scale.28
O2, carbon dioxide output
(CO2), and air flow were
measured on a breath-by-breath basis using the Vmax 229 monitor for
pulmonary and metabolic studies. The system was
calibrated with a standard gas of known concentration before each test.
These measurements were obtained with the subject in the upright
position before and during exercise and with the subject sitting in a
chair during the first 10 minutes of recovery. Baseline
O2 was calculated by averaging
the measurements made for 2 minutes before the beginning of
exercise.
Peak O2 was calculated as the
average of measurements made for 20 s before the end of exercise.
Anaerobic threshold (AT) was determined using the V slope
technique,29 and the result was confirmed by a graph on
which the respiratory equivalent for oxygen
(VE/O2) and carbon dioxide
(VE/CO2) were plotted
simultaneously against time. To evaluate
O2 kinetics during recovery in
groups I and II, the first-degree slope of
O2 for the first minute of the
recovery period was calculated by linear regression using an
appropriate computerized statistical program. The first minute was
chosen to guarantee that the measurements would reflect the alactic
phase of the repayment of oxygen debt.23 30 The time
required for a 50% fall from peak
O2 (T1/2 of
O2) was also calculated. When
it occurred in the middle of 2 sampling points, T1/2
of O2 was set at the second of
these points.22
In group III patients, the maximal respiratory pressure
measurements were consecutively obtained 2, 5, and 10 minutes after the
end of CPET. Consequently, in that group,
O2 kinetics could not be
practically measured during recovery.
Patients and normal volunteers were instructed to exercise until exhaustion. Endpoints of CPET were dyspnea, fatigue, leg weakness, and chest discomfort. Subjects who terminated CPET because of dizziness or chest pain or who developed a serious arrhythmia were excluded from the study.
Statistical Analyses
Results are presented as mean±SD unless otherwise stated.
The significance of differences between means was examined with
Student's t test. Correlation between
Pimax, Pemax, and peak
O2 were tested by
Pearson's correlation coefficient. The Mann-Whitney test was used to
compare differences between groups classified according to
Weber31 (see below). A repeated measurement ANOVA was
used to compare changes in Pimax measurements at
different times of recovery in group III. P<0.05 was
considered statistically significant.
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Results |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences |
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In the group I patients, the mean pulmonary capillary wedge pressure at rest was 14.4±7.3 mm Hg, and the mean left ventricular ejection fraction was 24.0±9.5%. Table 2
summarizes the results of CPET in
CHF patients versus healthy subjects. Both Pimax
and Pemax, at rest and after exercise, were
greater in controls than in CHF patients. Conversely,
T1/2 of O2
was longer in CHF patients than in healthy volunteers. The percent
change of Pimax or Pemax
after exercise was not statistically different between the two groups.
No control subject had a >10% reduction of
Pimax after CPET.
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In group III patients with 3 measurements of
Pimax during recovery, a repeated measurement
ANOVA showed statistically significant changes (F=5.6;
P<0.028). A decrease was found at 2 and 5 minutes after
CPET compared with preexercise values, whereas no difference was
observed 10 minutes after CPET (Figure 1).
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A total of 11 of the 45 group I patients (subgroup IA) had a >10%
decrease in Pimax after CPET. Table 3 summarizes the pertinent comparisons
between these 11 patients and the 34 patients whose
Pimax did not change significantly (subgroup IB).
There was no difference in preexercise Pimax and
Pimax% between patients in subgroups IA
and IB (Table 3). Subgroup IA had lower mean peak
O2, mean
O2 at the AT, and mean
O2/t-slope. There were no
significant differences between the 2 subgroups in left
ventricular ejection fraction, pulmonary capillary
wedge pressure, cardiac index, FEV-1%, FVC%, or FEV-1/FVC. Subgroup
IA patients showed a trend toward a higher degree of dyspnea (Borg
scale). Subgroup IB patients had lower mean peak
O2 (17.8±5.6 versus 26.9±4.9
mL · kg-1 ·
min-1; P<0.001), lower mean
O2 at the AT (13.6±4.6
versus 19.9±3.9 mL · kg-1 ·
min-1; P<0.001), lower mean
O2/t-slope (0.519±0.227
versus 0.889±0.327 L · min-1 ·
min-1; P<0.005), and greater
T1/2 (1.5±0.4 versus 1.1±0.2 minutes;
P<0.001) compared with controls (group II).
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The patients in group I were further subclassified using
Weber's scale based on peak
O231 : 12 patients were
in class A, 9 in class B, and 24 in class C/D. No patient in Weber
class A had a >10% reduction in Pimax after CPET;
however, 2 of 9 patients (22.2%) in Weber class B and 9 of 24 patients
(37.5%) in Weber class C/D did (Figure 2). The differences between these groups
were statistically significant (P=0.028). In group III, 4
patients were in class A, 2 in class B, and 4 in class C. Two of these
patients failed to return to within 10% of the preexercise
Pimax within 10 minutes.
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A weak correlation was measured between peak
O2 and
Pimax before CPET (r=0.33;
P=0.027) in group I patients. There was no correlation
between Pemax and peak
O2. In both patients and
controls, Pimax 10 minutes after the CPET
correlated significantly with
O2/t-slope
(r=0.39; P=0.003) (Figure 3). The correlation, although
weaker, was still significant when controls were removed
(r=0.31; P=0.039).
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Discussion |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences |
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This study showed that the pressure-generating capacity of the respiratory muscles is not reduced 10 minutes after CPET in the majority of CHF patients. However, when a fall in Pimax does occur, it is associated with altered oxygen kinetics, ie, the subgroup of CHF patients with Pimax<90% of baseline value after CPET (subgroup IA) had significantly longer recovery of basal metabolism (
O2/t-slope) and a
significantly lower AT and peak
O2 than the subgroup of CHF
patients whose Pimax did not decrease
significantly after CPET (subgroup IB).
Maximal Respiratory Pressures
The maximal respiratory pressures are considered reliable indices
of respiratory muscle strength.9 10 Thorough coaching and
patient motivation allows highly reproducible
measurements.13 A potential limitation of the method is
that higher maximal respiratory pressures can be reached through a
"learning effect."13 The design of this study, which
used the measurement of maximal respiratory pressures before exercise
as baseline to evaluate the changes occurring after exercise, aimed to
circumvent this potential problem because the learning effect, if
existent, would have resulted in an underestimation of the
Pimax reduction after exercise. This learning
effect may, thus, have accounted for the borderline (<10%) reduction
in Pimax after CPET in some of our patients.
CPET is a form of endurance test for the respiratory muscles capable of producing a decline in Pimax immediately after exercise in healthy subjects. This is also the case for CHF patients, as evidenced by the report of Mancini et al,20 who reported that the maximal respiratory pressures measured at peak exercise were lower than the values measured at rest. This reduction of Pimax at peak or immediately after exercise most likely represents high-frequency fatigue of the respiratory muscles, because beyond 2 minutes, a gradual return to normal occurs, at least in healthy human subjects. To our knowledge, the pattern of recovery of Pimax in CHF patients has not yet been studied.
Our finding that Pimax was not decreased 10 minutes after exercise in the majority of CHF patients indicates that the pattern of recovery of Pimax is similar to that observed in normal subjects,32 33 where a significant decline occurs within the first 2 minutes after CPET, with a gradual return to normal thereafter. This is further evidenced by the repeated Pimax measurements after the end of CPET in group III patients, who showed a decrease of Pimax at 2 and 5 minutes, but not at 10 minutes in comparison with preexercise values. However, this was not the case for all CHF patients. The large number of patients we studied allowed us to identify a subgroup of CHF patients whose Pimax was reduced 10 minutes after CPET, which probably reflected a component of low-frequency fatigue. Was this different respiratory muscle performance associated with oxygen kinetics as hypothesized?
Oxygen Kinetics
Comparison of Pimax and
Pemax before and after CPET in the same
individuals in relation to oxygen kinetics has not been previously
examined. Therefore, in this study, Pimax and
Pemax measurements were repeated at 10 minutes
into recovery from exercise. In agreement with previous findings, a
weak (although statistically significant) correlation, before and after
CPET, existed between Pimax and peak
O2.17 34
Assuming that the fall in
O2 during early recovery from
exercise is linear, O2
recovery in patients with CHF was examined in a linear regression
model. Our measurements applied to the fast component (alactic phase)
of the repayment of the oxygen debt.30 Investigators who
studied the repayment of oxygen debt have used
single23 35 36 and double exponential
equations36 to describe the fall in
O2 during the recovery period.
It was observed in stable workload protocols that the time constant and
half-time (T1/2) derived from it were independent of
the work level.35 Recently, Cohen-Solal et
al22 used the T1/2 of
O2, calculated as the time
required for a 50% fall in the peak
O2, to describe the fall in
O2 during recovery from
exercise in patients with CHF. A close correlation was found between
this T1/2 of
O2 and that derived from the
time constant of exponential equations.22 It was observed
during graded exercise in CHF patients that T1/2 of
O2 remained independent of the
level of exercise as long as workload remained above 50% of maximal.
Having to choose the second point when T1/2 of
O2 happens to fall between 2
sampling points is a methodological shortcoming, which may cause
considerable variability in the results, particularly when using the
breath-by-breath technique. We attempted to circumvent this problem by
using the O2/t-slope during
the early recovery period.
The value of O2/t-slope in the
early recovery period was significantly less in subgroup IA patients
than in subgroup IB patients. The association of postexercise
Pimax with oxygen kinetics is further supported
by the correlation of Pimax with
O2/t-slope found in our study.
This may be due to the slower recovery of muscle energy
stores,22 because the time course of energy stores
resynthesis resembles the recovery of maximum strength after exhaustive
exercise in man.24 25 The
pathophysiological mechanism of the slower recovery
of muscles' energy stores is not yet clear. Supinski et
al,37 in an animal model of heart failure, found that the
maximum phrenic arterial flow achieved during electrically
induced diaphragmatic fatigue was appreciably less and the duration of
postocclusive hyperemia in diaphragmatic muscle was
significantly longer in animals with heart failure. Furthermore,
hyperemic blood volume during the first minute after occlusion
was significantly lower (ie, the time to repay the blood volume debt of
the diaphragmatic muscle in animals with heart failure was prolonged).
It is, therefore, tempting to speculate that an analogous vascular
dysfunction occurs in the respiratory muscles of some CHF patients,
which would account for the decrease in Pimax and
the slower recovery of oxygen kinetics that was observed in this study.
Recent data suggest that oxygen delivery to working skeletal muscle, as
evaluated by nuclear magnetic resonance and near-infrared spectroscopy,
is impaired during recovery from maximal bicycle exercise in CHF
patients.38 39 Moreover, Mancini et al20
found serratus anterior muscle deoxygenation during
maximal bicycle exercise, consistent with respiratory muscle
ischemia. At the extreme end of this dysfunction, respiratory
muscle underperfusion during cardiogenic shock caused by tamponade in
dogs led to diaphragmatic fatigue.40
These observations are concordant with a significant reduction in peak
O2 and AT, as well as a lower
O2/t-slope during recovery
among subgroup IA patients. This association of respiratory muscle
function with indices of recovery oxygen kinetics in CHF patients has
not been reported before.
Patients with CHF have several histological and biochemical changes in their striated muscles, including fewer oxidative slow-twitch fibers, impaired aerobic-oxidative capacity, and an earlier shift toward anaerobic metabolism during exercise, causing the so-called oxygen debt.41 These changes are not homogeneous throughout the CHF population, and they are not attributed to changes in muscle blood flow, but rather to intrinsic alterations in the muscle.42 43 This variability in muscle metabolism and histology38 44 may partially explain the variability in Pimax after CPET among our patients.
In summary, respiratory muscle performance, expressed as maximal respiratory pressure after CPET, is not reduced (except transiently) in the majority of patients with heart failure. However, a long-lasting >10% decrease of maximal inspiratory pressure at late recovery was observed in CHF patients, with significantly lower exercise capacity and significantly delayed recovery of resting oxygen consumption. These observations provide new insights into the pathophysiological mechanisms of respiratory muscle performance in patients suffering from CHF.
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Acknowledgments |
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We thank Dr Theodoros Vasilakopoulos for his suggestions on the final form of this manuscript.
Received December 31, 1998; revision received May 5, 1999; accepted May 5, 1999.
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heart failure. Circulation. 1992;86:515A. Abstract.To
examine the relationship between respiratory muscle performance
and oxygen kinetics, 55 CHF patients (NYHA class I to III) and 11
healthy subjects underwent CPET on a treadmill. Eleven patients, who
had a >10% reduction of Pimax after exercise, had
significantly lower peak O2 (13.5±2.1
versus 17.8±5.6 mL · kg-1 ·
min-1; P<0.001) and lower first-degree
slope of O2 decline during early
recovery (0.365±0.126 versus 0.519±0.227l/min/min;
P=0.008) than the remaining patients (subgroup IB). The
reduction of Pimax at recovery after exercise is associated
with prolonged recovery of oxygen kinetics in CHF patients.
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