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* From the Cardiology Divisions (Drs. Wagner and Dubach), Kantonsspital Chur, Basel, Switzerland; University Hospital(Dr. Schwitter), Zurich, Switzerland; the University of Genoa (Dr. Gianrossi), Genoa, Italy; and Palo Alto Veterans Affairs Medical Center and Stanford University (Dr. Myers), Palo Alto, CA.
Correspondence to: Jonathan Myers, PhD, Palo Alto Veterans Affairs Health Care System, Cardiology 111C, 3801 Miranda Ave, Palo Alto, CA 94304; e-mail: DRJ993{at}aol.com
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Abstract |
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 TOP Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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O2) to return to baseline level
(recovery kinetics) is prolonged in patients with reduced ventricular
function, and the degree to which it is prolonged is related to the
severity of heart failure, markers of abnormal ventilation, and
prognosis. In the present study, we sought to determine the effect of
exercise training on O2 recovery
kinetics in patients with reduced ventricular function.
Methods: Twenty-four male patients with reduced ventricular
function after a myocardial infarction were randomized to either a
2-month high-intensity residential exercise training program or to a
control group. O2 kinetics in recovery
from maximal exercise were calculated before and after the study period
and expressed as the slope of a single exponential relation between
O2 and time during the first 3 min of
recovery.
Results: Peak
O2 increased significantly in the
exercise group (19.4 ± 3.0 mL/kg/min vs 25.1 ± 4.7 mL/kg/min,
p < 0.05), whereas no change was observed in control subjects. The
O2 half-time in recovery was reduced
slightly after the study period in both groups (108.7 ± 33.1 to
102.1 ± 50.5 s in the exercise group and 122.3 ± 68.7 to
107.5 ± 36.0 s in the control group); neither the change within or
between groups was significant. The degree to which
O2 was prolonged in recovery was
inversely related to measures of exercise capacity (peak
O2, watts achieved, and exercise time;
r = - 0.48 to - 0.57; p < 0.01) and directly
related to the peak ventilatory equivalents for oxygen
(r = 0.59, p < 0.01) and carbon dioxide
(r = 0.57, p < 0.01).
Conclusion: Two months of high-intensity training did
not result in a faster recovery of O2 in
patients with reduced ventricular function. This suggests that
adaptations to exercise training manifest themselves only during, but
not in, recovery from exercise.
Key Words: chronic heart failure • exercise training • oxygen uptake
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Introduction |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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O2), 6-min walk time,
autonomic balance, quality of life, and endothelial function.
Studies9
10
11
12
13
14
have observed that time to recovery of
O2 after exercise
(postexercise O2 kinetics) is
delayed in patients with chronic heart failure, and the degree to which
this response delayed is related to the severity of chronic heart
failure. The delay in postexercise O2
kinetics in patients with chronic heart failure appears to be related
to a delay in the recovery of energy stores in the active muscle, as
demonstrated9
using nuclear magnetic resonance
spectroscopy. A faster adjustment of O2
to a given workload at the onset of exercise after training has been
demonstrated in normal subjects,15
16
17
18
as has an
improvement in O2 recovery
time.15
In patients with chronic heart failure, an
improvement in this response might be reflected clinically in lessened
dyspnea after exertion, as a marker for lessened disease severity, and
presumably by an improvement in prognosis, since this index has been
suggested10
to predict outcomes in this condition.
To our knowledge, no controlled studies have been performed to assess
the effects of an exercise training program on
O2 kinetics in recovery in patients with
reduced ventricular function. We performed the present study to: (1)
further characterize the behavior of O2
recovery in these patients, and (2) investigate the effects of exercise
training on recovery kinetics of O2 in
patients with reduced ventricular function who were referred to a
residential cardiac rehabilitation facility in Switzerland.
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Materials and Methods |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Exercise Training
After stabilization and initial testing, patients in the
exercise group resided in a rehabilitation center in Seewis,
Switzerland, for a period of 8 weeks. Seewis is a small village in the
mountains with an elevation of 3,500 feet. The center has its own staff
of physicians, consisting of a medical director and three
interns/residents. Program components included education, exercise, and
low-fat meals prepared three times daily by the rehabilitation center
cook. Two approximately 1-h outdoor walking sessions daily were
performed, once in the morning and once in the afternoon. Walking
intensity was stratified into four levels based on clinical status,
exercise capacity, and performance on a 500-m walking test (50-m
increase in altitude) on a nearby hill. The patients were accompanied
by an exercise leader and a physician during these walking sessions. A
van equipped with emergency supplies followed the group.
In addition to these walking periods, the 12 patients in the exercise
group performed four 45-min periods of monitored stationary cycling per
week. The cycling sessions were designed to elicit an intensity equal
to roughly 60 to 70% of the patient’s peak
O2, and were increased
progressively over the 2 months as tolerated. Each of these sessions
was monitored closely by a medical resident at the rehabilitation
center. Heart rate, workload, and perceived exertion were recorded
every 5 min; adjustments were made in exercise intensity as
appropriate. Control patients received usual clinical follow-up at
home, and did not undergo any formal exercise program.
Exercise Testing
Maximal exercise tests were performed at baseline and 2 months
after randomization to the training or control groups. On the day of
testing, patients were requested to abstain from food, coffee, and
cigarettes for 3 h prior to the test. Standard pulmonary function
tests were performed. Maximal exercise testing was performed on an
electrically braked cycle ergometer using an individualized ramp
protocol. Briefly, this test entails choosing an individualized ramp
rate to yield a test duration of approximately 10 min.19
Arterial blood lactate samples were drawn every minute throughout the
test. A 12-lead ECG was monitored continuously, and BP was measured
manually every minute during exercise and throughout the recovery
period. The patient’s subjective level of exertion was quantified
every minute using the Borg 6 to 20 scale.20
All tests
were continued to volitional fatigue/dyspnea. Respiratory gas exchange
variables were acquired continuously throughout exercise using the
Schiller CS-100 metabolic system (Schiller AG; Baar,
Switzerland). Gas exchange variables analyzed included
O2, carbon dioxide production
(CO2), minute ventilation
(E), respiratory rate, tidal volume, oxygen pulse,
and respiratory exchange ratio. The lactate threshold was chosen using
a plot of the minute-by-minute lactate responses vs time by two
experienced observers (J.M. and P.D.).
The constant decay of
O2, expressed as the slope of
a single exponential relation between
O2 and time during the first 3
min of recovery, was calculated using with following equation:
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O2,
y0 is O2 at time zero, (the
beginning of the recovery phase), A and e are
constants, x is the time elapsed, and t is the
constant decay (Origin, version 2.5; Microcal Software; Northampton,
MA). Breath-by-breath values that fell outside the 95%
confidence limits of the calculated z distribution were excluded. The
time constant indicates the time required to achieve 63.2% of the
difference between peak and baseline values. The recovery half-time
represents the time required for a 50% fall from the peak
O2 value.
Statistics
Statistical software (Statgraphics Plus, Version 4; Statistical
Graphics Corporation; Bethesda, MD) was used to perform
multivariate analysis of variance procedures comparing hemodynamic, gas
exchange, and recovery responses between groups. Post hoc
multiple comparison procedures were performed using the Scheffe method.
Data are presented as mean ± SD.
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Results |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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O2 (Table 1)
. Ejection fraction was
unchanged in both the trained and control groups across the study
period. No untoward events occurred during any of the exercise testing
or training procedures during the 2 months of observation. Patients in
the exercise group were closely monitored for heart rate, workload, and
perceived exertion during their stationary cycling sessions and only
generally during walking sessions. During monitored cycling over the
2-month training period, the mean percentage of maximal heart rate
maintained was 83 ± 6%, the mean percentage of maximal workload was
78 ± 7%, and perceived exertion averaged 15.2 ± 2.
Maximal Exercise Testing
Exercise and ventilatory gas exchange data for each group are
presented in Table 2
. Both groups achieved mean maximal respiratory exchange ratios of
approximately 1.20 and mean perceived exertion levels of approximately
19 on pretests and posttests, suggesting that maximal efforts were
generally achieved. No differences were observed within or between
groups in maximal heart rate or BP. The exercise group demonstrated a
29% increase in maximal O2
(19.4 ± 3.0 to 25.1 ± 4.7 mL/kg/min, p < 0.01). Concomitant
increases in maximal E,
CO2, exercise time, and watts
achieved were observed in the exercise group. No differences between
tests were observed among control patients in maximal
O2, exercise time, or watts achieved.
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O2 at the lactate threshold increased
significantly (by 35%, p < 0.01) after the training period in the
exercise group. Conversely, small but insignificant decreases were
observed in control subjects. Similar increases in exercise time and
watts achieved at the lactate threshold were observed in patients in
the exercise group, whereas the control group demonstrated small
decreases in these variables. No differences were observed within or
between groups in heart rate, systolic or diastolic BP,
E, CO2,
respiratory exchange ratio, lactate, or perceived exertion at the
lactate threshold.
O2 time constants and half-time values
in recovery for both groups are presented in Table 3
, and the individual values for the half-time responses in recovery
among trained subjects are illustrated in Figure 1
. Both groups demonstrated decreases in these variables over the study
period, but none of the differences were significant within or between
groups. The time required for O2 to
recover from exercise was generally longer as fitness was reduced;
significant inverse relationships were observed between
O2 half-time in recovery and maximal
O2
(r = -0.57, p < 0.01), exercise time
(r = -0.48, p < 0.05), watts achieved
(r = -0.53, p < 0.01), and maximal heart rate
(r = - 0.42, p < 0.05). Half-time in recovery was
directly related to maximal
E/CO2
(r = 0.57, p < 0.01) and
E/O2
(r = 0.59, p < 0.01).
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Discussion |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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O2 and ventilation during
recovery in patients with chronic heart failure have been explained by
a delay in the recovery of energy stores in the muscle, as recently
demonstrated using 31P nuclear magnetic resonance
spectroscopy,9
although other factors, such as skeletal
muscle metabolic abnormalities, microcirculatory changes, sustained
hyperpnea, carbon dioxide retention, prolonged recovery of cardiac
output, and increased cost of breathing9
10
11
12
13
14
may
contribute to the characteristic response observed during recovery from
exercise in patients with chronic heart failure.
Because exercise training has been shown to partially normalize
skeletal muscle metabolic characteristics in patients with chronic
heart failure,24
25
and also abnormal ventilatory
responses to exercise,21
22
23
it follows that a program of
training would improve oxygen kinetics in recovery. The rate at which
O2 recovers from exercise has been used
as an index of oxidative capacity in healthy
subjects,9
10
12
15
26
and a growing body of literature
suggests that O2 kinetics in
recovery are a marker of skeletal muscle oxidative capacity in patients
with chronic heart failure.9
10
11
12
13
As reported by
others,10
11
12
we observed significant inverse
relationships between the extent to which
O2 was prolonged in recovery
and measures of exercise tolerance (peak
O2, watts achieved) and
hyperventilation
(E/O2,
E/CO2). To
our knowledge, the present study is the first to assess in a controlled
fashion the effects of exercise training on recovery kinetics in
patients with reduced ventricular function.
At baseline, the O2 half-times
in recovery (mean, 110 ± 7 s) we observed were similar to those
previously reported in patients with moderate-to-severe chronic heart
failure,10
11
12
which are substantially higher than those
reported in normal subjects11
15
26
and those with
coronary artery disease.11
27
Why exercise training
did not improve O2 recovery
time in the present study, despite the effects of training on peak
O2, is unclear. Previous
studies have demonstrated that exercise training results in a faster
recovery of O2 from maximal or
submaximal exercise in normal subjects,15
patients with
valvular heart disease,28
and in patients with spinal cord
injury subjected to functional electrical stimulation
training.29
However, such data in patients with chronic
heart failure are lacking. We did not measure
O2 kinetics in response to
submaximal exercise, as these patients were tested in a standard
fashion as part of their participation in a cardiac rehabilitation
program. It could be argued that the higher peak
O2 values after training
altered the slope of the decline in
O2 during recovery, and masked
any potential benefit reflected by the recovery-time constant.
Interestingly, however, the time constant in recovery has generally
been considered to be independent of the exercise level in studies
using constant work rates.9
13
30
Cohen-Solal et
al9
reported that the exercise level did not affect
O2 half-time in recovery when
O2 was > 50% of maximum.
Similarly, Zanconato and coworkers30
reported that the
time constant in recovery from brief, high-intensity exercise was
independent of the work rate, particularly when the work rate was above
the ventilatory threshold.
We hypothesized that a reduction in the time constant of
O2 in recovery, implying a
faster return of O2 to the
resting state, would have been an additional benefit of exercise
training in patients with reduced ventricular function. Had such a
response been observed, a reduction in what has been classically termed
the O2 debt or excess postexercise
O2 (EPOC) could be added to a
growing list of benefits of exercise training in these
patients.6
Although the mechanism underlying the EPOC has
been the subject of many different interpretations,26
a
reduction in the O2 recovery
time constant, and thus the EPOC, would certainly be related to a
faster recovery from dyspnea after a bout of exercise, permitting a
patient to perform more, or for a longer period of time, his or her
daily activities. The fact that we did not observe a change in the
O2 recovery time constant
after training may be due to characteristics unique to our population,
or the method that patients were tested that negated such an effect.
The use of a more complex modeling technique31
or a longer
recovery period may have reduced the variability and resulted in a
better fit to the recovery data. We did observe a substantial degree of
variability in the responses (Fig 1)
, and it could be argued that our
sample size lacked adequate power. However, our training responses were
considerable, and the control group exhibited a small reduction in the
O2 time constant, which was
similar to that observed in the trained group.
Limitations
The population studied had reduced ventricular function after a
myocardial infarction, but may not be representative of other studies
in which the disease was more chronic or ventricular function was more
severely reduced. As mentioned, the study population was small.
Although we observed a significant training effect, a larger sample
size may be needed to appropriately assess recovery
O2. Lastly, there is some
debate as to whether a single exponential relation or multiexponential
fitting for O2 in recovery is
most appropriate, although the majority of
studies9
10
12
27
28
assessing patients with
reduced ventricular function have used the single exponential model, as
we did.
Summary
Two months of high-intensity exercise training did not result in
an improvement in O2 kinetics in the
recovery period from exercise in patients with reduced ventricular
function following a myocardial infarction, despite a considerable
improvement in peak O2. This finding
implies that ventilatory gas exchange adaptations to exercise training
in patients with reduced ventricular function manifest themselves only
during, but not in recovery from acute exercise.
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Footnotes |
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E = minute ventilation;
CO2 = carbon dioxide production;
O2 = oxygen uptake Received for publication August 23, 2000. Accepted for publication April 11, 2001.
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References |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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This article has been cited by other articles:
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  P. Dall'Ago, G. R.S. Chiappa, H. Guths, R. Stein, and J. P. Ribeiro Inspiratory Muscle Training in Patients With Heart Failure and Inspiratory Muscle Weakness: A Randomized Trial J. Am. Coll. Cardiol., February 21, 2006; 47(4): 757 - 763. [Abstract] [Full Text] [PDF]
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 P. McDonough, B. J. Behnke, T. I. Musch, and D. C. Poole Effects of chronic heart failure in rats on the recovery of microvascular PO2 after contractions in muscles of opposing fibre type Exp Physiol, July 1, 2004; 89(4): 473 - 485. [Abstract] [Full Text] [PDF]
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 X.-G. Sun, J. E. Hansen, N. Garatachea, T. W. Storer, and K. Wasserman Ventilatory Efficiency during Exercise in Healthy Subjects Am. J. Respir. Crit. Care Med., December 1, 2002; 166(11): 1443 - 1448. [Abstract] [Full Text] [PDF]
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