| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Guest Access | Sign In via User Name/Password
|
|
|
|||||||
Guest Access | Sign In via User Name/Password |
|||||||||
* From the Department of Cardiology, St. Orsola Hospital, Brescia, Italy.
Correspondence to: Leandro Pavia, MD, Via Toscana 10, 25125 Brescia, Italy; e-mail: leopavia{at}tin.it
 |
Abstract |
|---|
 TOP Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
O2),
ventilation, or heart rate are similar to those in patients with heart
failure.
Methods: We performed a cardiopulmonary
exercise test with a ramping protocol in 18 healthy subjects, 18
patients with coronary artery disease, 19 patients with class A or B
congestive heart failure, and 19 patients with class C congestive heart
failure, according to the Weber classification. Peak oxygen uptake and
the kinetics of oxygen uptake, ventilation, and heart rate were
calculated and expressed as the slope of a single exponential relation
between O2 levels and time during the
first 3 min of recovery as
y(O2) = y0Ae
(-x/t).
Results: A difference in time of recovery of
O2 was found only between healthy
subjects and patients with more severe heart failure (class C)
(p < 0.05); no significant differences were observed among any of
the groups in ventilation or heart rate recovery responses.
Conclusion: O2 recovery time
is prolonged only in the presence of more severe heart failure. The
presence and degree of heart disease has no effect on ventilation or
heart rate recovery time.
Key Words: baseline oxygen consumption • congestive heart failure • exercise response • oxygen uptake
|
Introduction |
|---|
|
TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
O2) levels, an earlier
appearance of the ventilatory threshold, a reduced slope of the
increase in O2 vs time, and
inefficient ventilation. These abnormalities have been shown to
parallel the severity of this condition.1
2
3
4
5
6
The limited
cardiopulmonary reserve in these patients appears to affect not only
exercise responses but also the recovery phase. In healthy subjects,
the pattern of O2 in recovery,
expressed as O2 recovery
kinetics, is a rapid decline,7
8
and exercise training has
been shown to contribute to an even faster decline.9
However, among patients with chronic heart failure, the recovery of
O2 becomes prolonged, a
response that worsens as the condition becomes more
severe.10
11
12
13
14
In contrast, the response of heart rate in
the early recovery period does not appear to be affected by the degree
of exercise intolerance.11
13
Patients with coronary artery disease have reduced exercise capacity
and their response to exercise is characterized by a reduced submaximal
O2 /work rate ratio, a steeper
heart rate/O2 relation, chest
pain, and significant ST segment changes.15
16
The
hemodynamic response to exercise is characterized by a reduction in
maximal cardiac output and peak heart rate.17
18
19
20
However,
few data are available in regard to
O2 and heart rate kinetics in
recovery among patients with coronary artery disease. The purpose of
this study was to evaluate the rates of recovery of
O2, ventilation, and heart
rate among patients with coronary artery disease, and to compare their
responses to patients with chronic heart failure and healthy subjects.
|
Materials and Methods |
|---|
|
TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
All patients were tested while they received their usual drug therapy, including angiotensin-converting enzyme inhibitors, diuretics, nitrates, digitalis, or calcium antagonists in accordance with the prescription of the referring physician. Patients taking ß-blockers were specifically excluded. A standard echocardiogram was performed to assess left ventricular function.
Exercise Testing
All patients underwent a maximal cardiopulmonary exercise test
with an electromagnetically braked cycle ergometer in the
upright position using a ramp protocol.21
The ramp rates
used were 20 W/min in the control group, 20 or 15 W/min in the group of
patients with coronary artery disease, and 10 W/min in the group of
patients with congestive heart failure. All tests were monitored
continuously with two leads, V1 and V5. Ventilatory gas exchange
analysis was performed throughout exercise and for 3 min during the
recovery period.
The tests were performed using the Medical Graphics Corporation CAD/Net System 2001 device (Hans Rudolph Inc.; Kansas City, MO). A two-way, low-resistance breathing valve (Hans-Rudolph;) with a dead space of 90 mL was used, and expired air flow was recorded with a pneumotachometer (Medical Graphics). Before each test, the pneumotachometer was calibrated with a 3-L syringe and the gas analyzer was calibrated with a certified O2/CO2 concentration tank (O2, 12%; CO2, 5%). Gas exchange data and heart rate were recorded as eight-breath and eight-beat moving averages, respectively.22
The system computer calculated
O2 , minute ventilation
(E), carbon dioxide output
(CO2), ventilatory equivalents
for O2 and CO2
(E/O2 and
E/ (CO2),
and end-tidal O2 and CO2
pressures. The criteria for detecting the ventilatory threshold were a
systematic increase in the
E/O2 ratio
without an increase in
E/CO2 ratio
and a systematic increase in end-tidal O2
pressure without a decrease in end-tidal CO2
pressure.23
The constant decay of O2,
E, and heart rate, expressed as the slope of a
single exponential relation among
O2, E,
heart rate, and time during the first 3 minutes of recovery were
calculated with the following formula:
 |
O2, E, or
heart rate, respectively), y0 was the parameter at time zero (the
beginning of the recovery phase), A and e were constants, x was the
time elapsed, and t was the constant decay. Computer software was used
in the calculation (Origin, version 2.5; Microcal; Northhampton,
MA).
Statistical Analysis
The results are presented as mean ± SD. Differences between
groups were assessed by analysis of variance followed by Newman-Keuls
tests. Differences were considered significant at p < 0.05.
|
Results |
|---|
|
TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
O2 (measured in millimeters
per minute), O2 (measured in
millimeters per kilogram per minute), and workload were significantly
higher in the control group (p < 0.05) than in the other groups at
the ventilatory threshold and peak exercise. Peak heart rate was
significantly higher in the control group vs the other groups (Table 1)
. Significant differences also were observed in
O2 (measured in millimeters
per kilogram per minute) between the patients with coronary artery
disease and class A or B congestive heart failure vs patients with
class C congestive heart failure at both the ventilatory threshold
(p < 0.05) and peak exercise (p < 0.05).
|
O2
kinetics during the recovery phase in a healthy subject, a patient with
coronary artery disease, and a patient with class B and C congestive
heart failure. Significant but weak negative correlations were observed
between the rate of decline in
O2 and variables at the
ventilatory threshold, including
O2 (measured in millimeters
per minute) (r = -0.49), O2
(measured in millimters per kilogram per minute) (r = -0.42) and
watts (r = -46) (p < 0.05 for all three variables). Negative
correlations also were found between the recovery
O2 response and peak exercise
variables, including O2
(measured in millimeters per minute) (r = -0.60),
O2 (measured in millimters per
kilogram per minute) (r = -56),
CO2 (r = -0.59), and watts
(r = -0.52; all p < 0.05). We discovered no significant
correlation between recovery of
O2 and age. The recovery times
of ventilation and heart rate were not significantly correlated with
age or any exercise variables at the ventilatory threshold or peak
exercise.
|
|
|
Discussion |
|---|
|
TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
O2 immediately after maximal
exercise is not different from healthy subjects or patients with mild
or moderate heart failure; only among patients with relatively severe
heart failure is there a prolongation of the time required for
O2 to recover after exercise.
The slope of the increase in
O2 from rest to a constant
submaximal workload has been shown to be prolonged in congestive heart
failure,12
a finding that appears to be accentuated as
heart failure worsens.4
Our findings suggest that delayed
O2 responses also occur in
recovery from exercise in accordance with the severity of heart
failure.
The rate at which O2 recovers
from exercise has been used as an index of oxidative capacity in
healthy subjects.24
25
The rate of decrease in
O2 has been traditionally
related to the oxygen debt after exercise,26
which
involves an initial fast component (alactacic) and a second slow
component (lactacic).27
More recently, as the mechanisms
that mediate post-exercise O2
have proven more complex, the term excess postexercise oxygen
consumption has been used to absolve this entity from a strict
dependence on anaerobic metabolism.8
One factor that
contributes to the delayed recovery of
O2 is the prolonged recovery
time of the muscle phosphate/phosphocreatine ratio.28
29
30
31
A faster recovery time for this ratio has been demonstrated in
athletes.32
Other factors that could delay oxygen kinetics
during exercise and recovery in heart failure may involve delays in
circulatory transport of oxygen to and from metabolizing
tissue,33
34
gas exchange in pulmonary
tissues,2
or rate of uptake by the exercising or
recovering muscle tissues themselves. The importance of circulatory
factors is underscored by the observation that the half-time of
PCr in recovery is determined not only by the oxidative capacity
of the peripheral muscles,35
36
but also by blood
flow.28
36
Central factors also may help to explain the slower recovery of
O2 in patients with heart
failure. According to the Fick equation,
O2 is the product of cardiac
output, ie, heart rate multiplied by the stroke volume,
divided by the arteriovenous oxygen difference. During the recovery
phase, O2 remains
elevated in patients with left ventricular dysfunction, because cardiac
output remains high.34
38
39
The comparatively rapid
decrease in arteriovenous oxygen difference when cardiac output remains
elevated38
39
suggests that
O2 during early recovery
relies more on cardiac output than on arteriovenous oxygen
difference, unlike that during exercise when both variables contribute
more equally to O2.
Several studies have demonstrated an increase in contractility
associated with an increase in stroke volume40
41
42
or an
improvement in myocardial wall motion immediately after exercise due to
endogenous catecholamine stimulation in healthy
subjects.43
In patients with left ventricular dysfunction,
significant increases in stroke volume and ejection fraction also have
been reported during the early recovery period.34
The pathophysiologic basis for the rapid decline in arteriovenous oxygen difference after exercise previously observed may involve redistribution of blood flow to nonexercising tissues secondary to sympathetic-induced vasoconstriction44 45 46 or metabolic acidosis-induced vasoconstriction during exercise.47 This phenomenon may represent a compensatory response for an enhanced peripheral vascular tone to maintain the systemic arterial BP in the setting of reduced cardiac output.
Plotnick et al,48
using radionuclide angiography,
demonstrated in both healthy subjects and patients with coronary artery
disease an elevation of cardiac output and ejection fraction during the
early period of recovery. The absolute values differed between control
subjects and patients with coronary artery disease, but the trends
paralleled one another. In our study, the
O2 recovery times in patients
with coronary artery disease did not differ from healthy subjects.
Importantly, O2 kinetics
during the early recovery phase are considered independent of the
exercise level achieved, particularly if it was above the ventilatory
threshold49
or at > 50% of maximal exercise
capacity.13
This permitted a valid comparison between the
groups in the present study, despite the large differences in exercise
capacity. The negative correlation between exercise parameters at peak
exercise and at the ventilatory threshold confirms our observation that
O2 responses in recovery are
abnormal only in the presence of a severe reduction in exercise
capacity and abnormal left ventricular function.
In terms of heart rate kinetics in the early phase of recovery, we did not observe any differences among healthy subjects and our patient groups, we did not observe any significant relationships between heart rate responses in recovery and other exercise variables. This confirms the work of others,11 13 and suggests that the mechanisms that regulate heart rate during recovery are different from those during exercise in which increases in heart rate are the result of increases in sympathetic outflow and decreases in vagal outflow.16
The kinetics of ventilation during recovery were similar in all groups,
which contrasts the findings of some,10
13
but not all
previous investigations.11
Two previous reports have shown
that E recovery time is prolonged in heart failure
in parallel with the degree of exercise impairment.10
13
Riley11
however, reported that E
recovery time was actually faster in patients with heart failure
compared with controls.
In summary, during the early period of recovery, the rate of decline in
O2 is inversely related to
exercise capacity and is slowed only in the presence of class C heart
failure. The rate of recovery of heart rate and ventilation is similar
among healthy subjects, patients with coronary disease, and patients
with heart failure. Clinically,
O2 kinetics during recovery
from exercise appears to be an important marker of the severity of left
ventricular dysfunction10
11
12
13
14
and may even have an
important role in assessing prognosis in patients with congestive heart
failure.14
|
Footnotes |
|---|
CO2 = carbon dioxide output;
O2 = oxygen uptake;
E = minute ventilation Manscript received February 25, 1999; revision accepted April 7, 1999.
|
References |
|---|
|
TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  S. H. Mitchell, N. P. Steele, K. M. Leclerc, M. Sullivan, and W. C. Levy Oxygen Cost of Exercise Is Increased in Heart Failure After Accounting for Recovery Costs Chest, August 1, 2003; 124(2): 572 - 579. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Myers, R. Gianrossi, J. Schwitter, D. Wagner, and P. Dubach Effect of Exercise Training on Postexercise Oxygen Uptake Kinetics in Patients With Reduced Ventricular Function Chest, October 1, 2001; 120(4): 1206 - 1211. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
