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O2max during prolonged
high-altitude exposure
1 Ecole Nationale de Ski et d'alpinisme, 74401 Chamonix; 2 Association pour la Recherche en Physiologie de l'Environnement, 93017 Bobigny; 3 Laboratoire de Physiologie, hôpital Necker, 75015 Paris; 4 Laboratoire de Biochimie, hôpital Jean Verdier, 93140 Bondy; and 5 COMEX S.A., 13275 Marseille, France
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We hypothesize that plasma volume
decrease (
PV) induced by high-altitude (HA) exposure and intense
exercise is involved in the limitation of maximal O2 uptake
(
O2max) at HA. Eight male subjects were decompressed for 31 days in a hypobaric chamber to the
barometric equivalent of Mt. Everest (8,848 m). Maximal exercise was
performed with and without plasma volume expansion (PVX, 219-292
ml) during exercise, at sea level (SL), at HA (370 mmHg, equivalent to
6,000 m after 10-12 days) and after return to SL (RSL, 1-3
days). Plasma volume (PV) was determined at rest at SL, HA, and RSL by
Evans blue dilution. PV was decreased by 26% (P < 0.01) at HA and was 10% higher at RSL than at SL. Exercise-induced PV was reduced both by PVX and HA (P < 0.05).
Compared with SL, O2max was
decreased by 58 and 11% at HA and RSL, respectively. O2max was enhanced by PVX at
HA (+9%, P < 0.05) but not at SL or RSL. The more PV
was decreased at HA, the more
O2max was improved by PVX
(P < 0.05). At exhaustion, plasma renin and
aldosterone were not modified at HA compared with SL but were higher at
RSL, whereas plasma atrial natriuretic factor was lower at HA. The present results suggest that PV contributes to the limitation of
O2max during acclimatization
to HA. RSL-induced PVX, which may be due to increased activity of the
renin-aldosterone system, could also influence the recovery of
O2max.
hypoxia; blood volume; plasma lactate; gas exchange
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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ACUTE EXPOSURE TO
HYPOXIA decreases maximal O2 uptake
(O2max). This phenomenon is
related to several limiting factors, both central and peripheral, that
impair convective and/or diffusive O2 delivery to
exercising muscles (23, 29). Acclimatization to high altitude (HA) does not improve
O2max (23,
24, 27) even though the rise in red cell mass
enhances blood O2-carrying capacity. Indeed, other
acclimatization-related processes such as loss of muscle mass
(22) or decrease in maximal heart rate (17,
24) may alter some components of O2 transport.
Acclimatization to hypoxia also induces a decrease in plasma volume
(PV) (9, 16, 19). This process
could have multiple causes, including plasma protein loss
(26), increase in capillary permeability (7),
and dehydration or increased diuresis (6). Severe muscular work provokes a loss in PV that is due to fluid transfer from the
vascular bed into the interstitium and active muscles, resulting from
an increase in both muscle osmotic pressure and capillary hydrostatic
pressure (13). These two mechanisms suggest that PV during
maximal exercise in prolonged hypoxia could be decreased in an additive
manner. However, it is not known whether such a reduction in the
circulating volume associated with an elevated blood viscosity plays a
significant role on maximal O2 transport at high altitude.
The present study therefore tested the hypothesis that the decrease in
PV (PV) related to prolonged hypoxia and/or maximal exercise
contributes to the impairment of
O2max at HA. The role of PV
on O2max was examined by
means of plasma expansion during exercise at sea level (SL), at the
simulated HA of 6,000 m, and after HA exposure. On return to sea level
(RSL), O2max is known to
remain depressed (3), but the underlying mechanisms are not well understood. Undocumented PV alterations after extreme altitude
exposure could also influence
O2max recovery. To further examine the control of PV shifts, the fluid- and sodium-regulating hormones renin, aldosterone, and atrial natriuretic factor (ANF) were
also measured.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Operation Everest III was a simulated ascent of Mt. Everest in a hypobaric chamber at COMEX S.A. in Marseille, France. Complete details of this study have been described previously, including the selection and characteristics of the subjects, a description of the hypobaric chambers, the ascent profile, and the various hypotheses investigated (20).
Subjects. Eight male subjects participated in the experiment. Each subject underwent a medical examination and gave written, informed consent. The study was approved by the Ethics Committee of the University Hospital of Marseille, France. The subjects were not acclimatized to altitude before the study. Their mean ± SD age, height, and body mass were 27 ± 4 yr, 180 ± 6 cm, and 74.4 ± 6.7 kg, respectively.
Procedures.
All experiments were conducted in the hypobaric chamber at COMEX S.A.,
Marseille, France. The ascent profile is presented in Fig.
1, as described elsewhere
(20). Briefly, after a 10-day period of baseline
investigations at SL (760 mmHg), the subjects were transported by
helicopter to Observatoire Vallot (4,350-m altitude, 452 mmHg) where
they were preacclimatized for 7 days, without performance of any
scientific protocol. The subjects then descended to SL and were
transported to Marseille, where decompression from 422 to 253 mmHg
(8,848 m) started within 24 h and lasted 31 days. The HA studies
were performed 10-12 days after the beginning of decompression
during a 4-day period at 370 mmHg (6,000 m). The ambient pressure of
253 mmHg, which corresponds to the summit of Everest, was reached on
days 29-30. RSL studies were performed on days
1-3 after the end of HA exposure. Pure O2 was
breathed by the investigators, using a sealed helmet system, for a few minutes before decompression and during hypobaria to facilitate denitrogenation and to avoid nitrogen bubble formation. Expired gas was
evacuated by a vacuum pump so that O2 concentration in the
chamber remained constant at 21%. During studies, temperature and
hygrometry in the chamber were controlled between 18 and 24°C and 30 and 60%, respectively (20).
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Experiments with PVX.
To minimize exercise-induced PV, a plasma expander (Hesteril 6%,
6% hydroxyethyl starch, Fresenius) was infused in an antecubital vein
from the beginning of exercise until cessation. A special recommendation from the ethical committee was to restrict the infused
volume to 300 ml for all subjects. According to the mean body mass of
our subjects, this limitation corresponded to a volume of ~4 ml/kg.
Our objective was to infuse this volume of plasma expander over the
entire exercise period. The duration of incremental exercise was
therefore determined individually during a preliminary testing session,
and infusion flow was adjusted for each subject using a multiple
electric-syringe driver (Infusion Station; Vial Medical/Fresenius).
This system provided a constant infusion rate that was not altered by
the increase in arm venous pressure related to arm contractions during
cycling exercise. The individual infusion flow, determined at SL,
remained the same at HA and RSL. The volume of plasma expander infused
during exercise was 292 ± 24 ml at SL, 219 ± 22 ml at HA
(P < 0.05 vs. SL), and 290 ± 38 ml at RSL.
Gas exchange.
Gas exchange was measured breath by breath at rest and during
incremental exercise by using an integrated computer system (CPX/D
cardiopulmonary exercise system; Medical Graphics, Minneapolis, MN).
Minute ventilation was measured by a symmetrically disposed Pitot tube
flowmeter. O2 concentration was measured by a galvanic fuel
cell and CO2 by an infrared analyzer. The characteristics of this device have been described previously (21). The
gas exchange analyzer, located in the hypobaric chamber during all studies, was modified to ensure a correct measurement of gas exchange in hypobaria. Hypobaric hypoxia was associated with an increase in the
expired fraction of CO2 (but a decrease in the partial pressure of CO2) that exceeded the normal calibration range
for the CO2 analyzer. The CO2 gain was
therefore amplified, and the original CPX/D software was modified.
Preliminary tests using a gas exchange simulator (10)
showed that the measurements of O2 uptake
(O2) taken at rest and during exercise
(O2 ~2.7 l/min) with the modified gas
analyzer were reliable within 300-760 mmHg.
O2max corresponded to the
highest value of O2 averaged over a 30-s
time interval. Heart rate was measured continuously, as was as arterial
O2 saturation, by a pulse oximeter (Biox II, Ohmeda).
Blood analyses.
Resting plasma volume was determined by Evans blue dilution (T-1824).
After a 30-min resting period in the sitting position, 5 ml of T-1824
were injected into one arm. Blood was sampled from the opposite arm at
15-, 20-, and 25-min postinjection (19). Resting PV
(PVrest) was determined before the infusion of hydroxyethyl starch, three times in each subject, at SL, HA, and RSL. Hemoglobin concentration ([Hb]) was determined by spectrophotometry (CO
oximeter, model 270, Ciba Corning) and the hematocrit (Hct) by
micromethod, at rest and every 4 min, from the end of the 120-W
exercise period until exhaustion. Resting blood volume (BV) and red
cell volume (RCV) were calculated using the formulas BV = PV/(1 
Hct) and RCV = BV PV, respectively, and the
appropriate correction for trapped plasma and peripheral blood sampling
(8) was also used. The relative exercise-induced
PV (%) was calculated from [Hb] and Hct with the following
formula [Hct not corrected for Fcell ratio (overall
hematocrit/peripheral hematocrit)] (8)
![&Dgr;PV<IT>%=</IT>[([Hb]<SUB>pre</SUB><IT>/</IT>[Hb]<SUB>post</SUB>)](/content/vol89/issue1/fulltext/29/img001.gif)
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![×(100−Hct<SUB>post</SUB>)<IT>/</IT>(<IT>100−</IT>Hct<SUB>pre</SUB>)<IT>−1</IT>]<IT>×100</IT>](/content/vol89/issue1/fulltext/29/img002.gif)
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(1) |
PV (ml) was calculated as
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(2) |
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(3) |
80°C for further analysis. Plasma protein concentration was determined by end-point colorimetry. Plasma
albumin concentration ([Alb]) was measured by immunonephelometry, and
concentration of lactate was determined after perchloric
deproteinization by the end-point enzymatic ultraviolet method (Cobas
Fara-Roche).
Plasma renin ([Ren]) and aldosterone ([Aldo]) concentrations were
measured with an immunoradiometric assay (Sanofi Diagnostics Pasteur,
Marnes la Coquette, France) and a radioimmunoassay (Diagnostic Products, Los Angeles, CA), respectively. Plasma ANF concentration ([ANF]) was measured with a radioimmunoassay following an extraction step. Briefly, blood was collected on a tube containing EDTA and trasylol (a protease inhibitor), and plasma was separated and stored at
80°C until assay. One milliliter of plasma was then acidified with
3 ml of a 4% acetic acid solution, followed by deposition of 4 ml of
acidified plasma on a C18 Sep Pak column (Waters Millford)
that had been previously activated with methanol (5 ml). The column was
rinsed with 5 ml of distilled water. Elution was performed with 3 ml of
the following solution: 60% acetonitril and 0.1% trifluoroacetic
acid, in distilled water. Eluate was dried under nitrogen and assayed
afterward with a radioimmunoassay kit (Amersham International).
Statistics. Data are presented as means ± SD. A one-way ANOVA with repeated measures was used to compare the effect of altitude on resting parameters. A two-way ANOVA with repeated measures was performed to analyze 1) the effects of altitude and exercise in the control condition and 2) the effects of altitude and infusion during maximal exercise. A Dunnett's test was used for multiple comparisons. Relationships between two variables were evaluated by linear regression. Differences were considered significant at P < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Simulated HA effects.
Body mass decreased from 74.1 ± 6.5 kg at SL to 71.5 ± 6.1 kg (P < 0.01) at HA and to 71.2 ± 6.0 kg
(P < 0.01) after 31 days of hypobaric exposure.
PVrest decreased 26% from 3.68 ± 0.51 liters at SL
to 2.73 ± 0.63 liters at HA (P < 0.01). After HA
exposure, PVrest tended to be higher than at SL (4.06 ± 1.01 liters; +10%, P = 0.15). Individual PV values
show that, of eight subjects, seven experienced PVX after hypobaric
exposure (Fig. 2A). Resting RCV was not significantly increased between SL and HA (2.52 ± 0.43 vs. 2.57 ± 0.60 liters ) but was higher at RSL (3.24 ± 0.80 liters; Fig. 2B). BV was not significantly decreased
(P = 0.06) at HA compared with SL (5.30 ± 1.21 vs. 6.20 ± 0.90 liters) but was higher at RSL (7.31 ± 1.76 liters; Fig. 2C).
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PV induced by maximal exercise was similar before and after
hypobaric exposure but reduced at HA (Fig.
3). For a given absolute workload that
corresponded to the maximal workload at HA, PV was the same in the
three altitude conditions, with values of 310 ± 18, 317 ± 15, and 337 ± 22 ml at SL, HA, and RSL, respectively.
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O2max, expressed in liters
per minute, was lower at HA than at SL, and
O2max recovery remained incomplete
(14%) 1-3 days after the 31-day decompression (Table 1).
O2max, expressed per
kilogram of body mass, decreased 58% between SL and HA and remained
11% lower (P = 0.1) than the original SL value after hypobaric exposure (Fig. 4). The
discrepancy between both percentages for
O2max recovery (14 vs. 11%)
was related to the 3.9% decrease in body mass between SL and RSL
studies.
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O2max, whereas plasma
protein concentration was raised at rest only. Plasma [Alb] did not
change at HA (Table 2).
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O2max (Fig.
5). Conversely, the exercise-induced increase in plasma [ANF] was blunted at HA (Fig. 5). After altitude exposure, resting [Ren] and [Aldo] tended to be higher than at SL,
and both [Ren] and [Aldo] responses to exercise were exaggerated.
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O2max at HA was related to
the concomitant decline in PVrest
(%O2max = 0.497 × %PVrest 48.267; r = 0.72, P < 0.05) but not in PV at maximal exercise (Fig.
6A). O2max decrease at HA was
also related to the concomitant decline in resting BV
(BVrest;
%O2max = 0.257 × %BVrest 54.625; r = 0.73;
P < 0.05) and in BV at maximal exercise (Fig.
6B). Furthermore, O2max recovery at RSL was
related to the concomitant expansion 1) of
PVrest
(%O2max = 0.614 × PVrest 16.113; r = 0.74, P < 0.05) and of PV at maximal exercise (Fig.
6C), and 2) of BVrest (%O2max = 0.632 × %BVrest 20.628; r = 0.74;
P < 0.05) and of BV at maximal exercise (Fig.
6D).
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Effects of PVX.
At each altitude, PVX significantly attenuated exercise-induced PV
(Fig. 3). PVX did not influence any of the cardiopulmonary variables
except O2max at HA, which
increased 9% (P < 0.05; Table 1). When expressed per
kilogram of body mass, O2max
was also enhanced 9% by PVX at HA (Fig. 4). Conversely, PVX had no effect on O2max at SL or
RSL. PVX did not alter heart rate at maximal exercise or at 50% of
O2max (Table 1).
O2max was improved by PVX at
HA (%O2max = 1.157 × %PVrest 13.263; r = 0.89, P < 0.005). The relationship between BVrest and O2max
was also significant
(%O2max = 0.613 × %BVrest + 1.323; r = 0.93;
P < 0.001). The increase in
O2max with PVX at HA was
also related to the altitude-induced decrement in PV or BV during
maximal exercise (Fig. 7).
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| |
DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The main finding of the present study was that acute PVX during
incremental exercise to exhaustion slightly improved
O2max at HA in acclimatized
subjects. Conversely, plasma expander infusion at SL, before and after
a 31-day gradual decompression up to 253 mmHg, did not alter
O2max. This study also
provided insight on the recovery period after extreme altitude
exposure. Our results indicate that PV and BV expansion occur during
RSL because PV and BV were 0.7 and 1.1 liters higher, respectively,
after RSL compared with at SL. At RSL,
O2max did not return
completely to SL values. [Ren] and [Aldo] responses to exercise
were exaggerated at RSL, the only time they were affected by PVX.
HA exposure.
In the present study, exposure to the simulated altitude of 6,000 m
(after an 18-day gradual decompression starting at 4,350 m) provoked a
58% decrease in O2max,
which was higher than decreases previously reported for similar
altitudes by West et al. (30) and during Operation Everest
II by Cymerman et al. (3) (50 and 47%, respectively).
However, the magnitude of the differences observed between the present
and previous studies (58 vs. 47-50%) may be due to the large
range in individual responses, which could be equal to or greater than
the differences between these means.
O2max demonstrated during
acclimatization to severe hypoxia, but not at SL, raises the question of the involvement of PV shifts in the limitation of maximal
O2 transport at HA. At SL, after acute PVX,
O2max was found to be either
enhanced (2) or unchanged (11,
12, 14). In the present basal condition,
infusion during exercise did not improve maximal O2
transport, suggesting that, if resting PV is within the normal range,
the magnitude of PV associated with exercise would not contribute to
limit O2max. Prolonged
exposure to HA was associated with a 26% decrease in
PVrest, which was in agreement with previous data obtained
at similar altitudes (16). This plasma loss was unlikely
to be due to dehydration and/or increased diuresis because water intake
and urine output were well preserved over the first 16 days in
hypobaria (Westerterp, unpublished observation). Conversely, the
significant decrease in total circulating protein between SL and HA
(from 273 to 213 g) may be a primary factor in PV loss, as
suggested previously (26).
The insignificant increase in RCV observed in this study, from 35 ml/kg
at SL to 37 ml/kg at HA, may appear surprising. Classically, acclimatization is associated with a rise in red cell mass. However, recent work using an erythrocyte-labeling method indicated that RCV was
unchanged after 13 days at 4,300 m (26). Moreover, Grover et al. (5) demonstrated that RCV (determined by
rebreathing carbon monoxide) was not increased during the first 2 wk at
4,300 m, i.e., most individuals showed little or no increase or
decrease in RCV during this period. Indeed, a recent review has
emphasized the considerable individual variability in the RCV response
to altitude (5). These data therefore support the idea
that red cell mass expansion may take more than 2 wk of altitude
exposure, despite high levels of erythropoietin.
Finally, exercise-induced PV was similar at SL and RSL but decreased
at HA (Fig. 3). This lower leak of intravascular fluid at high altitude
was primarily related to the reduced maximal exercise intensity in this
condition, whereas the shorter exercise time was of less importance
(8).
At HA, although the fall in
O2max was too great to be
reversed to SL values by the infusion, the 219 ml (mean value) of plasma expander improved
O2max by 9%. This
observation supports the hypothesis that the depressed circulating
volume during maximal exercise in prolonged hypoxia may participate in
the limitation of O2max.
Previous studies completed at lower altitudes demonstrated that
O2max was not ameliorated
after isovolemic hemodilution (25) or erythrocyte infusion
(31). However, we are not aware of other reports
investigating acute PVX during maximal exercise in similar altitude conditions.
It is of interest to discuss the respective roles of acclimatization-
and exercise-induced PV on
O2max.
O2max decrement at HA was
significantly related to the concomitant decrease in PVrest
or BVrest and to the decrease in BV at maximal exercise (Fig. 6B). Second, the more PVrest or
BVrest and PV or BV at maximal exercise (Fig. 7,
A and B) were depressed at high altitude the greater the effect of PVX on O2 transport. On the other
hand, exercise at HA provoked an additional decrease in PV of ~11%
(317 ml), which was reduced to ~3% (72 ml) with PVX. However, the
individual improvement in
O2max with PVX was poorly
related to the PVX-induced reduction in plasma loss during exercise
(results not shown). Thus, if PV loss is a limiting factor of
O2 transport at high altitude, the mechanism could be
primarily linked to the large leak of plasma (~950 ml) associated
with prolonged exposure to hypoxia, whereas supplementary PV
occurring during exercise would be of less importance.
Because we did not measure any parameters of central or peripheral
circulation, we were not able to determine which mechanism PVX used to
enhance O2max at HA. One
could hypothesize that, facing a depressed circulating volume, even a
relatively small amount of PV expansion improved venous return, thus
improving cardiac output and blood flow to active muscles. Despite a
concomitant reduction in blood O2-carrying capacity, the
net result would be an amelioration in muscle O2 delivery.
Alternatively, if muscle oxygenation was impaired at HA by high blood
viscosity, rather than by volume depletion, PVX could be beneficial by
blunting the viscosity increase. However, this idea is not supported by the data of Sarnquist et al. (25), which indicated that
O2max at 5,400 m was not
improved after isovolemic hemodilution. In that study, the remarkable
finding was that O2max did
not change and was not impaired, despite the lower
O2-carrying capacity associated with hemodilution
(25).
Finally, the fact that maximal heart rate was not reduced with PVX,
both at SL and HA, is consistent with other data obtained at SL that
indicate no change in maximal heart rate with an acute PVX of
450-600 ml (2, 14). Conversely, maximal
heart rate at SL was reduced after a 700-ml PVX because of an increase
in stroke volume (11). The lack of a significant effect of
PVX on maximal heart rate in the present study was, therefore, most likely due to the limited volume of fluid infused.
Recovery after HA exposure.
Experiments performed at RSL provided additional insights on our
hypothesis. Even if O2max
recovery was not complete at RSL,
O2max (expressed in ml
· min
1 · kg1) was only 11% lower
than the initial value. In comparison, during Operation Everest II,
O2max after extreme altitude
exposure (within 2 days after the end of decompression) was more
reduced, being lower than the SL value by 20% (3). It is
of interest to relate the restoration of aerobic performance to PV
recovery. In eight subjects, six experienced "spontaneous" PVX
between SL and RSL. This observation is not in agreement with other
data obtained at altitudes 
4,300 m, indicating a subnormal PV during early recovery from altitude exposure (4,
26). Nevertheless, this phenomenon of PVX at RSL seems to
play a role in O2max recovery (Fig. 6C). Finally, the fact that infusion had no
effect on O2max at SL is not
surprising, because PVrest was normal or even supranormal.
Hormonal response. The lack of a significant decrease in [Ren] and [Aldo] at HA, as classically observed in hypoxia (15, 18, 32), could be partly explained by the great variability of our sample. Some subjects showed a suppression of exercise-induced rises in [Ren] and [Aldo] at HA, and others showed no change at all. However, the 15% decrease in BV experienced by our subjects at HA may have stimulated these sodium- and water-retaining hormones. Thus the antagonist effects of hypoxemia and hypovolemia may explain why [Ren] and [Aldo] did not change significantly at HA. The fact that the [ANF] response to exercise was reduced at HA, as demonstrated in previous studies (1, 18, 28), is probably explained by the large drop in heart rate and absolute work load. However, the most surprising hormonal responses occurred after recompression. At that time, [Ren] and [Aldo] responses to exercise were exacerbated, and infusion partially inhibited these responses, whereas [ANF] was not further increased. Globally, these hormonal changes indicated a trend toward an antidiuretic effect (increased renin-aldosterone activity) associated with RSL, which probably accounts for the concomitant PVX. This phenomenon could be related to a transient imbalance between two antagonist effects associated with reoxygenation, i.e., 1) an immediate withdrawal of hypoxia-induced inhibition and 2) a delayed suppression of hypovolemia-induced stimulation on the renin-aldosterone system.
In summary, this study demonstrated that acute PVX expansion, despite a concomitant reduction in [Hb], slightly amelioratedO2max at HA but not before
or after hypoxic exposure. Thus alterations in PV associated with
acclimatization may be involved in the impairment of O2
transport at HA. Furthermore, the PVX observed at RSL, which was
probably mediated by a rebound in renin and aldosterone secretion, could also be implicated in
O2max recovery. From a
practical point of view, the deleterious effect of a depressed
circulating volume on aerobic performance at altitude stresses the
importance of adequate hydration in the high mountain environment.
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ACKNOWLEDGEMENTS |
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We thank the administrative and technical crews of COMEX S.A. for assistance provided to the investigators and subjects during the study; Kim Bodin, Emmanuel Cauchy, Guillaume Despiau, Jean-François Finance, Mathieu Gayet, Guillaume Sabin, Philippe Serpollet, and Alexandre Héritier for patience and courage during this exceptional experience; and Vincent Marchand as well.
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FOOTNOTES |
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This study was made possible by grants from the Région Provence Alpes Côte d'Azur and Ministère Jeunesse et Sports.
This study was part of a larger study (Operation Everest III) investigating several physiological, physiopathological, and psychological mechanisms during exposure to extreme and prolonged hypobaric hypoxia.
Address for reprint requests and other correspondence: P. Robach, ENSA, BP 24, 74401 Chamonix, France (E-mail: med{at}ensa.jeunesse-sports.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. §1734 solely to indicate this fact.
Received 28 December 1998; accepted in final form 17 February 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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P < 0.05 PVX vs. control.
