Vol. 92, Issue 5, 1879-1884, May 2002
Early onset of pulmonary gas exchange disturbance during
progressive exercise in healthy active men
B.
Aguilaniu1,
P.
Flore1,
J.
Maitre1,
J.
Ochier1,
J. R.
Lacour2, and
H.
Perrault3
1 HYLAB, Clinique du Mail, F-38100 Grenoble,
France; 2 Laboratoire de physiologie de
l'exercice, 69921 Lyon Sud, France; and
3 Department of Kinesiology and Physical Education,
McGill University, Montreal, Canada H2W IS4
 |
ABSTRACT |
10.1152/japplphysiol.00630.1999.
Some recent studies of competitive
athletes have shown exercise-induced hypoxemia to begin in submaximal
exercise. We examined the role of ventilatory factors in the submaximal
exercise gas exchange disturbance (GED) of healthy men involved in
regular work-related exercise but not in competitive activities. From
the 38 national mountain rescue workers evaluated (36 ± 1 yr), 14 were classified as GED and were compared with 14 subjects matched for
age, height, weight, and maximal oxygen uptake
(
O2 max; 3.61 ± 0.12 l/min) and
showing a normal response (N). Mean arterial
PO2 was already lower than N (P = 0.05) at 40% O2 max and continued to
fall until O2 max (GED: 80.2 ± 1.6 vs. N: 91.7 ± 1.3 Torr). A parallel upward shift in
the alveolar-arterial oxygen difference vs.
%O2 max relationship was observed in
GED compared with N from the onset throughout the incremental protocol.
At submaximal intensities, ideal alveolar
PO2, tidal volume, respiratory
frequency, and dead space-to-tidal volume ratio were identical between
groups. As per the higher arterial PCO2 of GED
at O2 max, subjects with an exaggerated
submaximal alveolar-arterial oxygen difference also showed a relative
maximal hypoventilation. Results thus suggest the existence of a common
denominator that contributes to the GED of submaximal exercise and
affects the maximal ventilatory response.
alveolar-arterial oxygen difference; exercise ventilation, arterial
hypoxemia
| |
INTRODUCTION |
EXERCISE-INDUCED
ARTERIAL hypoxemia (EIH) has been a common finding in
endurance-trained young (3, 5) and master athletes (1, 2, 9, 15) that has also been described in regularly exercising young women (7, 11, 19, 20). The phenomenon defined as a decrease in arterial PO2
(PaO2) >10 Torr (5) has been related to
a number of factors including venoarterial shunt, ventilation, and/or diffusion limitations (5, 18). A
lower ventilation (E)-to-maximal oxygen uptake
(O2 max) ratio is generally
reported in athletic subjects exhibiting EIH compared with those who
did not, suggesting that a relative hypoventilation is a contributing
factor to EIH occurrence (12, 14). Similarly, a diffusion
limitation has been proposed, which could result from an incomplete
equilibration of oxygen between alveolar gas and pulmonary capillary
blood after a markedly shortened mean pulmonary capillary transit time
or from a potential alteration in the integrity of the
alveolar-capillary membrane or a combination of both (5, 6, 8,
18). Considering the systemic constraints imposed by maximal
exercise intensity, it seems likely that, independent of the extent of
their contribution, several concurrent mechanisms may act to express a
disturbance in gas exchange.
In some subjects, maximal EIH has been observed to begin even in
submaximal exercise and to worsen as work rate is increased (3,
7, 15-17). A common denominator in these studies may be the
high aerobic capacity of subjects. In the studies by Dempsey et al.
(3) and Rice et al. (16, 17), subjects were
highly trained competitive endurance athletes with
O2 max ranging between 58 and 82 ml · kg
1 · min1. Similarly,
Harms et al. (7) and more recently Wetter et al. (20) studied women endurance runners and found submaximal
EIH in subjects showing levels of
O2 max 43-70
ml · kg1 · min1. This
observation may suggest that submaximal gas exchange disturbance (GED)
is essentially related to the endurance athletic status or to smaller
relative lung size, such as seen in women, and predisposing to
ventilatory maldistribution and/or an imbalance between pulmonary capacity and demand for pulmonary oxygen transport.
In the present study, we examined arterial gases and ventilatory
adaptations from rest to maximal exercise in healthy men of normal
stature who were involved in regular work-related endurance exercise
and training but who did not engage in specific athletic competitive
activities. Similar to previous observations in athletes, our findings
indicate an early onset of excessive alveolar-arterial oxygen
difference (A-aDO2) in healthy nonathletic
subjects exhibiting a progressively decreasing PaO2.
We observed submaximal GED not to be accounted for by ventilatory
responses or by athletic status or body stature. An interesting
additional finding was that subjects showing an early onset of gas
exchange alteration were also those showing a relative hypoventilation
at maximal exercise.
| |
METHODS |
Subjects
Thirty-eight healthy nonsmoking male professional national
mountain rescue workers (age 36 ± 1 yr; weight 71.9 ± 1 kg;
height 176 ± 1 cm) volunteered to take part in the study. In
addition to their occupational physical activity, subjects took part in 13-16 h weekly of regular programmed outdoor physical activities such as mountain climbing and skiing to maintain and optimize their
fitness level and specific working skills. All participants signed an
informed consent form, and ethics approval was obtained from the
institution's ethics review board.
Evaluation Procedures and Protocols
Subjects were tested in the morning under standard laboratory
environmental conditions (barometric pressure 749-752 Torr; temperature 19-22°C; relative humidity 50-55%), 3 h
after a standard breakfast.
Resting pulmonary function tests.
Before completing the incremental maximal exercise test, all
participants were subjected to standard resting pulmonary function tests using a Masterlab spirometric system (Jaeger, Wurzburg, Germany)
and including maximal expiratory flow volume curves generated from
forced vital capacity and forced expiratory volume in 1 s (liters)
and the expired flow rates at 25 and 75% of vital capacity (l/s) by
use of criteria from the American Thoracic Society.
Maximal exercise protocol.
All subjects then completed an incremental maximal exercise test on an
electromagnetic braked cycle ergometer (Ergoline 800) using successive
increases of 30 W every 90 s until voluntary exhaustion.
Electrocardiograph recordings, oxygen uptake
(O2), expired CO2
(CO2), and E as well
as tidal volume (VT), breathing frequency, and respiratory
exchange ratio were obtained continuously throughout the exercise
protocol by using a breath-by breath automated exercise metabolic
system (CPX, Medical Graphics, St. Paul, MN). Values were averaged over
the last 30 s of each workload to coincide with the simultaneous
arterial blood sampling. Arterial blood samples were drawn from an
indwelling brachial arterial catheter at rest as well as during the
last 30 s of each workload of the incremental maximal exercise and
at the third and fifth minute of exercise recovery.
Treatment of data and blood sample analyses.
Arterial gas sample data obtained throughout the maximal exercise test
were examined for evidence of mild exercise-induced hypoxemia defined
as a fall in PaO2 from baseline rest >10 Torr on
non-temperature-corrected PaO2. Fourteen of the 38 subjects met this criteria and were classified as GED subjects. The
data from these 14 GED subjects were compared with those from 14 of the
24 subjects with no GED (N) matched for age, height, weight, and
maximal aerobic power. PaO2 values corresponding to
given relative exercise intensities between 30 and 100% of
O2 max were determined for each subject
by using an interpolation procedure from the mathematical model of best
fit from PaO2 values at each workload.
Determination of blood gases and blood lactate.
On sampling, blood was quickly analyzed for PaO2,
PaCO2, and pH at 37° by using the standard
electrodes (Radiometer ABL 330, Radiometer, Copenhagen, Denmark). The
instrument was calibrated before and several times during the course of
blood analysis by using precision buffers and gases. Oxygen hemoglobin
saturation was calculated by using blood PaO2 and
arterial pH determinations.
To correct PaO2 values for blood temperature during
exercise, a subgroup of 16 subjects (8 of each of the 14 subjects of
the GED and the N group) were asked to return to the laboratory to repeat the same exercise protocol while equipped with an esophageal temperature probe. Workload, O2, and
heart rate responses were identical to those of the initial test.
Esophageal temperature was monitored throughout the exercise. Results
indicated similar esophageal temperature kinetics in both GED and N
with an average 1.8 ± 0.2°C increase from rest to maximal
exercise as previously reported by others (7). A
temperature correction factor based on the average esophageal
temperature recording was then applied to all exercise
PaO2 and PaCO2 values by using the
following equations, where T is the temperature
A-aDO2 in PO2
was calculated from the alveolar gas equation by using
temperature-corrected (c) values for PaO2 and
PaCO2 and correcting for saturation vapor pressure of
water by using the equation PH2o = 5.556 × exp(0.058T). Dead space-to-tidal volume ratio
(VD/VT) was calculated by using the classic
Bohr equation corrected by the valve box dead space.
Samples for blood lactate determination were drawn 2 min after the end
of maximal exercise and were analyzed by use of a standard lactate
analyzer (Microzym, SGI, Toulouse, France).
Statistical Analyses
Values are reported as means ± SE. Mean comparisons
between GED and N subjects were achieved by using Student's
t-test for unpaired data. Mean comparisons at various
relative exercise intensities were achieved by using a two-way ANOVA
for repeated measures on the last factor. On finding of a significant
F ratio (P < 0.05), post hoc data
comparisons were achieved by using a Tukey's test to locate group
differences. Statistical significance was set at P < 0.05.
| |
RESULTS |
Anthropometric and Resting Pulmonary Function Parameters
Anthropometric and resting pulmonary function parameters are shown
in Table 1. All participants exhibited
normal pulmonary function tests. No differences in age, height, weight,
or ventilatory parameters were found between subjects of groups GED and
N.
View this table:
[in this window]
[in a new window]
|
Table 1.
Anthropometric and resting pulmonary function data in subjects with or
without exercise-induced gas exchange disturbance
|
|
Maximal Exercise Data
Maximal exercise data from GED and N subjects appear in Table
2. Results indicate similar maximal heart
rate, O2, E, E/O2, respiratory
exchange ratio, and plasma lactate between GED and N. GED exhibited
significantly lower PaO2 and higher
A-aDO2 than N with a significantly higher value
of PaCO2 and a lower pH. Maximal values of
VT, breathing frequency, calculated alveolar E, and estimated VD/VT were
not significantly different between GED and N.
View this table:
[in this window]
[in a new window]
|
Table 2.
Maximal exercise data with temperature correction in subjects with or
without exercise-induced gas exchange disturbance
|
|
Exercise Ventilatory and Pulmonary Gas Exchange Patterns
Figure 1 illustrates individual and
group mean PaO2 (Fig. 1A) as well as the
calculated A-aDO2 (Fig. 1B) at rest
as well as for submaximal and maximal exercise in both GED and N. Resting values of PaO2 and
A-aDO2 were not significantly different between groups. As expected in the N group, exercise-induced hyperventilation resulted in a gradual increase in mean PaO2 at higher
exercise intensities. In contrast, subjects of the GED group showed a
gradual decline in PaO2 with increasing exercise
intensity. A significantly lower mean PaO2 was
observed in GED compared with N for all exercise intensities equal to
or exceeding 40% O2 max. Post hoc contrasts revealed successive mean PaO2 exercise
values in GED to be significantly different from one another for all
points between 40 and 90% O2 max; the
latter point is not statistically significantly different from maximal
exercise. An increase of the A-aDO2 was
observed in both groups for increasing relative exercise intensities
equal to or exceeding 30% O2 max. Results indicate an upward shift in the mean
A-aDO2 curve in GED compared with N such that
values were significantly higher in GED for all exercise intensities.
The extent of between-group difference remained relatively constant
throughout the incremental exercise protocol widening only at
near-maximal exercise. Recovery PaO2 and
A-aDO2, 3 and 5 min after maximal exercise,
were not found to be significantly different between groups.
View larger version (31K):
[in this window]
[in a new window]
|
Fig. 1.
A: mean arterial PO2
(PaO2) values ± SE at rest, during progressive
submaximal and maximal exercise, and after 3 and 5 min of sitting
recovery for subjects in the gas exchange disturbance (GED) group
( ) and those of the normal response (N) group
( ). For the sake of clarity, individual values and
lines are shown only for the GED group. A significant difference
between groups is observed for an exercise intensity as low as 40%
maximal oxygen uptake (O2 max).
B: alveolar-arterial PO2 difference
[P(A-a)O2] at rest, during
progressive submaximal and maximal exercise, and after 3 and 5 min of
sitting recovery subjects of the GED and N groups. For the sake of
clarity, individual values and lines are shown only for the GED group.
A significant difference in
P(A-a)O2 is observed between GED
and N subjects throughout exercise. *P < 0.05 between
groups; **P < 0.01 between groups.
|
|
Individual and mean values of arterial oxygen saturation
(SaO2) corrected for pH and temperature are shown in
Fig. 2 for GED and N. Only a slight
nonsignificant decrease from baseline is found in N. Results indicate
mean SaO2 values in GED to be significantly lower than
those in N for exercise intensities exceeding 70%
O2 max, which is in agreement with an
impairment in oxygen transport.
View larger version (22K):
[in this window]
[in a new window]
|
Fig. 2.
Arterial oxygen saturation (SaO2; %)
corrected for pH and temperature at rest, during progressive submaximal
and maximal exercise, and after 3 and 5 min of sitting recovery for
subjects of the GED group () and those of the N group
(). For the sake of clarity, individual values and
lines are shown only for the GED group. A significant difference in
SaO2 is observed between GED and N subjects throughout
exercise. *P < 0.05 between groups;
**P < 0.01 between groups.
|
|
Individual and mean values of PaCO2 and calculated
alveolar oxygen tension (PAO2) for GED and
N are shown in Fig. 3 at rest as
well as during submaximal and maximal exercise. The general pattern of
the PaCO2 response indicates values to fall
significantly from baseline at 80%
O2 max in GED and at 90%
O2 max in N. No statistical differences
in mean PaCO2 were found between groups for submaximal
exercise intensities, except for near-maximal intensities (90 and 100%
O2 max), at which GED showed slightly
but significantly higher values than N with mean differences corresponding to 2.3 and 2.8 Torr, respectively. Recovery mean PaCO2 values remained lower than baseline 3 and 5 min
after maximal exercise but were not found to be significantly different
between groups.
View larger version (20K):
[in this window]
[in a new window]
|
Fig. 3.
A: mean arterial PCO2
(PaCO2) values ± SE at rest, during progressive
submaximal and maximal exercise, and after 3 and 5 min of sitting
recovery for subjects of the GED group () and those of
the N group (). *P < 0.05 between
groups. B: mean ± SE values of ideal alveolar
PO2 (PAO2) at
rest, during progressive submaximal and maximal exercise, and after 3 and 5 min of sitting recovery for subjects of the GED and N groups. No
significant difference between groups was observed.
|
|
As expected, ideal PAO2 increased
progressively with incremental exercise intensity in both groups; the
relative increases corresponding to ~12 and 17% in GED and N
respectively (Fig. 3B). No significant between-group
difference was observed for mean ideal
PAO2 at any point including recovery.
Figure 4 shows mean exercise ventilatory
parameters in GED and N. Results show similar VT and
breathing frequency responses with exercise and recovery in both
groups. Similarly, VD/VT was not different
between groups at any observation point of exercise or recovery.
View larger version (17K):
[in this window]
[in a new window]
|
Fig. 4.
Mean ± SE values of tidal volume (A),
respiratory frequency (B), and dead space-to-tidal volume
ratio (C) at rest, during progressive submaximal and maximal
exercise, and after 3 and 5 min of sitting recovery for subjects of the
GED and N groups. No significant difference between groups was
observed.
|
|
| |
DISCUSSION |
Previous studies have shown an alteration of submaximal pulmonary
gas exchange in athletic groups of young and older men and highly
trained women showing a significant EIH at maximal exercise (15-17, 19, 20). In this study, a GED at the early
onset of progressive maximal exercise was found in 37% of healthy
active men showing similarities in body stature and physical fitness status on account of the professional demands of their occupation as
mountain rescue workers. This prevalence is not far behind the ~50%
prevalence of EIH estimated at sea level in highly trained athletes
(5). This observation raises the question as to whether there exist predisposing factors in healthy individuals for
exercise-induced GED that might become magnified as a result of
endurance training. As previously suggested (3), endurance
training may lead to an imbalance between pulmonary oxygen transport
demands and oxygen delivery capacity on account of the cardiac output
adaptation unmatched by pulmonary structural and functional
adaptations. In addition, the pattern of repeated stress of intensive
exercise inherent to endurance training could act to enhance
inflammatory processes and secretory characteristics of pulmonary
airways and parenchyma (2, 13, 15), predisposing to an
exaggerated ventilation and/or perfusion maldistribution during exercise.
In the present study, a significantly higher
A-aDO2 was observed in GED subjects as early as
the first submaximal exercise determination (30%
O2 max) and increased thereafter
throughout the exercise protocol. The exaggerated
A-aDO2 could not be accounted for by any
difference between groups in ideal PAO2,
indicating that external ventilation was not a factor during mild or
moderate exercise intensities. The observed GED in the early phase of
exercise must therefore reflect an alteration of pulmonary oxygen
conductance per se linked to either a circulatory or a peripheral air
conductance component or a combination of both. A shortened pulmonary
transit time as a result of an enhanced cardiac output in well-trained individuals as well as a putative interstitial pulmonary edema have
been suggested as potential mechanisms for the reported hypoxemia of
maximal or near-maximal exercise (8, 10, 18). In the present study, a difference in cardiac output and ensuing pulmonary transit time is unlikely because both O2
and heart rate responses are the same in both groups and thus, also,
presumably cardiac output. It may also be argued that the level of
metabolic and circulatory demands for mild and moderate exercise are
too low to account for substantial shear stress failure on the
pulmonary vasculature. In agreement with this argument, our recovery
data indicate similar arterial gases and A-aDO2
between groups with and without exercise pulmonary gas disturbances,
decreasing the probability of a contribution by pulmonary edema.
Ventilation-perfusion mismatch currently appears as the most likely
explanation for the maximal EIH in healthy endurance-trained subjects
(5). Our data indicate subjects from both groups to have
identical dead space ventilation throughout the exercise protocol. This
result does not, however, exclude the possibility of an alteration in
peripheral airway ventilation leading to an exaggerated
ventilation-perfusion mismatch to explain the observed submaximal GED.
Recently, Wetter et al. (20) examined the link between
pulmonary gas exchange and airway function during prolonged exercise in
healthy fit women. Their results show 8 of 17 runners to exhibit low
PaO2 during steady-state exercise at 75%
O2 max but not at the previous
steady-state level of 50% O2 max. Their results revealed significant correlations between increased pulmonary closing volume and exercise SaO2 and
A-aDO2 and showed several subjects to exhibit
some abnormalities of airway resistance and/or reactivity, although
this was not related to the degree of exercise-induced gas exchange
impairment. Specific functional characteristics of small and large
airway function were not obtained in the present study such that this
relationship cannot be verified. On the other hand, in our study, as in
other previous reports of submaximal exercise GED (1, 2,
15-17), the maximal exercise challenge consisted of a ramp
protocol in which workload is increased every 1-2 min. In such
rapid incremental protocols, the time at each exercise stage may be
insufficient to allow for stability of ventilatory parameters. This
time factor might be especially important in the presence of
predisposing peripheral airway dysfunction, which could emphasize the
inhomogeneity of pulmonary mechanical time constants and lead to
maldistribution of ventilation and reduced alveolar oxygen clearance.
Finally, an interesting observation of the present study is the fact
that, as shown by PaCO2 data, subjects exhibiting an early exercise widening of A-aDO2 also
exhibited a lesser hyperventilation during near-maximal exercise. In
highly trained athletes, the extent of maximal EIH has been clearly
related to the degree of hyperventilation (12, 14). Why
subjects showing impairment in gas exchange in the early phases of a
progressive maximal exercise would also be those demonstrating a lesser
hyperventilation remains to be clarified. A common denominator for
these concurrent events could be peripheral airway constraints
contributing to maldistribution of pulmonary flow in the early phases
of exercise and potentially affecting the maximal exercise ventilatory
response through mechanical or reflex influences. It may thus be of
interest for future investigations to confirm the occurrence of
submaximal GED by using steady-state rather than rapid incremental
exercise protocols and to examine its relationship with peripheral
pulmonary airway characteristics and/or maximal exercise ventilation.
In conclusion, the present observations indicate that the
GED-susceptible healthy individuals exhibit an early onset of
alveolar-arterial oxygen widening throughout the incremental exercise
protocol, which appears independent of the ventilatory response. The
early phenomenon appears, however, to be compounded by a relative
hypoventilation as subjects exhibiting an early exaggerated
alveolar-arterial widening also exhibit a relative hypoventilation at
maximal exercise. The present observations of GED in 37% of subjects
matched for age, body stature, and physical fitness status suggest that
factors unrelated to an exaggerated systemic demand for pulmonary
capacities appear to be involved in the GED. The fact that alveolar
ventilation and ventilatory efficiency were similar in subjects
exhibiting a GED or not suggests the involvement of an exaggerated
ventilatory maldistribution as the main responsible factor. The extent
to which a cumulative effect of successive non-steady-state exercise loads contributes to the present observations also needs to be considered.
| |
FOOTNOTES |
Address for reprint requests and other correspondence: B. Aguilaniu, HYLAB, Clinique Du Mail, 45 av. Marie Reynoard, F-38100 Grenoble (E-mail:
b.aguilaniu{at}wanadoo.fr).
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement"
in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
10.1152/japplphysiol.00630.1999
Received 19 August 1999; accepted in final form 9 January 2002.
| |
REFERENCES |
1.
Aguilaniu, B,
Flore P,
Page E,
Maitre J,
Perrault H,
and
Lacour JR.
Effects of indomethacin and polyunsaturated fatty acid diet on exercise-induced hypoxemia in master athletes.
Eur J Appl Physiol
77:
81-88,
1998.
2.
Anselme, F,
Caillaud C,
Couret I,
Rossi M,
and
Préfaut C.
Histamine and exercise-induced hypoxemia in highly trained athletes.
J Appl Physiol
76:
127-132,
1994[Abstract/Free Full Text].
3.
Dempsey, JA,
Hanson PG,
and
Henderson KS.
Exercise induced arterial hypoxemia in healthy human subjects at sea level.
J Physiol (Lond)
355:
161-175,
1984[Abstract/Free Full Text].
4.
Dempsey, JA.
Is the lung built for exercise?
Med Sci Sports Exerc
18:
143-155,
1986[ISI][Medline].
5.
Dempsey, JA,
and
Wagner PD.
Exercise-induced arterial hypoxemia.
J Appl Physiol
87:
1997-2006,
1999[Abstract/Free Full Text].
6.
Edwards, MR,
Hunte GS,
Belzberg AS,
Sheel AW,
Worsley DF,
and
McKenzie DC.
Alveolar epithelial integrity in athletes with exercise-induced hypoxemia.
J Appl Physiol
89:
1537-1542,
2000[Abstract/Free Full Text].
7.
Harms, CA,
McClaran SR,
Nickele GA,
Pegelow DF,
Nelson WB,
and
Dempsey JA.
Exercise-induced arterial hypoxaemia in healthy young women.
J Physiol (Lond)
507:
619-628,
1998[Abstract/Free Full Text].
8.
Hopkins, SR,
Belzberg AS,
Wiggs BR,
and
McKenzie DC.
Pulmonary transit time and diffusion limitation during heavy exercise in athletes.
Respir Physiol
103:
67-73,
1996[ISI][Medline].
9.
Johnson, BD,
and
Dempsey JA.
Demand vs. capacity in the aging pulmonary system.
Exerc Sport Sci Rev
19:
171-210,
1991[Medline].
10.
Manier, G,
Moinard J,
and
Stoïcheff H.
Pulmonary diffusing capacity after maximal exercise.
J Appl Physiol
75:
2580-2585,
1993[Abstract/Free Full Text].
11.
McClaran, SR,
Harms CA,
Pegelow DF,
and
Dempsey JA.
Smaller lungs in women affect exercise hyperpnea.
J Appl Physiol
84:
1872-1881,
1998[Abstract/Free Full Text].
12.
Miyachi, M,
and
Tabata I.
Relationship between arterial oxygen desaturation and ventilation during maximal exercise.
J Appl Physiol
73:
2588-2591,
1992[Abstract/Free Full Text].
13.
Mucci, P,
Durand F,
Lebel B,
Bousquet J,
and
Préfaut C.
Interleukins 1-beta, -8 and histamine increases in highly trained, exercising athletes.
Med Sci Sports Exerc
32:
1094-1100,
2000[Medline].
14.
Powers, SK,
Martin D,
Cicale M,
Collop N,
Huang D,
and
Criswell D.
Exercise-induced hypoxemia in athletes: role of inadequate hyperventilation.
Eur J Appl Physiol
65:
37-42,
1992.
15.
Préfaut, C,
Anselme F,
Caillaud C,
and
Massé-Biron J.
Exercise-induced hypoxemia in older athletes.
J Appl Physiol
76:
120-126,
1994[Abstract/Free Full Text].
16.
Rice, AJ,
Scroop GC,
Gore CJ,
Thornton AT,
Chapman MAJ,
Greville HW,
Holmes MD,
and
Scicchitano R.
Exercise-induced hypoxemia in highly trained cyclists at 40% peak oxygen uptake.
Eur J Appl Physiol
79:
353-359,
1999.
17.
Rice, AJ,
Thornton AT,
Gore CJ,
Scroop GC,
Greville HW,
Wagner H,
Wagner PD,
and
Hopkins SR.
Pulmonary gas exchange during exercise in highly trained cyclists with arterial hypoxemia.
J Appl Physiol
87:
1802-1812,
1999[Abstract/Free Full Text].
18.
Schaffartzik, W,
Pool DC,
Derion T,
Tsukimoto K,
Hogan MC,
Arcos JP,
Bebout DE,
and
Wagner PD.
A/
distribution during heavy exercise and recovery in humans: implications for pulmonary edema.
J Appl Physiol
72:
1657-1667,
1992[Abstract/Free Full Text].
19.
Ste-Croix, CM,
Harms CA,
McClaran SR,
Nickele GA,
Pegelow DF,
Nelson WB,
and
Dempsey JA.
Effects of prior exercise on exercise-induced arterial hypoxemia in young women.
J Appl Physiol
85:
1556-1563,
1998[Abstract/Free Full Text].
20.
Wetter, TJ,
St-Croix CM,
Pegelow DF,
Sonetti DA,
and
Dempsey JA.
Effects of exhaustive endurance exercise on pulmonary gas exchange and airway function in women.
J Appl Physiol
91:
847-858,
2001[Abstract/Free Full Text].
J APPL PHYSIOL 92(5):1879-1884
8750-7587/02 $5.00
Copyright © 2002 the American Physiological Society
TOP
ABSTRACT
INTRODUCTION
![Pa<SUB>O<SUB>2</SUB></SUB>(c)<IT>=</IT>antilog [0.023<IT>×</IT>(T<IT>−</IT>37)]<IT>+</IT>log(Pa<SUB>O<SUB>2</SUB></SUB>)](/content/vol92/issue5/fulltext/1879/img001.gif)
![Pa<SUB>CO<SUB>2</SUB></SUB>(c)<IT>=</IT>Pa<SUB>CO<SUB>2</SUB></SUB><IT>×</IT>antilog [0.021<IT>×</IT>(T<IT>−</IT>37)]](/content/vol92/issue5/fulltext/1879/img002.gif)
