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Dr. Reybrouck is Professor of Exercise Physiology and Cardiovascular Rehabilitation, Department of Cardiovascular Rehabilitation, University Hospital Gasthuisberg, and Department Rehabilitation Sciences, University of Leuven.
Correspondence to: Tony Reybrouck, PhD, Department of Cardiovascular Rehabilitation, University Hospital Gasthuisberg, Herestraat, 3000 Leuven, Belgium; e-mail: tony.reybrouck{at}uz.kuleuven.ac.be
Clinical exercise testing has frequently focused on the
determination of maximal or symptom-limited oxygen uptake
(
O2). Its purpose has often
been the assessment of physical working capacity, which has shown to be
reduced in patents with cardiovascular disease,1
2
in
patients with congenital disease,3
and in hypertensive
patients.4
In addition, several studies have shown that a
low value for maximal O2 has a
prognostic value for cardiovascular mortality.5
6
However,
for activities of daily life, submaximal exercise testing is more
relevant.7
A considerable amount of clinical research has
been performed in this area.2
8
9
With the development of rapid gas analyzers and mass spectrometers, gas
exchange can easily be measured during nonsteady-state conditions. This
allows the investigator to study the kinetics of gas exchange, which
are a function of the increase of cardiac output during incremental or
square wave exercise testing. From a functional point of view, it is
more important to study the change of
O2 during nonsteady-state
exercise than to perform measurements of maximal aerobic capacity,
since the majority of physical activity is performed in conditions of
nonsteady state.
The experimental study in patients with cardiovascular disease,
published in this issue of CHEST (see page 329), has shown
that the speed of the response of the
O2 during subanaerobic
square wave exercise testing is delayed in patients with ischemic heart
disease. From a physiologic point of view, this has important
consequences. A slower adaptation of the
O2 leads to an earlier
onset of lactic acidosis and faster accumulation of oxygen deficit.
This induces a premature onset of dyspnea at the onset of
exercise.1
Furthermore, during recovery of exercise, the
oxygen deficit has to be repaid, which will lead to a subjective
feeling of difficulty or inability to perform a next bout of exercise.
The normal pattern for the increase of
O2 at the onset of exercise
can be described by a monoexponential function.10
Three
phases are normally considered.11
Phase 1 represents the
cardiodynamic phase and reflects the "bulk" increase in cardiac
output without an increase in arteriovenous oxygen difference. Phase 2
represents the adjustment to the metabolic adaptation or the widening
of the arteriovenous oxygen difference. Phase 3 reflects the attainment
of a steady-state value. A typical estimate for the speed of the
increase of O2 during a
subanaerobic square wave exercise test is the determination of the time
constant for O2. This
represents the time needed to reach 63% of the increase for
O2 from baseline to the
steady-state value with a normal value of 30 to 40
s.10
In normal individuals, the kinetics of leg blood flow
and presumably cardiac output have found to be faster than the kinetics
of O2,10
which
suggests that in normal conditions the oxygen delivery to the
exercising tissue is adequate. Both kinetics and amplitude of the
response of phase 1 and phase 2 can be impaired in patients with
cyanotic cardiovascular disease,11
in patients with
chronic heart failure,12
and in patients after surgical
correction of congenital heart disease.3
A clinical application of the determination of the time constant is
described in this issue of CHEST (see page 329), where
Adachi et al report a shortening of the time constant for
O2 after successful
percutaneous transluminal coronary angioplasty (PTCA), compared to the
values determined before the procedure, during the onset of a 50-W
exercise level of 6-min duration. On the other hand, in patients with
restenosis, no shortening or even an increase of the time constant for
O2 was reported. However,
it is difficult to differentiate whether the shortening of the time
constant reflects an improved function of the myocardium after a period
of relative ischemia (hibernating myocardium) or whether this reflects
an improvement of the rate-limiting steps of the oxidative metabolism
in skeletal muscle. It may be possible that patients after PTCA are no
longer symptom limited by exertional angina and become more active.
Therefore, the sensitivity of the improvement of oxygen kinetics as a
test of restenosis is difficult to prove.
Other and related measurements to study the dynamic response to
exercise are the determination of the early normalized oxygen deficit
during square wave exercise testing. Due to the inappropriate
(suboptimal) increase of the cardiac output at the early onset of
exercise, the organism has to rely on anaerobic energy sources with an
excess lactic acid accumulation. Therefore, at the onset of exercise,
O2 is subtracted from the
steady-state value, all breaths are cumulated, and the total oxygen
deficit is expressed as a percentage of the total oxygen cost of the
exercise level, above the resting value. Previous studies on this
topic, in patients with chronic heart failure8
and in
patients with congenital heart disease,13
have shown that
the normalized oxygen deficit is increased in these patients groups,
which suggest an inadequate oxygen delivery to the exercising tissue or
a metabolic inertia of the muscular tissue,14
which can be
due to deconditioning.
Finally, the measurement of O2
kinetics at low intensity (subanaerobic threshold) exercise may provide
useful information about the efficiency of the oxygen delivery to the
exercising tissue and may give some insight about the mechanisms of
exercise limitation in patients with cardiovascular disease.
References
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