| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Association pour la Recherche
en Physiologie de l'Environnement, ABSTRACT Robach, Paul, Daniel Biou, Jean-Pierre Herry, Denis Deberne,
Murielle Letournel, Jenny Vaysse, and Jean-Paul Richalet. Recovery
processes after repeated supramaximal exercise at the altitude of 4,350 m. J. Appl. Physiol. 82(6):
1897-1904, 1997.
hypoxia; plasma catecholamines; plasma lactate; plasma proteins; blood pH; oxygen uptake; ventilation; femoral blood velocity
INTRODUCTION MUSCLE POWER IN HUMANS during a supramaximal exercise
of short duration ( Besides the potential effect of hypoxia on
O2 transport during recovery, some
adaptative mechanisms that occur within a few days at high altitude may
impair performance during repeated sprints: 1) the decrease in buffer capacity
resulting from the compensation of respiratory alkalosis (24) may lead
to a more severe acidosis after the sprint and, therefore, limit the
restoration of power output, and 2)
the early decline in plasma volume (26) may interfere with recovery
processes at high altitude, because the sprint itself induces a severe
hemoconcentration during recovery (11). The present study, therefore,
examines the effect of prolonged exposure to hypoxia on the restoration
of muscle power during recovery. High-altitude experiments were
conducted 5-6 days after arrival at 4,350 m. At that time, the
changes in acid-base status and plasma volume had reached a
steady-state level (24), and any effects of symptoms of acute mountain
sickness on performance during sprint were avoided.
METHODS
We tested the hypothesis that prolonged exposure
to high altitude would impair the restoration of muscle power during
repeated sprints. Seven subjects performed two 20-s Wingate tests (WT1
and WT2) separated by 5 min of recovery, at sea level (N) and after
5-6 days at 4,350 m (H). Mean power output (MPO) and
O2 deficit were measured during
WT. O2 uptake
(
O2) and ventilation
(E) were measured continuously. Blood velocity in the femoral artery (FBV) was
recorded by Doppler ultrasound during recovery. Arterialized blood pH
and concentrations of bicarbonate
([HCO
3]), venous
plasma lactate
([La]),
norepinephrine ([NE]), and epinephrine ([Epi])
were measured before and after WT1 and WT2. MPO decreased between WT1
and WT2 by 6.9% in N (P < 0.05) and
by 10.7% in H (P < 0.01). H did not further decrease MPO. O2 deficit
decreased between WT1 and WT2 in H only
(P < 0.01). Peak
O2 after WT was reduced by
30-40% in H (P < 0.01), but
excess postexercise O2 consumption
was not significantly lowered in H. During recovery in H compared with N, E,
exercise-induced acidosis, and [NE] were higher,
[Epi] tended to be higher,
[La] was not
altered, and [HCO3] and
FBV were lower. The similar
[La]
accumulation was associated with a higher exercise-induced acidosis and
a larger increase in [NE] in H. We concluded from this
study that prolonged exposure to high altitude did not significantly impair the restoration of muscle power during repeated sprints, despite
a limitation of aerobic processes during early recovery.
45 s) is either not altered (6, 15) or only slightly decreased (19) by acute or chronic hypoxia. During recovery
after a supramaximal exercise, the restoration of muscle power requires
an O2 volume, defined as the
excess postexercise O2 consumption
(EPOC). The rapid EPOC component, in the early recovery, mainly
contributes to the replenishment of the high-energy phosphate stores,
as well as lactate removal by oxidation and glycogen resynthesis (1,
7). However, if a second supramaximal bout is performed shortly after
an initial maximal effort, the rate of energy release and,
consequently, power output will decrease (3, 4, 14). Using the same
exercise model as in the present study, we previously found that acute
hypoxic exposure did not significantly impair the restoration of power
output after sprint (21). However, Balsom et al. (2) also demonstrated
that the reduction in performance was larger when 10 successive sprints were performed in acute hypoxia. Nevertheless, in both cases, postexercise O2 uptake
(O2) was lower
in hypoxia, suggesting a reduced rate of oxidative processes during
early recovery.
O2 max) was
determined on the ergometer at sea level and on days
3-4 after arrival at high altitude. The test
protocol involved a 4-min warm-up at 60 W, followed by an incremental
exercise (30 W every 2 min) until the subject could not keep up the
pedaling rate [60 revolutions/min (rpm)]. Each subject
performed a preliminary force-velocity test (22) by pedaling maximally
during 5 s against loads from 2 to 10 kg to calculate the individual
optimal braking load for the Wingate test (WT). The force-velocity
relationship was determined at sea level only, and the same braking
load was used for normoxic and hypoxic WT experiments. In this study,
WT was a 20-s cycle exercise with maximal voluntary pedaling rate. Before each supramaximal test, subjects performed a 5-min warm-up at
60-90 W. During all WT and force-velocity tests, subjects remained seated on the saddle and were encouraged vigorously. The subjects were
trained for WT before the experiments.
E)
from two sensitive differential pressure transducers with a precision
of 2% for flows ranging from 6 to 172 l/min (17). The gas analyzers
were part of the integrated system and consisted of a galvanic fuel
cell for measurement of O2
concentration and an infrared CO2
analyzer. A reference gas bottle containing 12.1% O2 and 5.2%
CO2 was used for the calibration
of the analyzer. The delay time, response time to 90% of final value,
and precision were 0.54 s, 0.08 s, and 0.03% for the
O2 analyzer and 0.57 s, 0.11 s,
and 0.05% for the CO2 analyzer,
respectively. The breath-by-breath measurements of
E and
O2 were averaged over a
2-min interval at rest. Heart rate (HR) was measured continuously, as
well as arterial O2 saturation
(SaO2) by an ear pulse oximeter (Biox
II, Ohmeda). Mean arterial pressure (MAP) was collected over 20-s time
intervals during recovery by an automatic sphygmomanometer (Dinamap
1846 SX P, Critikon). Resting values for MAP were recorded as the mean
of three successive measurements.
Blood analyses.
Capillary blood from a prewarmed earlobe was sampled at rest (R), 1.5 min after WT1 (R11.5 min),
1.5 min after WT2
(R21.5 min), and 10 min
after WT2 (R210 min) and
then immediately analyzed in a blood-gas apparatus (Ciba Corning, model
248) for pH, bicarbonate concentration
([HCO3]), and
O2 and
CO2 pressure and content
(PO2 and
PCO2;
CO2 and
CCO2,
respectively). To collect blood anaerobically and to ensure a valid
PO2, a puncture was made with a
microlance for each sample. Consequently, each experiment required four
earlobe punctures. Simultaneously, forearm venous blood samples were
collected in heparinized tubes and immediately centrifuged. The
separated plasma was stored in liquid nitrogen within 30 min for
subsequent analyses. Concentrations of potassium
([K+]), sodium
([Na+]), and chloride
([Cl]) were
determined directly from the plasma by direct potentiometry with
specific electrodes, plasma protein concentration
([protein]) was determinetd by end-point colorimetry, and
concentrations of lactate
([La]) and
pyruvate ([Pyr]) were determined after perchloric acid deproteinization by end-point enzymatic ultraviolet method (Cobas Fara-Roche). Epinephrine ([Epi]) and norepinephrine
([NE]) concentrations were determined by a high-performance
liquid chromatography method with electrochemical detection (12).
Resting venous samples were used for the determination of hemoglobin
concentration and hematocrit by micromethod.
Blood velocity measurements.
The blood velocity in the right common femoral artery (FBV) was
monitored during rest and recovery by a continuous Doppler ultrasound
method. The frequency of the apparatus was 4 MHz. The probe was located
~3-6 cm distal of the inguinal ligament and positioned on the
skin with an adhesive strip. The probe was 7 mm thick and inserted into
a flat plastic plate (82 × 38 mm). Because of
muscle and skin movements during WT, FBV could not be recorded during
exercise, but only at rest and during recovery. However, the probe
characteristics ensured a correct position between the transducer and
the skin surface before and after exercise, with a constant angle
between the transducer and the femoral artery, provided that the
subject remained in the reference position during measurements (i.e.,
seated motionless on the ergometer with the trunk and the right leg in
a vertical axis). The angle between the transducer and the probe
surface was 54°. Because the continuous ultrasound method does not
take into account any sample volume, only forward velocity was measured
during recovery to avoid femoral venous artifacts. The intra- and
intersubject variability of this method were tested in our laboratory
during a separate experiment. The coefficients of variation were 11.6%
(intra-) and 127% (inter-) for peak FBV immediately after exercise
(unpublished data). The site of recording was marked on the thigh with
a pencil during the experiments at sea level and served as reference
for the recordings at 4,350 m. Instantaneous FBV was displayed from a
30-Hz sampling frequency and averaged over each cardiac cycle for
analysis. FBV monitoring was stopped at 4.5 min after WT1 so that
subjects could prepare themselves for WT2. FBV analysis started at 10 s
after the end of each WT and stopped at 4.5 and 6.5 min after the end of WT1 and WT2, respectively.
Calculations.
Accumulated O2 deficit during each
20-s exercise was calculated by a method described previously (16). The
incremental O2 max test allowed the determination of a linear relationship between power
and O2 for each subject.
The regression line was calculated from 8 to 10 and from 5 to 8 experimental points, for normoxia and hypoxia, respectively, with
coefficients of correlation always being 
0.99. On this line,
O2 demand during WT corresponded
to the intercept with MPO (i.e., the extrapolated
O2 value above O2 max), and
accumulated O2 demand was defined
as O2 demand times WT duration.
Accumulated O2 uptake was calculated as
integrated O2 over the 20-s
exercise period. Accumulated O2
deficit corresponded to the difference between accumulated
O2 demand 
accumulated O2 uptake.
EPOC established over the first 5 min after each WT
(EPOC5 min) was calculated
as the integrated O2 resting
O2 over this time
period. The same procedure was applied for total expired volume over
the first 5 min of recovery after WT1 and WT2
(VE5 min). O2 deficit,
EPOC5 min and
VE5 min
were calculated from breath-by-breath values. An index of total
peripheral resistance (TPRindex)
was calculated by the ratio between MAP and FBV. Finally, the rate of
FBV decrease over the first 4.5 min of recovery after each bout was
estimated by the half-time decrease
(t1/2 FBV) from
the end-exercise value to that at 4.5 min of recovery.
Statistics.
Data are means ± SD. A two-way analysis of variance with repeated
measures was performed to make comparisons between
1) altitude conditions and across
time for gas exchange, cardiovascular data, and blood samples, and
2) altitude conditions and exercise
bouts for power measurements and calculated data. A Dunnett's test was used for multiple comparisons (9). Linear regressions were performed by
using the least squares method. The two regression lines obtained at
sea level and at 4,350 m were compared by analysis of multiple linear
regression (9). Recovery O2
data were fitted for each subject by using nonlinear least squares
regression to a monoexponential model (8). The
t1/2
decrease was used to indicate the rate of decrease of
O2. Significant differences were accepted at P < 0.05.
RESULTS
O2 max.
O2 max decreased by
29% from 55 ± 6 ml · min1 · kg1
at sea level to 38 ± 7 ml · min1 · kg1
at 4,350 m.
Hematology.
Resting hemoglobin concentration and hematocrit increased
from 13.8 ± 1.6 g/dl and 39.4 ± 3.3% at sea level to 15.6 ± 1.7 g/dl (P < 0.01) and 45.3 ± 3.7% (P < 0.001) at 4,350 m,
respectively.
Mechanical power.
High altitude had no effect on MPO during WT1. A significant decrease
in MPO occurred between WT1 and WT2 (6.9% at sea level and 10.7% at
high altitude; Table 1). High altitude did
not lead to a larger decrease in MPO between WT1 and WT2. The
diminution in PPO between the two WT was significant at
high altitude (P < 0.05) but not at
sea level.
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
O2 peak was
significantly lower at 4,350 m over 0-40 s after WT1 and WT2, with
no difference observed later in recovery (Table
2, Fig.
1A).
O2 remained above
the resting level throughout the 14 min of recovery after WT2 at both
sea level and high altitude. The rate of decrease of
O2 after both tests was
faster in sea level than in high altitude;
t1/2 was 38 ± 8 and 36 ± 6 s at sea level, and 45 ± 7 (P < 0.05) and 45 ± 8 s
(P < 0.05) at high altitude, after
WT1 and WT2, respectively. Resting
E was
higher at high altitude (P < 0.01).
E was
increased at high altitude during the whole recovery interval studied
after each WT (Fig. 1B). In both
conditions, peak
E was
higher after WT2 than after WT1. E
remained above resting level throughout the 14 min of recovery after
WT2 at sea level and high altitude. Hypoxic exercise induced an
additional decrease in SaO2 below
resting level during recovery, between 30 and 60 s after WT1 and
10-150 s after WT2 (Fig. 1C). The decrease in O2 deficit between
WT1 and WT2 (Table 1) was 16% at high altitude
(P < 0.01) and 8% at sea level
(P = 0.05). A slight but not
significant diminution in
EPOC5 min was observed in
hypoxia, and
VE5 min
was higher at 4,350 m than at sea level throughout both recovery
periods (Table 1).
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
O2;
A), minute
ventilation
(E;
B), and
transcutaneous arterial
O2 saturation
(SaO2;
C) at rest, during repeated 20-s
exercise (WT1 and WT2), and during recovery, at sea level (
) and
after 5-6 days at altitude of 4,350 m (
). Symbols are means
(n = 7) from cycle-by-cycle values
averaged over 5-s time intervals. For clarity, error bars and
statistics are not shown (see text for
P values and means).
Cardiovascular variables. Peak FBV after WT1 and WT2 was 54 ± 9 and 58 ± 9 cm/s at sea level, 50 ± 10 and 53 ± 12 cm/s at high altitutde, respectively (Table 3). Peak FBV did not differ between sea level and high altitude. FBV was lower at high altitude than at sea level (P < 0.05) between 1 and 4.5 min after WT1 and between 30 s and 2 min after WT2. The t1/2 FBV was not modified by high altitude. The t1/2 FBV after WT1 and WT2 was 28 ± 12 and 53 ± 20 s at sea level, 30 ± 9 and 64 ± 41 s at high altitude, respectively. Hypoxia did not induce any alteration in MAP throughout recovery; and, finally, TPRindex was not modified at high altitude.
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
3] was lower at high altitude than at sea level at rest and during both recovery periods. Arterial
CO2 and
PO2, as well as
CCO2 and
PCO2 were lower at high altitude than
at sea level.
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
],
[Pyr], and
[La]-to-[Pyr]
ratio (Table 5). Furthermore, high altitude
did not modify [Na+],
[K+], and
[Cl]. Resting
[protein] was higher at 4,350 m and remained above the
sea-level value throughout recovery. Exercise induced a significant increase in [protein] throughout the whole recovery period.
High altitude significantly increased [NE] and tended to
increase [Epi] during recovery from repeated WT (Fig.
2).
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
) and after 5-6 days at the altitude of 4,350 m
(). Values are means ± SE for [NE]
(n = 7) and [Epi]
(n = 6). * Significantly different from sea level, P < 0.05;
significantly different from rest, P < 0.01.
The relationship between total work and hydrogen ion [H+] accumulation was not altered in high altitude (Fig. 3), although the increase in [H+] was greater at 4,350 m (P < 0.001). The same plasma lactate accumulation at sea level and at high altitude was associated with a greater increase in [H+] (P < 0.001) and a greater increase in [NE] (P < 0.01) at 4,350 m (Fig. 4). The slope of linear regression at 4,350 m was different (P < 0.05) from the corresponding slope at sea level for both relationships, i.e., [La
] against
[H+], and
[NE] against
[La].
[H+]), between
rest and recovery from repeated 20-s exercise
(R210 min) in 7 subjects,
at sea level () and after 5-6 days at altitude of 4,350 m
(). Regression equations are: sea level,
y = 0.212x 56.984, r = 0.86, P < 0.05; high altitude,
y = 0.248x 52.911, r = 0.90, P < 0.01.
[La]) and
blood H+ increase ( [H+]) and
(B) plasma norepinephrine increase
([NE]) and
[La] between rest
and recovery from repeated 20-s exercise (R210
min) at sea level () and after 5-6 days at
altitude of 4,350 m (); n = 7 subjects. Regression equations are: sea level,
y = 2.844x 17.619, r = 0.89, P < 0.01 (A); high
altitude, y = 5.661x 35.861, r = 0.91, P < 0.01; and sea level,
y = 0.777x + 9.164, r = 0.79, P < 0.05; high altitude,
y = 0.238x + 9.871, r = 0.87, P < 0.05 (B).
DISCUSSION
The primary finding of this study was that 5-6
days of exposure to 4,350 m did not reduce mechanical performance
during a repeated supramaximal 20-s cycle exercise. We demonstrated
that prolonged exposure to hypoxia did not impair the restoration of muscle power after sprint. During recovery at 4,350 m,
EPOC5 min was not
significantly lowered, despite a large but transient reduction in
O2 peak. Recovery at
4,350 m was also associated with a higher hyperventilation, a larger
drop in pH, and a greater catecholamine response but not with a change
in plasma lactate accumulation. Finally, plasma [protein]
was higher during recovery at high altitude.
O2 during recovery after
sprint.
The slight decrease in EPOC during recovery between both exercise bouts
at high altitude (14%, NS) was entirely due to a large reduction in
O2 at high altitude in the
first minute after exercise. Furthermore, the 30-40% decrease in
O2 peak after
exercise occurred at a time when ventilation was 20% higher at high
altitude. It is tempting to speculate that the difference observed in
O2 peak response
reflects a limitation in peak leg
O2 at 4,350 m. This hypothesis is supported by the finding that maximal leg
O2 is reduced in hypoxia
because of a decrease in leg O2
delivery but no increase in muscle
O2-diffusive capacity (20).
Immediately after sprint, it is likely that peak leg
O2 (and muscle
O2 diffusion) was also near
maximum, so that a reduced leg O2
supply induced a transient limitation in leg
O2. The hypothesis of a lower leg O2 delivery after sprint at
4,350 m was supported by the present data. On one hand, we observed a
marked decrease in arterial SaO2 within
the first minute after sprint and a decrease in arterial O2 content at 4,350 m. On the
other hand, the present Doppler ultrasound measurements, which were in
accordance with others' studies (10, 23), provide some information
with respect to alterations in femoral blood flow. We found no increase
in peak FBV after sprint at high altitude. Nevertheless, the fact that we found no relationship between the kinetics of
O2
(t1/2O2) and FBV (t1/2
FBV) during recovery suggests that the
O2 response after sprint does
not depend only on leg blood flow. Finally, the increase in plasma
[protein] during recovery after sprint at 4,350 m indicates
that sprint-induced hemoconcentration was larger after prolonged
exposure to high altitude. Thus an increased blood viscosity may be
involved in the transient limitation in O2 peak at
4,350 m via a limitation of
O2-diffusion processes at the
muscular level.
The fact that
[La] during
recovery was not altered at high altitude was consistent with the
performance data. The higher exercise-induced acidosis at 4,350 m
related to the same plasma lactate accumulation in both altitude
conditions (Fig. 4A) could be linked
to the decrease in [HCO3],
as has been shown in acclimatized lowlanders (25). The decrease in
buffer capacity at 4,350 m may also explain that the regression line
between performance and acidosis was shifted to a higher level of
H+ accumulation at 4,350 m (Fig.
3). Nevertheless, the changes in acid-base balance observed at high
altitude were not associated with an impairment in muscle power during
repeated sprints. High altitude also induced a larger increase in
catecholamine response during recovery, which may reflect a greater
sympathetic nervous activity. Considering that catecholamines are known
to activate muscle glycogenolysis (5, 13), the same plasma lactate
accumulation in both altitude conditions, related to a higher NE
response at high altitude (Fig. 4B),
may, therefore, reflect a desensitization of muscle 
-adrenoceptors
in response to permanent high adrenergic activity at 4,350 m, as shown
in heart -adrenoceptors with similar altitude conditions (18).
In summary, the repetition of supramaximal exercise after a prolonged
exposure to high altitude was associated with several changes observed
during recovery, such as transient decreases in arterial
SaO2 and
O2, higher acidosis,
hemoconcentration, and catecholamine response, and finally, no change
in blood lactate accumulation. At high altitude, the same blood lactate
accumulation was related to a higher adrenergic activity. However,
these changes were not associated with any significant impairment of
the restoration of muscle power.
ACKNOWLEDGEMENTS
The authors gratefully acknowledge the help of Dr. Nick Mason in preparing the manuscript.
FOOTNOTES
Address for reprint requests: P. Robach, Association pour la Recherche en Physiologie de l'Environnement, UFR de Médecine, 74 rue Marcel Cachin, 93012 Bobigny, France.
Received 8 April 1996; accepted in final form 27 January 1997.
REFERENCES
| 1. | Bahr, R. Excess postexercise oxygen consumptionmagnitude,
mechanisms and practical implications. Acta Physiol.
Scand. 144, Suppl.:
1-70, 1992.
|
| 2. | Balsom, P. D., G. C. Gaitanos, B. Ekblom, and B. Sjödin. Reduced oxygen availability during high intensity intermittent exercise impairs performance. Acta Physiol. Scand. 152: 279-285, 1994 . [Medline] |
| 3. |
Bogdanis, G. C.,
M. E. Nevill,
L. H. Boobis,
and
H. K. A. Lakomy.
Contribution of phosphocreatine and aerobic metabolism to energy supply during repeated sprint exercise.
J. Appl. Physiol.
80:
876-884,
1996
|
| 4. |
Bogdanis, G. C.,
M. E. Nevill,
L. H. Boobis,
H. K. A. Lakomy,
and
A. M. Nevill.
Recovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man.
J. Physiol. (Lond.)
482:
467-480,
1995 .
|
| 5. |
Cheetham, M. E.,
L. H. Bobbis,
S. Brooks,
and
C. Williams.
Human muscle metabolism during sprint running.
J. Appl. Physiol.
61:
54-60,
1986
|
| 6. | Coudert, J. Anaerobic performance at altitude. Int. J. Sports Med. 13, Suppl. 1: S82-S85, 1992. |
| 7. | Gaesser, G. A., and G. A. Brooks. Metabolic bases of excess post-exercise oxygen consumption: a review. Med. Sci. Sports Exercise 16: 29-43, 1984 . [Medline] |
| 8. | Garner, R. P., S. K. Powers, and G. Church. Effects of hypoxia and hyperoxia on ventilatory kinetics during recovery from exercise. Aviat. Space Environ. Med. 57: 1165-1169, 1986 . [Medline] |
| 9. | Glantz, S. A., and B. K. Slinker. Regression with two or more independent variables. In: Primer of Applied Regression and Analysis of Variance. New York: McGraw-Hill, 1990, p. 50-104. |
| 10. | Leyk, D., D. Essfeld, K. Baum, and J. Stegemann. Influence of calf muscle contractions on blood flow parameters measured in the arteria femoralis. Int. J. Sports Med. 13: 588-593, 1992 . [Medline] |
| 11. |
Lindinger, M. I.,
G. J. F. Heigenhauser,
R. S. McKelvie,
and
N. L. Jones.
Blood ion regulation during repeated maximal exercise and recovery in humans.
Am. J. Physiol.
262 (Regulatory Integrative Comp. Physiol. 31):
R126-R136,
1992 .
|
| 12. |
Mazzeo, R. S.,
G. A. Brooks,
G. E. Butterfield,
D. A. Podolin,
E. E. Wolfel,
and
J. T. Reeves.
Acclimatization to high altitude increases muscle sympathetic activity both at rest and during exercise.
Am. J. Physiol.
269 (Regulatory Integrative Comp. Physiol. 38):
R201-R207,
1995 .
|
| 13. |
Mazzeo, R. S.,
and
P. Marshall.
Influence of plasma catecholamines on the lactate threshold during graded exercise.
J. Appl. Physiol.
67:
1319-1322,
1989
|
| 14. |
McCartney, N.,
L. L. Spriet,
G. J. F. Heigenhauser,
J. M. Kowalchuk,
J. R. Sutton,
and
N. L. Jones.
Muscle power and metabolism in maximal intermittent exercise.
J. Appl. Physiol.
60:
1164-1169,
1986
|
| 15. | McLellan, T. M., M. F. Kavanagh, and I. Jacobs. The effect of hypoxia on performance during 30 s or 45 s of supramaximal exercise. Eur. J. Appl. Physiol. Occup. Physiol. 60: 155-161, 1990. [Medline] |
| 16. |
Medbø, J. I.,
A.-C. Mohn,
I. Tabata,
R. Bahr,
O. Vaage,
and
O. M. Sejersted.
Anaerobic capacity determined by maximal accumulated O2 deficit.
J. Appl. Physiol.
64:
50-60,
1988.
|
| 17. |
Porszasz, J.,
T. J. Barstow,
and
K. Wasserman.
Evaluation of a symmetrically disposed Pitot tube flowmeter for measuring gas flow during exercise.
J. Appl. Physiol.
77:
2659-2665,
1994
|
| 18. |
Richalet, J.-P.,
P. Larmignat,
C. Rathat,
A. Kéromès,
P. Baud,
and
F. Lhotse.
Decreased cardiac response to isoproterenol infusion in acute and chronic hypoxia.
J. Appl. Physiol.
65:
1957-1961,
1988
|
| 19. | Richalet, J.-P., M. Marchal, C. Lamberto, J.-L. Le Trong, A.-M. Antezana, and E. Cauchy. Alteration of aerobic and anaerobic performance after 3 wk at 6,542 m (Mt. Sajama) (Abstract). Int. J. Sports Med. 13: 87, 1992. |
| 20. |
Richardson, R. S.,
D. R. Knight,
D. C. Poole,
S. S. Kurdak,
M. C. Hogan,
B. Grassi,
and
P. D. Wagner.
Determinants of maximal exercise O2 during single leg knee-extensor exercise in humans.
Am. J. Physiol.
268 (Heart Circ. Physiol. 37):
H1453-H1461,
1995 .
|
| 21. | Robach, P., P. Bouchet, D. Deberne, M. Letournel, and J.-P. Richalet. Cardiopulmonary kinetics during recovery after repeated supramaximal exercise in hypoxia (Abstract). In: Hypoxia and the Brain, edited by J. R. Sutton, G. Coates, and C. S. Houston. Burlington, VT: Queen City Printers, A97, 1995. |
| 22. | Vandewalle, H., G. Pérès, J. Heller, and H. Monod. All out anaerobic capacity tests on cycle ergometers. Eur. J. Appl. Physiol. Occup. Physiol. 54: 222-229, 1985. [Medline] |
| 23. |
Walløe, L.,
and
J. Wesche.
Time course and magnitude of blood flow changes in the human quadriceps muscles during and following rhythmic exercise.
J. Physiol. (Lond.)
405:
257-273,
1988.
|
| 24. | Ward, M. P., J. S. Milledge, and J. B. West. Haematological changes and plasma volume. In: High Altitude Medicine and Physiology (2nd ed.). London: Chapman & Hall Medical, 1995, p. 217-239. |
| 25. | West, J. B. Lactate during exercise at extreme altitude. Federation Proc. 45: 2953-2957, 1986 . [Medline] |
| 26. |
Wolfel, E. E.,
B. M. Groves,
G. A. Brooks,
G. E. Butterfield,
R. Mazzeo,
L. G. Moore,
J. R. Sutton,
P. R. Bender,
T. E. Dahms,
R. E. Mc Cullough,
R. G. McCullough,
S.-Y. Huang,
S.-F. Sun,
R. F. Grover,
H. N. Hultgren,
and
J. T. Reeves.
Oxygen transport during steady-state submaximal exercise in chronic hypoxia.
J. Appl. Physiol.
70:
1129-1136,
1991
|
This article has been cited by other articles:
|
|
 |
|
  P. Robach, M. Dechaux, S. Jarrot, J. Vaysse, J.-C. Schneider, N. P. Mason, J.-P. Herry, B. Gardette, and J.-P. Richalet Operation Everest III: role of plasma volume expansion on VO2max during prolonged high-altitude exposure J Appl Physiol, July 1, 2000; 89(1): 29 - 37. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
ABSTRACT
