| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Department of Kinesiology, University of Waterloo, Waterloo, Ontario N2L 3G1; 2 Ottawa Heart Institute, University of Ottawa, Ottawa, Ontario K1Y 4E9; 3 Division of Sports Medicine, University of British Columbia, British Columbia, Canada V6T 1Z3; and 4 Department of Anesthesiology, University of Washington, Seattle, Washington 98124
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
To investigate the hypothesis that respiratory
gas exchange and, in particular, the O2 consumption
(
O2) response to exercise is altered
after a 21-day expedition to 6,194 m, five male climbers (age 28.2 ± 2 yr; weight 76.9 ± 4.3 kg; means ± SE) performed a
progressive and prolonged two-step cycle test both before and 3-4
days after return to sea level. During both exercise tests, a
depression (P < 0.05) in
O2 (l/min) and an increase
(P < 0.05) in minute ventilation (E
BTPS; l/min) and respiratory exchange ratio were observed after
the expedition. These changes occurred in the absence of changes in
CO2 production (l/min). During steady-state submaximal
exercise, net efficiency, calculated from the rates of the mechanical
power output to the energy expended (O2)
above that measured at rest, increased (P < 0.05) from
25.9 ± 1.6 to 31.3 ± 1.3% at the lighter power output and
from 24.4 ± 1.3 to 29.5 ± 1.5% at the heavy power output.
These changes were accompanied by a 4.5% reduction (P < 0.05) in peak O2 (3.99 ± 0.17 vs. 3.81 ± 0.18 l/min). After the expedition, an increase
(P < 0.05) in hemoglobin concentration (15.0 ± 0.49 vs. 15.8 ± 0.41 g/100 ml) was found. It is concluded that,
because resting O2 was unchanged, net
efficiency is enhanced during submaximal exercise after a mountaineering expedition when the exercise is performed soon after
return to sea level conditions.
exercise; aerobic; O2 consumption; hypoxia
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
AMONG THE MANY CHANGES
PROPOSED to occur with altitude acclimatization is a change in
net mechanical efficiency (16). According to this
hypothesis, at a given level of submaximal exercise, the net energy
cost, as measured by O2 consumption
(O2), is reduced, and, consequently,
mechanical efficiency is enhanced (16). Although this
hypothesis is appealing, because the adaptation could potentially allow
more work to be performed with the limited O2 available, the evidence is not impressive.
One experimental model that has been commonly utilized to investigate
the effects of altitude acclimatization involves initial sea level
testing of lowlanders, followed by additional testing soon after
arrival at altitude or during acute exposure to simulated altitude, and
after a period of residence either at altitude or in hypobaric hypoxic
conditions (17, 39). In general, studies examining the
response of lowlanders to both acute and chronic hypoxia have reported
either no effect (2, 39) or an increase (31)
in whole body steady-state O2 during
constant-load exercise. When an increase in whole body
O2 has been found, increases in resting
O2 appear responsible (31).
One factor that could mitigate against reductions in whole body
O2 is the additional energy costs
associated with ventilation (4). The increase in minute
ventilation (E) that occurs with acute hypoxia
(4), and which may be potentiated with sustained exposure
(4), could mask changes in efficiency in the working leg
muscles. This possibility has been examined by measuring
O2 across the working leg muscles in
conjunction with measures of whole body
O2. Using this approach, Wolfel et al.
(39) have found evidence of a lower leg
O2 with unchanged total body
O2 as a result of a lower leg blood flow
and a lower arteriovenous O2 difference during both acute
and chronic hypoxic conditions. These results have not been confirmed
by others (2, 31).
Another approach that has been used to examine the effects of
acclimatization is to measure the exercise response under normoxic conditions. Under this strategy, the energy costs associated with ventilation are considerably reduced and the more persistent effects of
chronic hypoxia on increased red cell volume and arterial
O2-carrying capacity can be examined (35).
Surprisingly, this model has rarely been employed. Of the few
studies available, exercise in normoxia after acclimatization, although
reducing the ventilatory response (2), has not resulted in
either lower total body O2 or
O2 in the working legs (2,
3).
This issue of mechanical efficiency has also been examined in
high-altitude residents during a brief sojourn to near-sea level conditions (16). On the basis of comparisons with sea
level residents, both trained and untrained, it was found that the
O2 measured during progressive exercise
at sea level was lower in the highlanders (16). The
difference in O2 costs could be explained by a lower resting metabolic rate.
In this study, we report on the effects of a 21-day expedition to an
altitude of 6,194 m (Mount Denali). By having the mountaineers report
to the laboratory a few days before and within 3 days after the
expedition, we were able to avoid many of the problems associated with
deacclimatization that have characterized other studies
(27). Under such conditions, we hypothesized that
steady-state submaximal exercise performed at the same absolute power
both before and after the expedition will result in lower
O2 costs that cannot be explained by changes in
resting O2. As a consequence, net efficiency is increased with acclimatization.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Subjects
The data are from five men who participated in an expedition to Mount Denali. On average, the age (means ± SE) was 28 ± 2 yr, weight was 76.9 ± 4.3 kg, and height was 173.6 ± 3.6 cm. An additional member of the expedition, a woman, was not included because we did not have a complete data set. All male climbers were regularly active, including during the months immediately preceding the expedition, and all had a history of mountain climbing. The testing protocols were approved by the Office of Human Research and Animal Care (University of Waterloo, Waterloo, Ontario, Canada), and written consent was obtained from each participant as required. The expedition itself was self-initiated without involvement of the University of Waterloo or any of the scientists involved.Experimental Design
To examine the effects of the expedition to Mount Denali, testing was conducted at the University of Waterloo (altitude = 317 m). Approximately 1 wk before the beginning of the climb, the mountaineers were transported to the laboratory, where a series of tests (Pre) was conducted over a 3-day period. On day 1, the participants performed a progressive cycle test to fatigue for measurement of peakO2
(O2 peak) and related parameters. Also
on day 1, a short submaximal kicking test was performed for measurement of O2 and blood flow. This
test preceded the progressive cycle test. Approximately 2-3 h were
allowed between tests. On day 2, a two-step prolonged cycle
test was performed to measure gas exchange and selected blood
properties. The results of the progressive and prolonged tests are
reported in this paper. Three days after the expedition (Post), the
climbers were transported back to the laboratory to perform the same
series of tests in the same order.
The expedition to Mount Denali extended over a 21-day period. The mountaineers flew to Talkeetna, Alaska (300 m), and established a base camp (2,160 m) on day 1. Ascent to the summit (6,194 m) was achieved on day 18. By day 8, the climbers achieved an altitude of ~50% of the summit, and, by day 14, 75% of the objective was realized. By day 20, the volunteers had arrived at the initial base camp and returned to Talkeetna. Three days later, the group arrived at the University of Waterloo for posttesting.
Testing Protocols
Progressive exercise.
Approximately 60 min before the progressive test, the participants
reported to the laboratory. During this period, weights and heights
were recorded, and preparations were made for blood sampling and the
monitoring of respiratory gas exchange and heart rate. For blood
sampling, a small Teflon catheter with a three-way stopcock was placed
in a dorsal vein of a prewarmed hand and kept warm throughout the
exercise with a heating pad. Heart rate was determined by standard
electrocardiograph techniques. Gas exchange [O2, CO2 production
(CO2), and E] was
measured by use of an open-circuit system as previously described
(18). An electrically braked cycle ergometer (Quinton
870), calibrated on each testing day using standardized weights, was
used for all exercise tests. In addition, the gas analyzers (Beckman
OM-11 and LB-2) and the pneumotachograph (Hewlett Packard 4730 A) were
calibrated on each testing day (both before and after the expedition).
Common reference gases, with the gas percentages precisely determined,
were used for the calibration. The pneumotachograph was calibrated by
using a 3-liter syringe, emptied to produce a flow rate similar to that found in exercise.
Prolonged exercise.
The prolonged cycle exercise protocol consisted of 40 min of exercise
performed for 20 min at each of two power outputs, designed to elicit
~60% and 75% of prealtitude
O2 peak. As with the progressive test,
subjects were instrumented for respiratory, heart rate, and blood
sampling. These measurements were performed at rest before the exercise
and, in the case of the heart rate and respiratory gas exchange
measurements, during the final 4- to 5-min segment of each power
output. Resting measurements for all variables were obtained after the
subjects had been sitting quietly on the cycle for an ~15-min period.
Blood samples were collected over a 30-s period before 3, 20, and 40 min of exercise. All procedures, including calibration and data
collection, were essentially as reported for the progressive test. For
the submaximal tests, all subjects consumed a liquid supplement
consisting of one can of Ensure (1.045 kJ: 14.8% protein, 31.5% fat,
and 53.7% carbohydrate; Ross Laboratories, Montreal, PQ, Canada) ~4
h before the beginning of exercise. No other supplements, including
coffee, were permitted on the day of the test.
O2, used as a measure of
energy expended, was converted to joules per milliliter (20.93 J/ml), assuming a respiratory exchange ratio (RER) of 1.0. It was not possible
to calculate an energetic equivalent based on the actual ratio because
this value was >1, particularly during the Post tests.
Analytical techniques.
Whole blood was extracted and used for the measurement of lactate,
hematocrit (Hct), and Hb. For lactate, the blood was deproteinized by
using ice-cold perchloric acid, centrifuged to remove the pelleted proteins, and neutralized with ice-cold KHCO3. Samples were
stored at 
80°C until analyzed by fluorometric techniques
(21). Hct was measured in triplicate using standard
techniques (38) and corrected for trapped plasma (0.96)
and venous-to-whole body Hct difference (0.91). Hb was also measured in
triplicate using standard cyanomethemoglobin methods. Changes in plasma
volume (PV) before and after the expedition were determined using both
Hct and Hb (38) obtained during rest before the prolonged
exercise test. Changes in PV during the exercise were calculated using
only the Hct values (37). Protein was measured on the
serum by standard techniques.
80°C. During a given analytical session, all samples
for a given subject and for a given property were performed in
duplicate during the same analytical session.
Measurements of arterial O2 saturation
(SaO2) were made from the fingertip using oximetry
(Ohmeda model 3700). Fingertips were carefully cleaned with alcohol
before the probe was attached. The validity of the oximeter was
previously established (29). Moreover, we have also found
a close relationship between SaO2 obtained from
arterial blood obtained from the radial artery and the oximeter during
exercise (unpublished observations).
Statistical Procedures
The effect of the altitude expedition was determined by both one-way and two-way ANOVA procedures for repeated measures. One-way ANOVA was employed with a single measurement (i.e.,O2 peak, peak E, and
so forth) obtained before and after the expedition. Two-way ANOVA
procedures were used when several measurements were made during
exercise (i.e., O2,
CO2, lactate, and so forth), both
before and after acclimatization. When significance was found, Newman-Keuls procedures were applied to locate differences between specific means. Significance was set at the 0.05 level.
| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Resting Blood Measurements
After the expedition to Mount Denali, both resting Hct and Hb concentration were elevated (Table 1). PV, calculated using both Hct and Hb changes, decreased by ~10% after acclimatization. Acclimatization also resulted in an ~6.2% decrease in total protein. At rest, arterial Hb saturation with O2 was estimated at 96% both before and after the expedition.
|
Progressive Exercise
After the expedition, a small but significant decline was observed inO2 peak obtained during progressive
exercise to fatigue (Table 2). The
decline was observed only when O2 peak was expressed in absolute (l/min), and not relative
(ml · kg
1 · min1), terms.
Body mass, measured before (76.9 ± 3.7 kg) and after the
expedition (75.5 ± 2.9 kg), was unchanged.
Acclimatization did not result in a lower peak
CO2. The peak values for the other
variables examined, namely heart rate, E, RER, and
power output, were all unchanged with acclimatization. Also unchanged with acclimatization were the peak concentrations of blood lactate (7.21 ± 0.35 vs. 5.65 ± 0.70 mM) and the blood
catecholamines epinephrine (246 ± 53 vs. 216 ± 56 pg/ml)
and norepinephrine (1,796 ± 210 vs. 1,674 ± 266 pg/ml).
|
O2, measured during the final 20 s
of each step increase in power output, was lower after the expedition
(Fig. 1A). The lower value was
not specific to any time point but rather represented a general effect.
Unlike O2,
CO2 was not changed before and after
acclimatization (Fig. 1B). In contrast to
O2, E was higher
during exercise after acclimatization (Fig. 1C). For all variables, a general progressive increase was shown with each increment
in power output. Blood lactate concentration was also found to be
altered with acclimatization (Fig.
2A). At rest and during
initial 25- W load pedaling, lactate concentration was higher
postacclimatization than preacclimatization. At the higher exercise
intensities, lactates were lower after acclimatization than before.
With progressive exercise, a lower percent SaO2 was observed (Fig. 2B). In general, SaO2
remained higher during exercise after the altitude expedition than
before; however, the difference was not significant. No effect of the
expedition was observed on heart rate, regardless of the exercise
intensity (Fig. 2C).
|
|
Changes in the catecholamines, norepinephrine and epinephrine, were
found for both exercise and acclimatization. With exercise, both
norepinephrine and epinephrine increased with increases in power output
(Fig. 3, A and B).
However, these hormones reacted differently to acclimatization. For
norepinephrine, a generally higher value was found that was not
specific to any time point. In contrast, the concentration of
epinephrine was unchanged after acclimatization.
|
Submaximal Exercise
As expected, the two-stage prolonged exercise test resulted in increases inO2,
CO2, and E (Table
3). After acclimatization, O2 was depressed by 9.7% at 20 min and
by 7.7% at 40 min of exercise. A similar effect was not found for
CO2. Both E and RER
were higher at postacclimatization compared with preacclimatization. In
the case of RER, higher values were observed at rest and at 20 and 40 min of exercise. For E, the higher values observed were not specific to any time point. Exercise heart rates were reduced
at both 20 and 40 min with acclimatization (Fig.
4A). In contrast, resting
heart rates were higher after the expedition than before. Blood lactate
concentration, although increased with exercise, was not affected by
the expedition (Fig. 4B).
|
|
Net mechanical efficiency, calculated during steady state for both exercise intensities, was 25.9 ± 1.6% and 24.4 ± 1.3% during the first and second step, respectively, before the expedition. After the expedition, the respective values were 31.3 ± 1.3% and 29.5 ± 1.5%. Acclimatization resulted in an increase in net efficiency.
Of the plasma catecholamines norepinephrine and epinephrine, only
norepinephrine was blunted after acclimatization (Fig.
5, A and B). The
lower norepinephrine was observed only during exercise and not at rest.
As with norepinephrine, epinephrine increased with exercise. Although
lower epinephrine values were observed after the expedition, the
differences were not significant.
|
Declines in arterial oxyhemoglobin saturation were initially observed
at 20 min of exercise and persisted at 40 min of exercise (Fig.
6A). The decline in saturation
was not affected by the state of acclimatization.
|
As expected, reductions in PV occurred with exercise (Fig. 6B). Before acclimatization, the decline was progressive, averaging 4.0% at 20 min and 6% at 40 min. The magnitude of the PV reduction was not altered with acclimatization.
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
As hypothesized, we found a lower
O2, measured during identical
progressive and prolonged work protocols after the expedition compared
with before the expedition. Because resting
O2 was unchanged (before submaximal
exercise), increases in net efficiency are indicated with
acclimatization. For the submaximal test, net efficiency was found to
increase ~21% regardless of power output. This study appears to be
the first report of changes in mechanical efficiency in lowlanders
after an altitude expedition or after acclimatization when the exercise
is performed under sea level conditions. A higher mechanical efficiency
has been suggested in highland residents during submaximal exercise at
sea level compared with conditioned lowland residents
(16); however, the differences do not appear to be due to
differences in 
efficiency, as obtained from the slope of the
O2-work rate relationship (9).
It should be emphasized that there is little chance that measurement
error could explain the lower O2 that we
observed after acclimatization. In an accompanying paper that addresses
muscle blood flow and O2 kinetics
(22), a similar result was found. This observation was
made while using a different gas-exchange system that was independently
calibrated, a different ergometer, and a different test protocol.
Because we measured whole body O2, it
was not possible to determine whether the lower
O2 was mediated by changes in
the locomotor muscles used in cycling or in the nonlocomotor components such as the muscles of ventilation. However, in this study, the lower
O2 did not appear to be due to a
decreased cost of ventilation because E was
generally higher, during both progressive and prolonged exercise, after
acclimatization. It would appear probable, given the magnitude of the
difference between O2 measured before and after acclimatization and the fact that the muscles involved in
cycling account for most of the total body
O2 (11, 28), that the
decrease in O2 is explained, in large
part, by a reduced O2 utilization in the
working locomotor muscles. Teleologically, the lower
O2 could be explained by a shift toward
a greater glycolytic involvement in ATP regeneration, a shift toward a
greater carbohydrate preference over fats in oxidative phosphorylation, and/or an increased ability of the excitation and contraction processes
to perform work at lower energy costs.
An acclimatization-dependent increase in anaerobic glycolysis during submaximal exercise does not appear probable given the studies that provide evidence that just the opposite occurs, namely, a reduction in anaerobic-based metabolism. During exercise after acclimatization, reductions in lactate production (5), lactate exchange across the working limbs (3), and lower blood (10) and muscle (13) lactates have been reported.
In general, adaptations to chronic hypoxia in hypoxia-intolerant
mammals appear to favor increased exploitation of available O2 (14, 15). The second possibility, namely,
increasing carbohydrate dependency during acclimatization, could lower
O2 costs because complete oxidation of
glycogen yields more ATP per mole of O2 than the complete
oxidation of fats (16). Studies using stable isotopes have
reported increases in glucose oxidation during exercise while subjects
were resident at altitude (6, 32), in conjunction with
decreases in fat oxidation (31). However, it is not clear what effect the increased glucose utilization has on
O2 during exercise. Studies reporting
increases in glucose utilization have not found decreases in
O2 with acclimatization (6,
32). Moreover, because a reduction in the muscle glycogen
depletion rate also appears to be part of the acclimatization process
(13, 40), it is possible that some of the glucose is being
diverted to glyconeogenesis. Alternatively, it is possible that the
glycogen-sparing effect with acclimatization is due to reductions in
anaerobic glycolysis (5, 13).
Regardless of the effect of the acclimatization-induced shift toward increased glucose utilization, a shift in substrate cannot explain the effect of the expedition on the increases in net efficiency reported in this paper. It should be emphasized that, although our calculations of the energetic equivalent were based on a standardized ratio of 1.0, the actual ratio obtained (i.e., 0.95 Pre vs. 1.0 Post) would not alter our conclusions regarding the increase in net efficiency after the altitude expedition.
It would appear that the increase in net efficiency occurs as a consequence of the reduced energy needs of one or more of the processes involved in excitation and contraction. The major energy-consuming processes in the contracting muscle are associated with Na+/K+ exchange across the sarcolemma and T tubule, Ca2+ pumping into the sarcoplasmic reticulum (SR), and actomyosin cycling (19). The ATP requirements of these processes are supplied by three ATPases, namely the Na+-K+-ATPase, the SR Ca2+-ATPase, and the myosin ATPase. It is possible that, given the requirements of the exercise tasks, decreased cation or actomyosin cycling could occur without compromise to excitation and contraction events. Alternatively, increased efficiency could result in increases in the coupling between the number of cations pumped per ATP utilized, as in the case of Ca2+ cycling (23). Increased efficiency may also result from the metabolic adaptations that occur with acclimatization. The decrease in metabolic by-product accumulation, such as ADP, Pi, and H+, that occurs after acclimatization would be expected to increase the amount of free energy released from ATP hydrolysis (26) and, consequently, depress the need to maintain hydrolysis rates at preacclimatization levels. Although the significance remains to be established, it is of interest that the altitude expedition induced a downregulation in muscle Na+-K+-ATPase content (12) and supposedly in maximal Na+-K+-ATPase activity (7). On the basis of Michaelis-Menton enzyme kinetics, a lower maximal Na+-K+-ATPase activity should reduce reaction rates at a given substrate concentration (26). At present, it is unclear how acclimatization affected the SR Ca2+- ATPase and the myosin ATPase. It is of interest that Hochachka et al. (16) have reported a higher mechanical efficiency in long-term high-altitude residents (4,200 m) compared with trained lowlanders when measured under sea level conditions, an adaptation that they also attribute to increased efficiency of one or more of the processes involved in excitation and contraction.
It has been shown that the type I (slow twitch), in contrast to the type II (fast twitch), muscle fiber is considerably more efficient in performing isometric tasks or tasks requiring relatively lower velocities (8). Acclimatization-induced transformation of fiber types could conceivably underlie changes in mechanical efficiency. However, in this study, the fiber types and subtypes were unaltered by the expedition (12). Interestingly, the mountaineers contained an abnormally high percentage of type I fibers in the vastus lateralis before the expedition. This observation was made previously in experienced mountaineers (27).
Acclimatization also resulted in a reduction in exercise heart rate
during each step of the two-stage exercise protocol, even though
resting heart rate was elevated. The reduction in heart rate could be
explained, at least in part, by the lower exercise O2 and, consequently, the reduced
cardiovascular demand in conjunction with the lower leg blood flow that
probably resulted (2). Unlike the effects of
acclimatization measured during exercise in hypoxia (3),
in our findings, SaO2 was not elevated during exercise in normoxia after the expedition to Mount Denali. Exercise, both before
and after the expedition, did result in a significant reduction in
SaO2. As in a previous study (34), we
have shown that, within 1 wk of deacclimatization, Hb concentration
remains significantly elevated. Because resting SaO2
was not affected by altitude residence, arterial O2 content
would be elevated (2, 39). Given that preservation of
arterial O2 delivery to working muscle appears to be a high
priority, the increases in arterial O2 content should have
implications to cardiac function and muscle blood flow (2, 39).
In addition to the lower exercise O2,
acclimatization also altered several variables measured during the
two-step submaximal exercise test employed in this study. As an
example, a higher exercise E and RER were observed
after acclimatization, both of which can be explained by the higher
resting values. Higher E values have also been
reported at rest during acclimatization to 4,300 m (4).
However, higher resting E values were not observed
at sea level after a 10-day deacclimatization period (34).
The increase in E that we observed could result from increased chemoreceptor sensitivity (20, 30, 36), which still persists for a few days after acclimatization but is lost as the
deacclimatization period is extended. Interestingly, the higher
exercise RER values that we observed after acclimatization are not due
to increases in CO2, because
CO2 remained unaltered, but to the
reduction in O2.
The adaptations that were observed during the progressive exercise are
generally similar to those reported for the two-stage submaximal
protocol. As an example, O2 was lower,
E was higher, and CO2
was unchanged with acclimatization, regardless of the test protocol
employed. However, in the progressive test, blood lactates were clearly
depressed with acclimatization but only at the higher power outputs. At
the lower power outputs, blood lactates were higher after
acclimatization. The results that we have observed at the higher
intensities are consistent with what was reported by Grassi et al.
(10) after a 1-wk deacclimatization from an expedition to
5,050 m. A curious difference was observed between the two exercise
protocols regarding the effects of acclimatization on the heart rate
response. During the prolonged exercise protocol, heart rate was
depressed after the expedition. Such effects were not observed during
the progressive exercise. These differences might be explained as a
result of differences in the blood catecholamine response to exercise
and acclimatization. During the progressive exercise, blood
norepinephrine was elevated, an adaptation that could be explained by
the progressive increase in resting blood norepinephrine that occurs
with acclimatization (1, 24, 25). During the prolonged
exercise session, blood norepinephrine was blunted during exercise.
Differences in the effects of acclimatization also occurred between
tests for blood epinephrine concentration. Whereas acclimatization
resulted in a lower blood epinephrine response during progressive
exercise, no significant changes were observed during the submaximal
exercise protocol. After acute exposure, chronic altitude residence
results in a lower blood epinephrine response during prolonged exercise
(25). The most probable reason for the differences in the
acclimatization response between the two exercise protocols,
notwithstanding the different challenges imposed, is the period of
deacclimatization. The progressive test was conducted some 2 days
earlier than the prolonged submaximal test. Given the role of the
sympathoadrenal system in regulating a wide range of physiological
responses, including cardiovascular and metabolic, the differences that
we observed on the acclimatization effects between the two tests may be
related to the period of deacclimatization.
In summary, we found that, when tested under sea level conditions, a chronic acclimatization to altitude results in a range of adaptations, the most conspicuous being an increase in net efficiency. Although it is appealing to credit the effects observed to chronic hypoxia, other influences may be important. Acclimatization, as experienced by a mountaineering expedition, results in exposure to a variety of other stressors, including cold, food and water restriction, and exhaustive work. The independent and interactive effects of each of these variables remain uncertain.
| |
ACKNOWLEDGEMENTS |
|---|
The financial support by the Natural Sciences and Engineering Research Council (NSERC) and the Ottawa Heart Institute is gratefully acknowledged.
| |
FOOTNOTES |
|---|
Address for reprint requests and other correspondence: H. J. Green, Dept. of Kinesiology, Univ. of Waterloo, Waterloo, ON, Canada N2L 3G1 (E-mail: green{at}healthy.uwaterloo.ca).
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 27 August 1999; accepted in final form 28 April 2000.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Antezana, AM,
Kacini R,
Le Trong JL,
Marchal M,
Abousahl L,
Dubray C,
and
Richalet JP.
Adrenergic status of humans during prolonged exposure to altitude of 6,542 m.
J Appl Physiol
76:
1055-1059,
1994
2.
Bender, PR,
Groves BM,
McCullough RE,
McCullough RG,
Huang SY,
Hamilton AJ,
Wagner PD,
Cymerman A,
and
Reeves JT.
Oxygen transport to exercising leg in chronic hypoxia.
J Appl Physiol
65:
2592-2597,
1988
3.
Bender, PR,
Groves BM,
McCullough RE,
McCullough RG,
Trad L,
Young AJ,
Cymerman A,
and
Reeves JT.
Decreased exercise muscle lactate release after high altitude acclimatization.
J Appl Physiol
67:
1456-1462,
1989
4.
Bender, PR,
McCullough RE,
McCullough RS,
Huang SY,
Wagner PD,
Cymerman A,
Hamilton AJ,
and
Reeves JT.
Increased exercise SaO2 independent of ventilatory acclimatization at 4,300 m.
J Appl Physiol
66:
2733-2738,
1989
5.
Brooks, GA,
Butterfield GE,
Wolfe RR,
Groves BM,
Mazzeo RS,
Sutton JR,
Wolfel EE,
and
Reeves JT.
Decreased reliance on lactate during exercise after acclimatization to 4,300 m.
J Appl Physiol
71:
333-341,
1991
6.
Brooks, GA,
Butterfield GE,
Wolfe RR,
Groves BM,
Mazzeo RS,
Sutton JR,
Wolfel EE,
and
Reeves JT.
Increased dependence on blood glucose after acclimatization to 4,300 m.
J Appl Physiol
70:
919-927,
1991
7.
Clausen, T,
and
Nielsen OB.
The Na+-K+ pump and muscle contractility.
Acta Physiol Scand
152:
365-373,
1996.
8.
Crow, MT,
and
Kushmerick MJ.
Chemical energetics of slow- and fast-twitch muscles of the mouse.
J Gen Physiol
79:
147-166,
1982
9.
Gaesser, GA,
and
Brooks GA.
Muscular efficiency during steady-state exercise: effects of speed and work rate.
J Appl Physiol
38:
1132-1139,
1975
10.
Grassi, B,
Marzorati M,
Bordini M,
Colombini A,
Conti M,
Marconi C,
and
Cerretelli P.
Peak blood lactate and blood lactate vs. workload during acclimatization to 5,050 m and deacclimatization.
J Appl Physiol
80:
685-692,
1996
11.
Grassi, B,
Poole DC,
Richardson RS,
Knight DR,
Erickson BK,
and
Wagner PD.
Muscle O2 uptake kinetics in humans: implications for metabolic control.
J Appl Physiol
80:
988-998,
1996
12.
Green, HJ,
Roy B,
Grant S,
Burnett M,
Tupling R,
Otto C,
Pipe A,
and
McKenzie D.
Downregulation in muscle Na+-K+-ATPase following a 21-day expedition to 6,194 m.
J Appl Physiol
88:
634-640,
2000
13.
Green, HJ,
Sutton JR,
Wolfel EE,
Reeves JT,
Butterfield GE,
and
Brooks GA.
Altitude acclimatization and energy metabolic adaptations in skeletal muscle during submaximal exercise.
J Appl Physiol
73:
2701-2708,
1992
14.
Hochachka, PW.
Mechanism and evolution of hypoxia-tolerance in humans.
J Exp Biol
201:
1243-1254,
1998[Abstract].
15.
Hochachka, PW,
Gunga HC,
and
Kirsch K.
Our ancestral physiologic phenotype: an adaptation for hypoxia tolerance and for endurance performance?
Proc Natl Acad Sci USA
95:
1915-1920,
1998
16.
Hochachka, PW,
Stanley C,
Mathewson GO,
McKenzie DC,
Allen PS,
and
Parkhouse WS.
Metabolic and work efficiencies during exercise in Andean natives.
J Appl Physiol
70:
1720-1730,
1991
17.
Houston, CS,
Sutton JR,
Cymerman A,
and
Reeves JT.
Operation Everest II: man at extreme altitude.
J Appl Physiol
63:
877-882,
1987
18.
Hughson, RL,
Kowalchuk JM,
Prime WM,
and
Green HJ.
Open-circuit gas exchange analysis in the non-steady state.
Can J Appl Sport Sci
5:
15-18,
1980[Medline].
19.
Kushmerick, MJ.
Energetics of muscle contraction.
In: Handbook of Physiology: Skeletal Muscle. Bethesda, MD: Am. Physiol. Soc, 1983, sect. 10, chapt. 7, p. 189-236.
20.
Levine, BD,
Friedman DB,
Engfred K,
Hanel B,
Kjaer M,
Clifford PS,
and
Secher NH.
The effect of normoxic or hypobaric hypoxic endurance training on the hypoxic ventilatory response.
Med Sci Sports Exerc
24:
769-775,
1992[ISI][Medline].
21.
Lowry, OH,
and
Passonneau JV.
A Flexible System of Enzymatic Analysis. New York: Academic Press, 1972, p. 146-218.
22.
MacDonald MJ, Green H-J, Naylor HL, Otto C, and Hughson RL.
Reduced oxygen uptake during steady state exercise after a 21 day
mountain climbing expedition to 6,194 m. Can J Appl Physiol
In press.
23.
MacLennan, DH.
Molecular tools to elucidate problems in excitation-contraction coupling.
Biophys J
58:
1355-1365,
1990
24.
Mazzeo, RS,
Bender PR,
Brooks GA,
Butterfield GE,
Groves BM,
Sutton JR,
Wolfel EE,
and
Reeves JT.
Arterial catecholamine response with acute and chronic high-altitude exposure.
Am J Physiol Endocrinol Metab
261:
E419-E424,
1991
25.
Mazzeo, RS,
Wolfel EE,
Butterfield GE,
and
Reeves JT.
Sympathetic response during 21 days at high altitude (4,300 m) as determined by urinary and arterial catecholamines.
Metabolism
43:
1226-1232,
1994[ISI][Medline].
26.
Newsholme, EA,
and
Leech AR.
Biochemistry for the Medical Sciences. New York: Wiley, 1983, p. 357-379.
27.
Oelz, O,
Howald H,
Di Prampero P,
Hoppeler H,
Claassen H,
Jenni R,
Bühlmann A,
Ferretti G,
Brückner J,
Veicsteinas A,
Gussoni M,
and
Cerretelli P.
Physiological profile of world-class high-altitude climbers.
J Appl Physiol
60:
1734-1742,
1986
28.
Poole, DC,
Gaesser GA,
Hogan MC,
Knight DR,
and
Wagner PD.
Pulmonary and leg O2 during submaximal exercise: implications for muscular efficiency.
J Appl Physiol
72:
805-810,
1992
29.
Powers, SK,
Dodd S,
Freeman J,
Ayers GD,
Samson H,
and
McKnight T.
Accuracy of pulse oximetry to estimate HbO2 fraction of total Hb during exercise.
J Appl Physiol
67:
300-304,
1989
30.
Reeves, JT,
McCullough RE,
Moore LG,
Cymerman A,
and
Weil JV.
Sea-level PCO2 relates to ventilatory acclimatization at 4,300 m.
J Appl Physiol
75:
1117-1122,
1993
31.
Roberts, AC,
Butterfield GE,
Cymerman A,
Reeves JT,
Wolfel EE,
and
Brooks GA.
Acclimatization to 4,300 m altitude decreases reliance of fat as a substrate.
J Appl Physiol
81:
1762-1771,
1996
32.
Roberts, AC,
Reeves JT,
Butterfield GE,
Mazzeo RS,
Sutton JR,
Wolfel EE,
and
Brooks GA.
Altitude and 
-blockade augment glucose utilization during submaximal exercise.
J Appl Physiol
80:
605-615,
1996
34.
Savourey, C,
Garcia N,
Besnard Y,
Guinet A,
Hanniguet AM,
and
Bittel J.
Pre-adaptation, adaptation, and de-adaptation to high altitude in humans: cardio-ventilatory and haematological changes.
Eur J Appl Physiol
73:
529-535,
1996[ISI].
35.
Savourey, C,
Garcia N,
Caravel JP,
Gharib C,
Pouzeratte N,
Martin S,
and
Bittel J.
Pre-adaptation, adaptation and de-adaptation to high altitude in humans: hormonal and biochemical changes at sea level.
Eur J Appl Physiol Occup Physiol
77:
37-43,
1998[ISI][Medline].
36.
Schoene, RS,
Roach RC,
Hackett PH,
Sutton JR,
Cymerman A,
and
Houston CS.
Operation Everest II: ventilatory adaptation during gradual decompression to extreme altitude.
Med Sci Sports Exerc
22:
804-810,
1990[ISI][Medline].
37.
Van Beaumont, W.
Evaluation of hemoconcentration from hematocrit measurements.
J Appl Physiol
31:
712-713,
1972.
38.
Van Beaumont, W,
Greenleaf JE,
and
Juhos L.
Disproportional changes in hematocrit, plasma volume, and proteins during exercise and bed rest.
J Appl Physiol
33:
55-61,
1972
39.
Wolfel, EE,
Groves BM,
Brooks GA,
Butterfield GE,
Mazzeo RS,
Moore LG,
Sutton JR,
Bender PR,
Dahms TE,
McCullough RE,
Huang SY,
Sun SF,
Grover RF,
Hultgren HN,
and
Reeves JT.
Oxygen transport during steady state, submaximal exercise in chronic hypoxia.
J Appl Physiol
70:
1129-1136,
1991
40.
Young, AJ,
Evans WJ,
Cymerman A,
Pandolf KB,
Knapik JJ,
and
Maher JJ.
Sparing effect of chronic high-altitude exposure on muscle glycogen utilization during exercise.
J Appl Physiol
52:
857-862,
1982
This article has been cited by other articles:
|
|
 |
|
  M. J. Truijens, F. A. Rodriguez, N. E. Townsend, J. Stray-Gundersen, C. J. Gore, and B. D. Levine The effect of intermittent hypobaric hypoxic exposure and sea level training on submaximal economy in well-trained swimmers and runners J Appl Physiol, February 1, 2008; 104(2): 328 - 337. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Neya, T. Enoki, Y. Kumai, T. Sugoh, and T. Kawahara The effects of nightly normobaric hypoxia and high intensity training under intermittent normobaric hypoxia on running economy and hemoglobin mass J Appl Physiol, September 1, 2007; 103(3): 828 - 834. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. A. Duhamel, J. G. Perco, and H. J. Green Manipulation of dietary carbohydrates after prolonged effort modifies muscle sarcoplasmic reticulum responses in exercising males Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2006; 291(4): R1100 - R1110. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. A. Duhamel, H. J. Green, J. G. Perco, and J. Ouyang Effects of prior exercise and a low-carbohydrate diet on muscle sarcoplasmic reticulum function during cycling in women J Appl Physiol, September 1, 2006; 101(3): 695 - 706. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. D. Noakes, P. E. di Prampero, C. Capelli, T. Zaobornyj, L. B Valdez, A. Boveris, M. Ashenden, T. W. Secomb, S. Dufour, E. Ponsot, et al. Comments on Point:Counterpoint "Positive effects of intermittent hypoxia (live high:train low) on exercise performance are/are not mediated primarily by augmented red cell volume" J Appl Physiol, December 1, 2005; 99(6): 2453 - 2462. [Full Text] [PDF]
|
|
|
|
 |
|
 C. Marconi, M. Marzorati, D. Sciuto, A. Ferri, and P. Cerretelli Economy of locomotion in high-altitude Tibetan migrants exposed to normoxia J. Physiol., December 1, 2005; 569(2): 667 - 675. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. F. Coyle Improved muscular efficiency displayed as Tour de France champion matures J Appl Physiol, June 1, 2005; 98(6): 2191 - 2196. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. U. Saunders, R. D. Telford, D. B. Pyne, R. B. Cunningham, C. J. Gore, A. G. Hahn, and J. A. Hawley Improved running economy in elite runners after 20 days of simulated moderate-altitude exposure J Appl Physiol, March 1, 2004; 96(3): 931 - 937. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. D. Noakes, J. E. Peltonen, and H. K. Rusko Evidence that a central governor regulates exercise performance during acute hypoxia and hyperoxia J. Exp. Biol., March 11, 2002; 204(18): 3225 - 3234. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Boning and H. J. Green Efficiency After Altitude Acclimatization J Appl Physiol, August 1, 2001; 91(2): 1014 - 1015. [Full Text] [PDF]
|
|
|
|
|
|
H. Green, B. Roy, S. Grant, C. Otto, A. Pipe, D. McKenzie, and M. Johnson Human skeletal muscle exercise metabolism following an expedition to Mount Denali Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2000; 279(5): R1872 - R1879. [Abstract] [Full Text] [PDF]
|
|
| ||||||||
Post > Pre
(P < 0.05). Main effects (P < 0.05) of
exercise were found for all variables.
