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1 Institute for Exercise and
Environmental Medicine, ABSTRACT Levine, Benjamin D., and James Stray-Gundersen.
"Living high-training low": effect of moderate-altitude
acclimatization with low-altitude training on performance.
J. Appl. Physiol. 83(1): 102-112, 1997.
altitude; hypoxia; training; exercise; sports
INTRODUCTION ALTITUDE TRAINING is frequently used by competitive
athletes to improve sea-level performance (14). However, the objective benefits of altitude training are controversial (21). On one hand,
acclimatization to high altitude results in central and peripheral
adaptations that improve oxygen delivery and utilization (4, 8, 26, 31,
34, 38, 44). Moreover, hypoxic exercise may increase the training
stimulus, thus magnifying the effects of endurance training (7, 41).
Conversely, hypoxia at altitude limits training intensity (23), which
in elite athletes may result in relative deconditioning.
Numerous anecdotal reports since the 1940s have suggested that
endurance athletes may achieve some benefit from altitude training for
sea-level performance (3, 12, 15). However, incomplete characterization
of athletic performance, lack of appropriate controls, and small
subject numbers have complicated the interpretation of the majority of
previous studies of altitude training (3, 11, 12, 15, 17, 18). When
appropriate control groups have been included, living and training at
altitude have not been proven to be advantageous compared with
equivalent training at sea level (1).
We reasoned that if athletes could live at moderate altitude, above
2,500 m (22), but train at low altitude, below 1,500 m, they could
acquire the physiological advantages of altitude acclimatization for
maximizing oxygen transport, without the detraining associated with
hypoxic exercise (24). The present study was designed to test this
hypothesis by examining 1)
competitive athletes, already well trained under supervised conditions
at sea level; 2) adequate numbers of
subjects to allow sufficient statistical power to detect meaningful
differences among treatment and control groups;
3) a balanced, randomized design
providing both sequential and parallel controls;
4) high-dose iron supplementation in
iron-deficient athletes to ensure appropriate acclimatization to high
altitude; and 5) comprehensive
characterization of performance including track and laboratory-based
markers.
METHODS Subjects
Study Design
The principal objective of this study was to test the hypothesis
that acclimatization to moderate altitude (2,500 m) plus training at
low altitude (1,250 m), "living high-training low," improves
sea-level performance in well-trained runners more than an equivalent
sea-level or altitude control. Thirty-nine competitive runners (27 men,
12 women) completed 1) a 2-wk
lead-in phase, followed by 2) 4 wk
of supervised training at sea level; and
3) 4 wk of field training camp
randomized to three groups: "high-low"
(n = 13), living at moderate altitude
(2,500 m) and training at low altitude (1,250 m); "high-high"
(n = 13), living and training at
moderate altitude (2,500 m); or "low-low"
(n = 13), living and training in a
mountain environment at sea level (150 m). A 5,000-m time trial was the
primary measure of performance; laboratory outcomes included maximal
O2 uptake
(
O2 max), anaerobic capacity (accumulated O2 deficit),
maximal steady state (MSS; ventilatory threshold), running economy,
velocity at O2 max, and blood compartment volumes. Both altitude groups significantly increased O2 max
(5%) in direct proportion to an increase in red cell mass volume
(9%; r = 0.37, P < 0.05), neither of which changed
in the control. Five-kilometer time was improved by the field training
camp only in the high-low group (13.4 ± 10 s), in direct
proportion to the increase in
O2 max
(r = 0.65, P < 0.01). Velocity at
O2 max and
MSS also improved only in the high-low group. Four weeks of living
high-training low improves sea-level running performance in trained
runners due to altitude acclimatization (increase in red cell mass
volume and O2 max) and maintenance of sea-level training velocities, most
likely accounting for the increase in velocity at
O2 max and MSS.
O2 max) of 5% (3 ml · kg
1 · min1)
with an SD of 3.2 ml · kg1 · min1,
requiring 11 athletes/group (
= 0.80, 
= 0.05). Athletes were required to be competitive at a distance between 1,500 m and the marathon and to have a recent personal best 5,000-m time (or
equivalent) of <16:30 for men and <18:30 for women. All were
sea-level residents and could not have been to altitude above 1,500 m
for a period exceeding 1 wk in the previous 10 mo. All subjects gave
their voluntary written informed consent to a protocol approved by the Institutional Review Board of the University of Texas Southwestern Medical Center at Dallas.
Fig. 1.
The study consisted of the following phases:
1) initial time trial and series of
laboratory tests for familiarization;
2) sea-level (SL) "lead-in"
phase designed to overcome effect of supervised training and to begin
aggressive iron supplementation to normalize serum ferritin;
3) full set of laboratory testing to
serve as baseline; 4) 4 wk of
sea-level training in Dallas, TX, designed to maximize fitness in all
athletes and to serve as a longitudinal sea-level control;
5) 2nd set of baseline measurements before field training camp; and 6) 4 wk of training camp with athletes divided into 3 groups by using a
balanced randomized design: living high (2,500 m), training low (1,250 m; 1); living high (2,500 m), training high (2,500-2,700 m; 2);
and living low (150 m), training low (150 m; 3). After 4 wk of training
camp, athletes returned to Dallas for
7) repeat series of laboratory testing and 8) repeat 5-km (5K) time
trials each week for total of 3 wk to determine optimal timing of
competition.
[View Larger Version of this Image (21K GIF file)]
O2 max was on
the fourth day, and the anaerobic capacity test was on the fifth day
after return from altitude. This testing session was compared with the last testing session before the training camps, with all testing performed in the same order, and served as the primary experimental comparison. Over the subsequent 2 wk, the athletes performed primarily easy base running, supplemented by short, fast runs, with a 5,000-m time trial at the end of each week. The purpose of this phase was to
determine the optimal time for competition after return from the
altitude training camp or control.
Evaluation of Performance
The primary outcome measure of this study was running performance, as measured both on a track and in the laboratory on a treadmill. An outline of the testing schedule is included in Fig. 1. Track evaluation. 5,000-m time trial. Multiple time trials over 5,000 m were conducted on a 400-m track. Time trials were performed at sea level in Dallas at 7:00-8:00 AM (temperature 22-26°C, humidity 80-100%, wind 0-10 km/h). To avoid racing strategies, all starts were staggered by at least 2 min. Treadmill evaluation.
O2 MAX.
O2 max was measured
with a modified Astrand-Saltin protocol (3) involving incremental
exercise on a treadmill. After a brief warm-up, subjects ran at 9.0 miles/h (mph) for men and 8.0 mph for women at 0% grade for 2 min. The
grade was then increased 2% every 2 min until exhaustion, which
usually occurred after 6-8 min. Oxygen uptake
(O2) was measured by using
the Douglas bag method, gas fractions were analyzed by mass
spectrometer (Marquette MGA 1100), and ventilatory volume was measured
with either a Tissot spirometer or dry-gas meter (Collins).
O2 max was
defined as the O2 measured
from at least a 40-s Douglas bag. In nearly all cases, a plateau
in O2 was observed with
increasing work rate, confirming the identification of
O2 max. However, to
verify that O2 max
was achieved, on a separate day a supramaximal treadmill run was
performed, with the measurement of
O2 and anaerobic capacity
as described below. The highest value of
O2 achieved on either test
was accepted as
O2 max. In
addition, heart rate was monitored continuously (Polar CIC, Port
Washington, NY), and fingertip capillary blood was obtained during the
second minute of each stage for the measurement of lactate
concentration [Yellow Springs Instruments (YSI) 23L, Yellow Springs,
OH].
MAXIMAL STEADY STATE (MSS).
MSS was estimated from the ventilatory threshold according to standard
criteria (2) as follows. During the incremental test of
O2 max,
breath-by-breath O2 was
calculated and displayed online by using gas fractions measured at the
mouth by mass spectrometer (Marquette), and ventilation
(E) by
turbine flowmeter (VMM, Interface Associates). The
O2 at ventilatory threshold
for all tests was determined by a single, blinded, experienced observer during simultaneous examination of multiple plots of
O2 vs. E,
O2 vs.
E/O2,
O2 vs.
CO2 production
(CO2), and
O2 vs.
E/CO2
by using either commercial (First Breath, Marquette) or proprietary
software.
ANAEROBIC CAPACITY.
Anaerobic capacity was estimated from the accumulated oxygen deficit,
according to the method of Medbo et al. (28). Briefly, subjects had
their uphill running economy measured during two, 5-min submaximal runs
up an 8% grade (5 and 6 mph for women, 6 and 7 mph for men), during
which O2 was measured with
the Douglas bag method. After at least 4 h of rest, subjects performed
a supramaximal run at 8% grade with the speed chosen individually to
exhaust the subject between 2 and 4 min. The accumulated oxygen deficit was defined as the difference between the predicted
O2 (calculated from
submaximal economy and time) and the measured
O2 (28). In addition, the
total treadmill time was used as a high-intensity short-duration
(3-min) performance marker. Immediately after the supramaximal run,
fingertip capillary blood samples were collected every 2 min for 10 min
during recovery to identify peak lactate concentration.
SUBMAXIMAL RUNNING ECONOMY AND PERFORMANCE.
Submaximal economy during flat treadmill running was estimated from the
relationship between O2 and
treadmill speed during three, 5-min submaximal runs at 0% grade: 8, 10, and 12 mph for men; 8, 9, and 10 mph for women.
O2 at each level was
measured from a 1-min Douglas bag obtained from the third to fourth
minutes. Running economy was defined as the slope of the regression
relating O2 to treadmill
speed. Velocity at
O2 max was also
calculated by identifying the treadmill speed that would elicit
O2 max, on the basis
of the flat running economy regression equation and O2 max.
E, heart
rate, and capillary lactate were measured during each stage. Cardiac
output was also measured during these runs by using a foreign
gas-rebreathing method, with acetylene as the soluble and helium as the
insoluble gas (42). Recent modifications in our laboratories designed
to facilitate measurement during high-velocity treadmill running have
been validated against standard invasive methods, with an
r2 of 0.91 and an
SE of the estimate of 1.1 l/m over a range of cardiac output from 2.75 to 27.0 l/min compared with both direct Fick and thermodilution (32).
Stroke volume was calculated from cardiac output and heart rate, and
arteriovenous oxygen difference [(a-v)DO2]
was calculated from O2 and
cardiac output. For purposes of statistical comparison, physiological
variables at 10 mph and 0% grade were used as index markers of
submaximal running performance.
Other Laboratory Measures
Blood compartments. Plasma volume, blood volume, and red cell mass volume were measured at each testing time point at sea level. Plasma volume was measured by using the Evans blue dye indicator dilution technique (30). Briefly, after at least 30 min of quiet, supine rest, a known quantity of Evans blue dye was injected through a peripheral intravenous catheter, and venous blood was drawn at 10, 20, and 30 min after injection for the measurement of absorbance at 620 and 740 nm via spectrophotometry (DU 600, Beckman). Hematocrit was measured via microcapillary centrifuge, and blood volume was estimated by dividing plasma volume by 1
hematocrit, using appropriate corrections for trapped plasma
and peripheral sampling (30). Red cell mass volume was defined as blood
volume plasma volume.
Evaluation of Training
Training logs. Each runner kept a detailed training logbook that included duration and intensity of each workout, along with resting and training heart rate (Polar). Logs also included descriptions of well-being, fluid intake, body weight, and quantity and quality of sleep and were reviewed weekly by investigators and staff. Diet was also monitored to ensure adequate nutrition. Training stimulus. To derive an index that would allow us to quantify the training stimulus (that stimulus induced by a training session that results in an adaptative response) and compare training among the three groups, we used the method of Bannister and Wenger (5) for the calculation of the training impulse (TRIMPS). This method multiplies the duration of a training session by the average heart rate achieved during that session, weighted for exercise intensity (5). Total training time and an estimate of training distance were calculated from the information in the training logs. Training characterization. To precisely quantify the metabolic requirements of a typical training session, we measured running velocity,O2,
E, heart rate, and lactate duringtypical base and interval training under all
the conditions at which training occurred during the study: sea level
(Dallas and San Diego, both 150 m), low altitude (Salt Lake City, 1,250 m), and moderate altitude (Deer Valley, 2,700 m) after 2 wk of
acclimatization. O2 in the
field was measured with a small telemetry device (K2, Cosmed) that
combines a turbine flowmeter built into a face mask to measure
E, with a
polarographic electrode to measure expired oxygen fraction, assuming a
respiratory quotient of 1.0 (which may underestimate
O2 at very high work rates)
(25). Testing sessions were conducted over measured trails, allowing
the calculation of running velocity. Heart rate was measured simultaneously (Polar), and samples of fingertip capillary blood were
obtained immediately after each characterization session for the
measurement of lactate concentration (YSI).
Statistics
Analytic approach. The primary statistical comparison was between the testing sessions before and after the altitude training camp or sea-level control and was analyzed with a two-way, repeated-measures analysis of variance by using commercially available software (Winstar, Anderson Bell). An interaction statistic F-value < 0.05 was considered statistically significant and was then followed by Student-Newman-Keul's post hoc test for multiple comparisons to determine the source of the difference. The relationship between the change inO2 max and
the change in red cell mass volume, as well as the change in
O2 max and the change
in 5,000-m time before and after the training camp, were compared by
using linear regression and Pearson's coefficient. All data are
expressed as means ± SD.
RESULTS
Subjects
Subject characteristics for all three groups are shown in Table 1, which includes the 39 subjects who completed all testing and training phases of the study. Only two subjects dropped out during the course of the study. One subject left because of homesickness. One subject suffered from chronic Epstein-Barr virus infection and was unable to complete the training at altitude. No data from these two subjects are included in the analysis. At baseline and after the sea-level control training period, there were no statistically or physiologically significant differences among the three groups in terms of 5,000-m time,O2 max, or blood
compartment volumes.
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Training
There was no significant difference in sea-level training by any criteria among the groups (Fig. 2, A-C). During the field training camps, all three groups had small but similar increases in total training duration and total training distance, from sea level in Dallas to the field training camp, with no significant difference among the groups. This increase was predominantly because the first and last weeks of training in Dallas included the laboratory testing. Similar to training at sea level in Dallas, there was no significant difference among groups for training during the training camp for either TRIMPS, training duration, or estimated total mileage, supporting the conclusion that training was closely matched among the groups during both 4-wk mesocycles.
Base training at sea level (Dallas and San Diego) was performed at
82-84% of sea-level 5,000-m race pace, which required 71% of
O2 max, 85% of maximal
heart rate, and lactate values of 3.5 mmol/l (Table
2). With increasing altitude, there was a
trend for base training to be performed at progressively slower speed and at a lower percentage of sea-level
O2 max, which reached statistical significance at 2,700 m. However, base training heart rate
was similar under all three conditions, suggesting that base training
was performed at similar relative work rates, even though the absolute
work rates were less (slower speeds). For 1,000-m interval sessions,
training at sea level (Dallas and San Diego) was accomplished at 110%
of sea-level 5,000-m race pace, 87% of sea-level
O2 max, 96% of
sea-level maximal heart rate, and lactate values of 10 mmol/l. For
unclear reasons, lactate measured after the interval sessions in San
Diego was significantly lower than in Dallas. With increasing altitude,
running speed, O2, and heart
rate were all lower than at sea level. Despite the relative oxygen lack
at moderate altitude, peak lactate was significantly lower at 2,700 m
than at either sea level or 1,250 m (33).
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Response to Training
Blood compartment volumes (Table 1). Plasma volume tended to increase in the high-low and high-high groups by training at sea level in the heat in Dallas (5%, P = 0.08) and decreased back to baseline after training in the cooler mountain environments. Plasma volume was unchanged in the sea-level control group throughout the study. Living at moderate altitude, regardless of training altitude, resulted in a significant increase in red cell mass volume of 9% (P < 0.01), which was not observed in the sea-level control. Blood volume changes paralleled the changes in plasma volume during sea-level training in Dallas, when red cell mass volume did not change. In contrast, after subjects lived at moderate altitude, the reduction in plasma volume was offset by an increase in red cell mass volume, leaving total blood volume unchanged but with an increase in oxygen-carrying capacity (increased hemoglobin concentration). Laboratory treadmill performance.O2 MAX.
After the 2-wk lead-in phase, an additional 4 wk of training at sea
level in Dallas did not increase
O2 max in any
group, confirming the fact that the athletes had reached a plateau in aerobic power induced by this training program at sea level (Fig. 3). However, after an additional 4 wk of
living at moderate altitude, both high-low and high-high groups
increased O2 max
significantly by an additional 5% (P < 0.05 for each). Approximately one-half of the subjects increased
O2 max by achieving a
higher work rate (higher grade) on the incremental treadmill test. The
other half was able to increase the proportion of work performed
aerobically at the highest work rate and therefore had a higher
O2 at the same peak treadmill
grade. In contrast, there was no change in O2 max in the sea-level
control despite an equivalent supervised training program. The change
in O2 max was loosely
but significantly correlated with both the change in red cell mass
volume during the training camp (r = 0.37, P = 0.02) and the change in
hemoglobin concentration (r = 0.40, P = 0.01).
MSS. Similar to
O2 max,
O2 at MSS did not change in
any group during 4 wk of supervised training at sea level in Dallas
(Fig. 4). However, in contrast to
O2 max, MSS increased
significantly only in the high-low group after the altitude training
camp (P < 0.05).
O2) at maximal
steady state, determined from ventilatory threshold, at baseline, after
sea-level training in Dallas (sea level), and after altitude training
camp or sea-level control (altitude). Group characteristics and figure
symbols are defined as in Fig. 2.
* P < 0.05 compared with
previous time point.
ANAEROBIC CAPACITY. There were no significant changes in accumulated oxygen deficit in any group after training at either sea level or altitude (Table 1). Uphill treadmill run time did not change in any group after training at sea level in Dallas. After the field training camp, uphill treadmill run time increased only in the high-high group (159 ± 10 to 182 ± 13 s, P < 0.05). SUBMAXIMAL ECONOMY AND PERFORMANCE. Treadmill running economy was stable throughout the study and did not change in any group from any training stimulus (Table 3). Similarly stable was the relationship between cardiac output (Table 3) and
O2 (slope of
cardiac
output/O2), which was constant in all groups at all measured time points. However, at velocities near 5,000-m time-trial speeds (12 mph for men), cardiac output tended to be lower in both altitude groups
(P = 0.09), and
(a-v)DO2
was significantly higher (P = 0.01).
Velocity at O2 max
increased significantly after the altitude training camp only in the
high-low group (P < 0.05, Table 1).
At our index submaximal level of 10 mph and 0% grade, there were
initial improvements in heart rate and lactate in all three groups
after 4 wk of training at sea level in Dallas but no further changes in
these variables after altitude or sea-level field training camps.
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O2 max (Fig.
6) (r = 0.65, P < 0.00001).
O2 max)
and change in 5,000-m time trial performance (5K) after training camp for all subjects. Group characteristics and symbols are
defined as in Fig. 2, except for men (squares) and women (circles).
DISCUSSION
The principal new observation from this study is that acclimatization
to moderate altitude, when combined with training at low altitude,
results in an improvement in sea-level running performance over 5,000 m
in already well-trained, competitive runners. Such an improvement was
not observed when acclimatization was combined with training at
moderate altitude, or with an equivalent supervised training camp at
sea level. The mechanism of this improvement appears to be twofold: an
altitude-acclimatization effect, increase in blood oxygen-carrying
capacity and O2 max,
which was translated into improved performance by low-altitude
training, with maintenance of training velocities and oxygen flux,
presumably allowing an increase in velocity at
O2 max and
MSS.
High-Altitude Acclimatization Effect
The rationale for this study was based on the assumption that, if altitude training works to improve sea-level endurance performance, then the physiological benefits of altitude training must derive from either the development of acclimatization, an enhancement of the training effect by hypoxic exercise, or both (23). Acclimatization to high altitude includes a number of physiological adaptations that might theoretically improve oxygen transport during exercise. Ventilatory adaptations could improve alveolar oxygenation in some athletes (13) but are likely to be short lived. Structural and biochemical adaptations in skeletal muscle may be more robust and could improve oxygen extraction and substrate utilization (4, 8, 26, 31, 34, 41, 44). All have been reported in animal models and frequently in humans. However, probably the most important adaptation that would improve sea-level performance is an increase in red blood cell mass (43), which increases the oxygen-carrying capacity of the blood and improves aerobic power (9, 16, 20). In the present study, we have demonstrated that 4 wk of living at an altitude of 2,500 m was sufficient to stimulate erythropoietin secretion (37) and increase red blood cell mass volume by ~10%. This increase in oxygen-carrying capacity of the blood is on the order of magnitude observed in previous studies of acute erythrocyte infusion that demonstrated a similar improvement inO2 max (9). In this
study, the significant, albeit loose, correlation between both the
increases in red blood cell mass volume and hemoglobin concentration
and the increase in
O2 max observed in both
groups living at moderate high altitude suggests that this endogenous
"erythrocyte infusion" is at least partially responsible for the
improvement in maximal aerobic power. Moreover, at running speeds on
the treadmill that approximated 5,000-m race velocity, the increase in
oxygen-carrying capacity allowed a lower cardiac output and therefore
more peripheral diffusion time and oxygen extraction [i.e.,
increased
(a-v)DO2],
as well as providing for additional cardiac flow reserve. Finally, the close correlation between the increase in
O2 max and the
improvement in 5,000-m time after the field training camp argues
strongly that this is a key adaptation during altitude training and a
necessary mechanism for improving sea-level performance.
However, this adaptation, by itself, may be necessary but not
sufficient to improve sea-level performance. Thus the
high-high group was exposed to exactly the same living conditions at
2,500 m and had similar increases in red cell mass volume and
O2 max as the high-low
group, yet they did not increase running performance over 5,000 m at
sea level. The only difference between these two groups was the
training site, which in the high-high group was also at moderate
altitude.
Low-Altitude Training
Training (as opposed to living) at moderate altitude is associated with relatively severe hypoxemia, with oxyhemoglobin saturations reported to be <80% during typical base training (19). This hypoxia results in a decrease in maximal aerobic power of ~1% for every 100 m above 1,500 m (11). Particularly for well-trained athletes, there are more marked reductions in aerobic power even at lower altitudes (41). Thus elite athletes are not able to sustain the high work rates at altitude necessary to maintain competitive fitness (35). In the present study, this limitation was manifested most clearly during interval training that was performed nearly 15% slower, and at 20% lowerO2, than comparable training
at sea level. Despite an equivalent effort
(E was 16% greater than at sea level), heart rate and lactate were also
significantly lower at 2,700 m, consistent with previous reports of
decreased maximal heart rate and maximal lactate after acclimatization
to high altitude (33). Such a reduction in interval-training intensity in trained runners has recently been shown to decrease running performance over 5,000 m despite a pre- servation of
O2 max (27). It thus
appears likely that, in the high-high group, the increase in red blood
cell mass and O2 max
was offset by a reduction in training velocity and oxygen flux, leading
to no change in running performance.
In contrast to the training in the high-high group, who performed all
interval training at 2,700 m, similar training at 1,250 m in the
high-low group was only slightly (6%) slower than at sea level and was
accomplished at virtually the same
O2, heart rate, and lactate
concentration. Although the mechanism is not entirely clear, such a
maintenance of training velocity and oxygen flux is likely to be
critical toward sustaining competitive performance, as has been
recently shown in runners who decrease training volume but maintain
intensity (6). This difference in training between high-high and
high-low groups appeared to be the most important factor that, combined
with the increase in
O2 max induced by altitude acclimatization, allowed for both an increase in the O2 at MSS and the velocity
at O2 max only in
the high-low group.
Whether these characteristics associated with "low-altitude
training" are specifically responsible for the improvement in 5,000-m time or simply markers for some other skeletal muscle adaptation is not clear. Adaptations such as increases in MSS would be
expected to have a greater impact on longer distance events, during
which competition occurs at some fraction below O2 max, than on 5,000-m
performance, which is run essentially at
O2 max. One previous
study has demonstrated an increase in muscle buffer capacity after a
period of "high-high" altitude training (29) associated with an
increase in oxygen deficit and an increase in treadmill run time. In
the present study, we did observe an increase in uphill treadmill run
time in our high-high group, raising the possibility of an increase in
buffer capacity. However, we did not observe any changes in anaerobic
capacity, as measured by the accumulated oxygen deficit. The difference between the study of Mizuno et al. (29) and ours may derive from the
fact that their athletes changed training modalities, from running to
skiing, during their sojourn at altitude. They also did not have any
controls doing similar ski training at sea level.
We were concerned with the observation that in the present experiment, the concurrent sea-level control, if anything, tended to have a worse 5,000-m performance after the training camp compared with before, although this did not reach statistical significance. We suspect that, because all time trials were conducted in the heat of the Texas summer, a loss of heat acclimatization in the cooler mountains outside of San Diego, without the benefit of altitude acclimatization, may have been responsible for some of this apparent deterioration. We also considered the possibility that the athletes in the San Diego control might not have been as motivated as the altitude groups on the basis of previously held expectations of a benefit from altitude training. However, the new Olympic training center represents the state of the art in training facilities available to American Olympic athletes and would not be available to the athletes in this study under other circumstances. Virtually all the athletes were therefore very excited about the opportunity to go to San Diego, thus eliminating any sense of disappoinment that might occur on the basis of randomization to the sea-level control. Moreover, these athletes are by nature very competitive, and the athletes in San Diego were, if anything, more motivated to perform better on return from the camp to prove that their training experience was every bit as good as their altitude counterparts. Over the course of the training cycle, it was clear that these athletes were receiving an outstanding training experience. They bonded as a group, performed extremely well in the interim races to which they were assigned during the month, and uniformly felt that they had improved significantly. The observed and reported differences are therefore even more remarkable in this regard.
On closer inspection, the majority of this seeming decline was due to unusually poor performances in two of our women athletes. Because we had only four female athletes in each group, which might increase the variability, as an additional check we also examined the 5,000-m performance for all men in the study separately. As can be seen in Fig. 5B, the results for men only were less variable, with no clear change in performance in the low-low or high-high group, and an even greater improvement in the high-low group. We believe that further studies involving larger numbers of female athletes will be necessary to confirm the applicability of this study to all women. However, we speculate that as long as adequate iron is made available through supplementation, the results will be consistent for all athletes, regardless of gender.
In conclusion, well-trained competitive runners living at moderate
altitude increased red cell mass and oxygen-carrying capacity of the
blood and increased
O2 max after
return to sea level. This increase in
O2 max was translated
into improved performance by the maintenance of near sea-level training
velocities and oxygen flux when interval training was
performed at low altitude, resulting in an increase in
O2 at MSS and velocity at
O2 max. Running performance over 5,000 m at sea level therefore improved only in the
runners who lived at moderate altitude and trained near sea level
(high-low group) but not in those who lived and trained at moderate
altitude or lived and trained at sea level, after equivalent training
programs.
ACKNOWLEDGEMENTS
Many individuals and organizations provided extraordinary support for this project, without which it could not have been completed. Electronic Data Systems Corp. graciously provided housing for the athletes in Dallas, as did the Presbyterian Village North community. The US Olympic Training Center in Chula Vista, California, provided housing and meals for the athletes in San Diego. SmithKline Beecham laboratories kindly provided the iron supplement (Feosol). The Deer Valley Club allowed the use of their training facilities in Utah. Stacey Blaker, Nancy Mordecai, Tia Petersen, Kevin Robinzine, Mark Schecter, Wyman Schultz, and Christie Zolfoghary provided invaluable technical assistance with athlete care, testing, and training. Lisa Baker provided technical assistance with all the blood work. We also were assisted each summer by many outstanding students and interns, whose contribution should be acknowledged. Dr. Jay T. Kearney from the US Olympic Committee and Dr. Harmon Brown from US Track and Field provided strong continued support, and Dr. Birgit Friedmann from the University of Heidelberg provided invaluable assistance with training and medical care of the athletes, technical assistance, and analysis of the ventilatory threshold curves. We also would like to thank Dr. Eric Bannister for allowing us to use his program for the calculation of TRIMPS.
FOOTNOTES
Address for reprint requests: B. D. Levine, Institute for Exercise and Environmental Medicine, 7232 Greenville Ave., Dallas, Texas 75231 (E-mail: Levineb{at}wpmail.phscare.org).
Received 19 June 1996; accepted in final form 14 February 1997.
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K. Katayama, Y. Sato, Y. Morotome, N. Shima, K. Ishida, S. Mori, and M. Miyamura Cardiovascular response to hypoxia after endurance training at altitude and sea level and after detraining J Appl Physiol, April 1, 2000; 88(4): 1221 - 1227. [Abstract] [Full Text] [PDF]
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R. F. Chapman, J. Stray-Gundersen, and B. D. Levine Individual variation in response to altitude training J Appl Physiol, October 1, 1998; 85(4): 1448 - 1456. [Abstract] [Full Text] [PDF]
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ABSTRACT
