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John Rankin Laboratory of Pulmonary Medicine, Department of Preventive Medicine, University of Wisconsin, Madison, Wisconsin 53705
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ABSTRACT |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Twenty-eight
healthy women (ages 27.2 ± 6.4 yr) with widely varying fitness
levels [maximal O2
consumption (
O2 max),
31-70 ml · kg
1 · min1]
first completed a progressive incremental treadmill test to O2 max (total
duration, 13.3 ± 1.4 min; 97 ± 37 s at maximal workload), rested for 20 min, and then completed a constant-load treadmill test at maximal workload (total duration, 143 ± 31 s). At
the termination of the progressive test, 6 subjects had maintained arterial PO2
(PaO2) near resting levels, whereas 22 subjects showed a >10 Torr decrease in
PaO2 [78.0 ± 7.2 Torr, arterial O2 saturation
(SaO2), 91.6 ± 2.4%], and
alveolar-arterial O2 difference (A-aDO2,
39.2 ± 7.4 Torr). During the subsequent constant-load test, all
subjects, regardless of their degree of exercise-induced arterial
hypoxemia (EIAH) during the progressive test, showed a nearly identical
effect of a narrowed
A-aDO2
(
4.8 ± 3.8 Torr) and an increase in
PaO2 (+5.9 ± 4.3 Torr) and
SaO2 (+1.6 ± 1.7%) compared with at
the end point of the progressive test. Therefore, EIAH during maximal
exercise was lessened, not enhanced, by prior exercise, consistent with
the hypothesis that EIAH is not caused by a mechanism
which persists after the initial exercise period and is aggravated by
subsequent exercise, as might be expected of exercise-induced
structural alterations at the alveolar-capillary interface. Rather,
these findings in habitually active young women point to a functionally
based mechanism for EIAH that is present only during the exercise
period.
maximal exercise; diffusion; repeat exercise effects
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INTRODUCTION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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AN EXCESSIVE WIDENING of the alveolar-arterial
O2 difference
(A-aDO2), which
leads to exercise-induced arterial hypoxemia (EIAH), occurs during
severe exercise in many highly fit humans (7, 25) and in the
Thoroughbred horse (2, 31). This failure of homeostasis may occur as a
result of functionally based mechanisms that are present only during
the exercise period, such as a transient maldistribution of alveolar
ventilation-to-pulmonary capillary flow ratio
(A/
c)
and/or alveolar-capillary diffusion disequilibrium. For
example, a mismatch of increased cardiac output with expansion of the
pulmonary capillary vasculature might cause diffusion disequilibrium
during exercise via a markedly reduced red blood cell transit time in
the lung (7, 15). On the other hand, recent evidence points to
structural changes at the alveolar-capillary interface
induced by heavy exercise. Such structurally based mechanisms for EIAH
may have long-lasting effects.
EIAH and pulmonary hemorrhage have been shown to occur in Thoroughbred
racehorses during severe exercise, presumably as a result of stress
failure of the blood-gas barrier; these results are achieved via high
pulmonary capillary transmural pressures (31). In humans, lung
diffusion capacity for carbon monoxide (DLCO) is
reduced for up to 1 h after strenuous exercise (4, 9, 17), and
A/c
inequalities have been shown to persist during the postexercise period
after ventilation and cardiac output have returned to baseline values
(26). EIAH has been associated with an increase in histamine release
(1), which may be related to an inflammatory reaction at the pulmonary
capillary level, potentially contributing to a mild interstitial edema.
In addition, the inhibition of histamine release has been associated
with an improvement in gas exchange (23). Recent reports of higher
concentrations of red blood cells and protein in bronchoalveolar lavage
fluid after brief intense exercise in athletes (14) do not necessarily imply abnormalities in gas exchange but do support the hypothesis that
mechanical stress is the mechanism for altered blood-gas barrier
function in the human.
Given the indirect evidence for alveolar capillary damage in the human,
we hypothesized that subsequent exercise after heavy exercise,
especially in those subjects with EIAH, would increase the severity of
the EIAH and perhaps even cause significant EIAH in those subjects who
did not initially experience it. We previously documented a high
incidence of EIAH in active females during progressive exercise to
maximal O2 consumption
(O2 max); the EIAH was
caused primarily by an excessively widened
A-aDO2, with a
lack of sufficient compensatory hyperventilation (11). The
description of these responses and the analysis of the potential
mechanisms can be found in the previous paper (11). These female
subjects, particularly those in habitual training, were especially
appropriate to test our current hypothesis because they displayed such
a wide
A-aDO2 and an
exceptionally high prevalence of EIAH.
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METHODS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Details of our methods are provided in the recent paper by Harms et al. (11), and in the present paper we summarize only the essential techniques and protocols.
Subjects.
Of the 29 women who participated in the previous study (11), 28 completed the present study. All subjects were nonsmokers, ages
18-42 yr (mean, 27.2 ± 6.4 yr), with resting pulmonary
function within normal limits (total lung capacity, vital capacity, and forced expiratory volume per 1 s were 106 ± 3% predicted). Resting DLCO
averaged 26.4 ± 4.5 ml · min1 · Torr1.
Taking into account any differences in Hb or hematocrit between our
subjects and the population in which the reference equations were
developed, the
DLCO for
our subjects was 88 ± 16% of that predicted according to Crapo and
Morris (6) and 86 ± 15% of that predicted according to Knudson et
al. (16). None of the subjects was anemic (Hb, 12.8-15.5 g/dl),
and all subjects were free of any history or symptoms of
cardiopulmonary disease, including exercise-induced asthma. In
additional studies (19), all subjects showed a normal increase in their
maximal flow-volume envelope immediately after exercise. There was a
wide variation in fitness levels
(O2 max, 31-70
ml · kg1 · min1;
82-202% of value predicted on the basis of gender and age). Twenty-four of the subjects were runners (including 13 former collegiate runners and 1 former Olympian), and all competed regularly in middle- and long-distance races. Twenty of the subjects ran at least
3 times/wk, averaging 36.3 mi./wk (range, 5-90 mi./wk). Four
subjects were sedentary. Informed consent was obtained in writing from
each subject, and all procedures were approved by the Institutional
Review Board of the University of Wisconsin-Madison. All tests were
performed during the follicular phase of the menstrual cycle, as
determined by progesterone levels (0.8 ± 0.4 g/ml; range, 0.2-1.3 g/ml) and self-reported basal temperature recordings over a 30-day period. None of our subjects reported abnormalities with her
menstrual cycle in the 6 mo before testing.
Apparatus. During all tests, subjects breathed through a low-resistance two-way valve (model 2400, Hans Rudolph), and expired gases were sampled at the mouth via a Perkin-Elmer mass spectrometer (model 1100). Inspiratory and expiratory flow rates were measured separately by pneumotachographs. All signals were displayed on a chart recorder, sent through an analog-to-digital board, and sampled on a computer at 75 Hz. Esophageal temperature was measured from a thermocouple placed intranasally in the lower one-third of the esophagus (Mon-a-Therm 6500).
Arterial blood was obtained from a 20-gauge indwelling plastic catheter inserted in the brachial or radial artery after 1% lidocaine anesthesia was given. Multiple blood samples of 3-4 ml were drawn anaerobically over 20-30 s during a 15-min rest period in the sitting position (on and off the mouthpiece), during the final minute at each grade during a progressive treadmill test toO2 max, and at
regular intervals during a constant-load O2 max test. A
minimum of two blood samples (usually 3-5) was obtained at each
workload. Measurements of arterial
PO2, PCO2, and pH were made with a
blood-gas analyzer calibrated with tonometered blood (Radiometer
ABL300), and arterial O2
saturation (SaO2) and Hb concentration
were measured with a CO-oximeter (Radiometer OSM3). Calculated
SaO2 levels (on the basis of the normal
average oxyhemoglobin dissociation curve and measured changes in body temperature and pH) were in close agreement with measured
SaO2 levels
(r = 0.94). Blood gases were
corrected for in vivo esophageal temperature changes during
exercise. Esophageal temperature increased 1.7 ± 0.6°C from
rest to maximal exercise during the progressive incremental
O2 max test
and increased 1.2 ± 0.4°C during the constant-load
O2 max test
(P < 0.004).
Protocol.
Each subject completed a progressive incremental treadmill exercise
test to O2 max,
followed by a 20-min rest period, and then a second
O2 max test at a
constant workload equivalent to or greater than (10 of the 28 subjects)
the maximal workload achieved during the incremental test. For the
progressive O2 max test, a 5-10 min warm-up period at 4-6 miles per hour (mph)
with 0% grade was followed by increasing the speed of the treadmill by
2 mph every 2.5 min until a comfortable speed of 6, 8, or 10 mph was
reached. At this stage, the slope of the treadmill was increased 2%
every 2.5 min until volitional fatigue was reached. All 28 subjects met
the criteria for
O2 max (26), showing a plateau in O2 consumption
(O2; <150 ml increase)
over the last two workloads. For the constant-load
O2 max test, a 3- to
5-min warm-up period was followed by increasing the treadmill, over a
30-s period, to the predetermined speed and grade, on the basis of the
maximal workload achieved on the progressive test, and the subjects
exercised until volitional fatigue.
Analysis.
Comparisons between mean values obtained at the end point of the
maximal workload of the progressive
O2 max test
and at the endpoint of the constant-load
O2 max test were made
by paired t-test. Pairwise comparisons
were made for the 12 variables of interest, and the Bonferroni
adjustment (
/number of t-tests) was
used to modify the level of significance accordingly
(P < 0.004). Mean values for each
variable were also compared at equivalent time points (isotime) within
each of the exercise protocols. Our analysis in this study involved
only the data obtained at rest and at maximal exercise. Data obtained
during all submaximal workloads during the progressive exercise
protocol in these same subjects were reported previously (11).
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RESULTS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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O2 and work
rate.
The total duration of the progressive protocol was 13.3 ± 1.4 min,
with the time spent at the end (maximal) workload averaging 97.3 ± 36.9 s. The duration of the repeat constant-load protocol was
significantly longer (P < 0.004)
than the final workload of the progressive test at 143.0 ± 31.3 s.
The average maximal workload for the progressive test was 8.2 ± 1.7 mph at 6.9 ± 1.9% grade. On the repeat constant-load test, the
grade of the treadmill was increased (1.7 ± 0.5%) for 10 of the 28 subjects, so that the average workload for all 28 subjects
was higher than the maximal workload for the progressive test at 8.2 ± 1.7 mph and 7.5 ± 1.7% grade
(P < 0.004). However, the
O2 achieved at the
end point of the maximal workload of the progressive test (54.7 ± 9.0 ml · kg1 · min1)
was not different (P > 0.004) from
the O2 achieved at the end of
the constant-load test (54.5 ± 8.8 ml · kg1 · min1).
The similiarity in O2 between
tests was consistent with the relative plateau in
O2 achieved over the final
two workloads of the progressive test.
Comparison of resting values.
Table 1 shows the average resting values measured before
the progressive test and the constant-load test. The subjects were still hyperventilating at the end of the 20-min recovery period between
the two tests, as resting arterial
CO2 pressure
(PaCO2) was lower (32.1 ± 4.0 vs.
37.5 ± 3.4 Torr, P < 0.004) and
resting arterial PO2
(PaO2) was higher (102.7 ± 9.7 vs. 100.0 ± 3.7 Torr, P < 0.004) before the constant-load test compared with resting values
measured under steady-state control conditions before the progressive
test. The pH was more acid (P < 0.004) before the constant-load test, compared with the resting
(control) pH measured before the progressive test, due to the lower
HCO3 concentration
([HCO3];
P < 0.004).
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Comparisons at end exercise.
The 28 subjects were divided into three groups based on the change
(
) in PaO2 and the degree of the
resulting EIAH from rest to the end of the progressive exercise test to
O2 max. Six subjects experienced no EIAH (group 1,
PaO2 less than 10 Torr) and had the lowest average
O2 max of all three
groups (45.4 ± 7.9 ml · kg1 · min1).
Group 2 (n = 7) had lowered
PaO2 by 10 to 20 Torr
(mild EIAH). Group 3 (n = 15) decreased
PaO2 by more than 20 Torr (severe EIAH; SaO2 = 90.9 ± 2.4%; range
86.2-92.5%).1
Groups 2 and
3 had similiar
O2 max values (56.6 ± 4.5 and 57.5 ± 8.9 ml · kg1 · min1,
respectively). The greater the EIAH across groups, the wider was the
A-aDO2 and the
smaller was the hyperventilatory response.
O2 max,
the decrease in PaO2 or
SaO2 from rest to end exercise
was not as great, and the
A-aDO2 was not
as wide, as at the end of the progressive test (Table 2). A
significant hypocapnia occurred in both tests, with mean
PaCO2 averaging 0.9 Torr lower
(P < 0.004) at the end of the
constant-load test. Thus, on average, in all 28 subjects, the 5.9 ± 4.3 Torr higher PaO2 on the
constant-load vs. end-progressive test was due to a 4.8 ± 3.8 Torr narrower
A-aDO2 and a
1.0 ± 1.5 Torr lower PaCO2 [i.e., 0.6 ± 1.7 Torr higher alveolar PO2
(PAO2)].
All three groups, regardless of their degree of EIAH in the
progressive test, showed a nearly identical effect of narrowing
their A-aDO2 and increasing their PaO2 and
SaO2 between the end of the progressive test and the constant-load
O2 max test.
SaO2 was 2.0 ± 0.9% higher in
group 3 and 1.5 ± 0.9% higher in
the entire group at the end of the repeat constant-load
vs. the progressive test. The higher
SaO2 was primarily a result of a higher
PaO2 (5.9 ± 4.3 Torr,
P < 0.004) and lower body
temperature (0.5 ± 0.3°C, P < 0.004) at the end of the constant-load vs. the
progressive test.
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Comparisons at isotime.
Because the constant-load
O2 max test
was 46 s or 72% longer (P < 0.004)
on average than the end workload of the progressive test, we also
compared blood-gas data at equivalent time points in both tests (i.e.,
progressive test, 82.1 ± 32.4 s; constant-load test, 86.0 ± 29.8 s). Figure 1 shows the individual data
for the isotime points of the progressive vs.
constant-load tests. Mean data are shown in Tables 2 and 3. The results
were similiar to the end point comparisons. That is, the
A-aDO2 was not
as wide and the PaO2 and
SaO2 were higher at the same time point
of the constant-load test compared with the progressive test.
The magnitude of the increase in PaO2
and decrease in
A-aDO2, with
the constant-load vs. progressive test, was slightly
less for the isotime comparison vs. the end point time
comparison. There were no differences between mean values for any of
the ventilatory variables at isotime points of the two tests (Table 3).
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Time course effects during exercise. Mean exercise time was 97 s for the final (maximal) workload of the progressive test and 143 s for the repeat constant-load test at maximal workload, and it varied widely (32-174 vs. 86-220 s, progressive vs. constant-load tests, respectively). The time course for the change in PaO2 during maximal exercise was similiar for the two exercise tests (Fig. 2). In both instances, when EIAH occurred, the PaO2 fell within the first minute of maximal exercise and was maintained at the lower level for the duration of the exercise. There were no instances, with either test, in which PaO2 fell further beyond the initial minute of the exercise, and only four instances (all in the repeat constant-load test) in which PaO2 tended to rise over the duration of the test. In these cases, the average increase in PaO2 was 6.0 ± 3.6 Torr between 47.5 ± 13.2 and 142.5 ± 59.1 s.
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3.4 ± 3.0 Torr; constant-load test, 0.3 ± 3.1 Torr) and then
either stayed constant or, in the constant-load test, tended to rise
slightly with time (+3.5 ± 1.5 Torr) in 12 of the 28 subjects (Fig.
3A). Due to a progressive decrease
in [HCO3], arterial pH
decreased progressively with time in both tests (Fig.
3B).
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DISCUSSION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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We determined the effects of a repeat bout of maximal
exercise on EIAH in a group of 28 female subjects who had experienced varying degrees of EIAH during a progressive exercise test. In contradiction to our hypothesis that a second bout of maximal exercise
would increase the severity of the EIAH observed during a progressive
exercise test to
O2 max, we found that
the decrease in PaO2 or
SaO2 was not as great, and the
A-aDO2
was not as wide, during a repeat constant-load exercise test at
O2 max work rate, as at
the end workload of the progressive exercise test. This reduced EIAH
that was experienced on repeat maximal exercise occurred regardless of
the degree of EIAH in the initial progressive test.
Comparison with prior studies. Two previous studies addressed the question of repeat exercise effects in men who were athletes; results were similiar (5, 9). However, only a small number of subjects were studied (7-8 subjects), and EIAH was rare or nonexistent.
In agreement with our results, Hanel et al. (9) found no differences in PaO2, PaCO2, SaO2, or pH during two 6-min "all-out" bouts of ergometer rowing, separated by a 2-h recovery period. In the seven subjects who completed the two exercise bouts, the SaO2 averaged 95% (range, 86-96%) during the first rowing period (PaO2, 77-102 Torr) and 94% (range, 90-96%) during the second rowing period (PaO2, 77-99 Torr). Although it is evident that at least one subject experienced EIAH, no data were reported for individual subjects so as to determine whether the response was different in those subjects who showed impaired gas exchange during the first exercise bout. Caillaud et al. (5) reported that the drop in PaO2 and the increase in A-aDO2 observed during an incremental exercise test toO2 max were accentuated
during submaximal exercise in a second incremental test. However, they
found no difference between the two tests in pulmonary gas exchange
(PaO2,
A-aDO2, and
PaCO2) at maximal exercise. Exercise was
performed on a cycle ergometer, using a 30-W/min ramp increase in work
rate (mean duration, 13 min), with a 30-min recovery period separating
the two tests. Among the eight subjects, the average
PaO2 at maximal exercise was 86 Torr,
with a mean
A-aDO2 <32
Torr. Because blood-gas measurements were not corrected for changes in
body temperature during the exercise,
PaO2 was actually higher and
A-aDO2 was
significantly narrower than data reported in the study. Therefore,
these subjects appeared to experience only marginal or no EIAH.
In agreement with our results, these previous studies (5, 9) show that
simply repeating maximal exercise will not cause EIAH. However, the
development of EIAH during the first exercise period is crucial to
testing our hypothesis. If the subjects are not hypoxemic after the
first period of maximal exercise, there would be no reason to suspect
that the high capillary pressures experienced during the exercise
induced any ultrastructural changes to the blood-gas barrier which
would impair gas exchange during the second period of heavy exercise.
Implications for mechanisms causing EIAH. Our results demonstrate that the EIAH experienced during the initial progressive exercise test cannot be attributed to a mechanism(s) that persists long after the exercise and/or one which is aggravated by subsequent exercise bouts. These data thus appear to speak against our basic premise that the high vascular pressures experienced in heavy exercise, which cause structural stress failure of the capillary endothelium, are responsible for the EIAH. The evidence for parenchymal damage is based on direct histological findings obtained postexercise in the Thoroughbred horse (31), in situ findings in the isolated perfused lung (3, 29, 32, 34), and indirectly in the human (1, 4, 14). Certainly the evidence for damage in the human athlete seems clear and it appears to be long lasting after maximal exercise (14); however, this does not mean that the structural changes were sufficiently widespread or that they caused a diffuse interstitial edema of a magnitude which would interfere with pulmonary gas exchange. Evidence for accumulation of extravascular lung water as a result of severe exercise has been controversial (4, 8). Our concern in the present study was not whether significant edema actually occurred during severe exercise but whether it caused the EIAH. If heavy progressive exercise had produced widespread permeability changes in the capillary endothelium sufficient to cause the EIAH, we would expect to see a further progressive widening of the A-aDO2 and a fall in PaO2 with continued exposure to high vascular pressures with repeated maximal exercise. We did not.
Our findings are most consistent with a functionally based mechanism for EIAH that is present only during the exercise period or shortly thereafter. These mechanisms include nonuniformities in the distribution ofA/c
and/or failure of alveolar to end pulmonary capillary
equilibrium for O2 (7, 30). The
increase in
A/c
mismatch during exercise could be attributable to nonuniform pulmonary
vasoconstriction or vasodilation (30), the development of mild
interstitial pulmonary edema (26), and/or mechanical time-constant inequalities in the airways (30). In the highly trained
subjects, it is also possible that short red blood cell transit times,
in at least a portion of the pulmonary circulation, might occur
secondary to the maximal expansion of the pulmonary capillary blood
volume at a time when pulmonary blood flow continues to increase (7,
15). Our present findings cannot distinguish between these factors.
Two sets of our own findings concerning the nature of EIAH do support
our suggestion of a functional basis for EIAH. First, hypoxemia was
observed to develop in the first minute or so during both the maximal
workload of the progressive test and the constant-load test at maximal
workload, and hypoxemia did not worsen thereafter (Fig. 2). Second, and
more importantly, a previous report of exercise responses in these
women subjects showed that, of the 22 subjects with EIAH at maximal
exercise, the majority showed excessive
A-aDO2 and
significant EIAH beginning to develop during submaximal exercise (at
50-75% of O2 max)
(11). In earlier studies (7), EIAH was also detected at submaximal
exercise intensities in many highly trained young men who were
athletes. Given the greater likelihood of increasing pulmonary
capillary transmural pressures as maximal exercise is prolonged, at
least over a few minutes, and the unlikelihood of moderate exercise
intensity causing excessive pulmonary vascular pressures sufficient to
cause injury to the vascular endothelium, these findings also support
our proposal for a functional transient cause of EIAH.
Effects of experimental protocol on EIAH.
We used a nonrandomized application of two quite different exercise
tests, with the longer progressive maximal test always preceding the
shorter (repeat) constant-load
O2 max test.
Thus we were unable to specifically dissect out the effects of
progressive vs. constant-load test protocols on EIAH or
the effect of test duration per se on EIAH. We think it unlikely that
these differences in the progressive vs. constant-load
type of maximal exercise test would explain our negative findings with
repeat maximal exercise. First, we note that the repeat constant-load
test was longer and usually at a slightly higher work load than the
peak work load of the progressive test. Second, although the occurrence
of EIAH during incremental exercise to
O2 max has been well
documented (7, 12, 15, 22), EIAH has also been observed during intense exercise at a constant work load (7, 9, 13). In the present study,
although the hypoxemia was not as severe or prevalent in the repeat
constant-load test, it was still present in the majority of subjects
who experienced EIAH in the progressive test.
6.8 to
9.8 Torr) which was less during intermittent vs. progressive
exercise (the intermittent exercise consisted of 1-min supermaximal
exercise and 3-min rest periods). They argued that the postexercise
hyperventilation, which increased
PAO2, improved gas exchange during the subsequent exercise bout. Similarly, our subjects also were hyperventilating while at rest after the termination of the 20-min recovery period and before the repeat exercise bout. However, during the repeat maximal
exercise, the ventilatory response was almost identical to that at the
maximal workload of the progressive exercise and therefore was not a
factor in explaining the improved PaO2
on this repeat maximal exercise bout. It is not entirely clear why the
developing acidosis during maximal exercise was not associated with a
hyperventilatory response either at end exercise or over the time
course of the exercise (see Fig. 3). In many, but not all, of our women
subjects, expiratory flow limitation was significant at maximal
exercise and was shown to constrain the ventilatory response (19).
An alternative explanation for the moderate but significant improvement
in gas exchange during repeat maximal exercise might be provided by
Widimsky et al. (33), who showed that pulmonary vascular resistance was
lower during repeat exercise of moderate intensity, compared with the
initial period of exercise, also of moderate intensity. If this effect
could also be documented at maximal exercise, then perhaps
this reduced vascular resistance might lead to a more
uniform perfusion distribution and a narrower A-aDO2 with
repeat exercise. However, these proposed mechansims for the higher
PaO2 and narrowed
A-aDO2 during
the repeat test are purely speculative. Given the differences between
the two exercise protocols, we caution against overinterpretation of
the small (but quite consistent) improvement in gas exchange.
Implications for postexercise reductions in DLCO. Our results question the relevance of the postexercise reduction in DLCO to the pulmonary O2 exchange during exercise. It has been argued that the persistent decrease in DLCO for many hours after maximal exercise indicates a structural alteration to the alveolar capillary membrane (18, 20, 24). However, it has also been reported that a second bout of maximal ergometer rowing did not worsen the decrease in postexercise DLCO, nor was the reduction in DLCO related to the decrease in PaO2 or SaO2 during the exercise (9). These findings also argue against significant injury to the blood-gas barrier, thus affecting pulmonary gas exchange during heavy exercise, and question the physiological importance of the postexercise decrease in resting DLCO. Later studies that measured regional electrical impedence and atrial natriuretic peptide concentration indicated that about one-half of the postexercise reduction in resting DLCO was explained by a redistribution of pulmonary blood volume to more distal regions (10). Any reduction in central blood volume would be restored during subsequent exercise.
In summary, we demonstrated that previous maximal exercise does not precipitate widening of the A-aDO2 or worsening of EIAH during maximal exercise. These results suggest that EIAH is not caused by a mechanism which persists after the initial exercise period and is aggravated by subsequent exercise, as might be expected of exercise-induced structural alterations at the alveolar-capillary interface. Rather, our present findings, along with evidence of EIAH onset at submaximal exercise (11), are more consistent with a functionally based mechanism
likely
A/c
maldistributionwhich is present only during the exercise period or
shortly thereafter.
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ACKNOWLEDGEMENTS |
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This work was supported by the National Heart, Lung, and Blood Institute and (in part) by Research Fellowships from the American Heart Association of Wisconsin (to C. M. St. Croix) and from the Parker B. Francis Foundation (to C. A. Harms).
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FOOTNOTES |
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1 In group 3, 11 of the 15 subjects also showed EIAH during submaximal exercise. These submaximal data are discussed in detail in a previous paper (11).
Address for reprint requests: C. M. St. Croix, John Rankin Laboratory of Pulmonary Medicine, Dept. of Preventive Medicine, 504 N. Walnut St., Univ. of Wisconsin-Madison, Madison, WI 53705.
Received 1 December 1997; accepted in final form 18 May 1998.
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REFERENCES |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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; group 2, 
;
group 3, 
. These data were obtained
after 82 ± 32 s of progressive test and 86 ± 30 s of
constant-load test. See mean values in Table 
