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Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas 75231; and University of Texas Southwestern Medical Center, Dallas, Texas 75235
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ABSTRACT |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Moderate-altitude living (2,500 m), combined with low-altitude training (1,250 m) (i.e., live
high-train low), results in a significantly greater improvement in
maximal O2 uptake
(
O2 max) and performance over equivalent sea-level training. Although the mean
improvement in group response with this "high-low" training model
is clear, the individual response displays a wide variability. To
determine the factors that contribute to this variability, 39 collegiate runners (27 men, 12 women) were retrospectively divided into
responders (n = 17) and nonresponders
(n = 15) to altitude training on the
basis of the change in sea-level 5,000-m run time determined before and
after 28 days of living at moderate altitude and training at either low
or moderate altitude. In addition, 22 elite runners were examined
prospectively to confirm the significance of these factors in a
separate population. In the retrospective analysis, responders
displayed a significantly larger increase in erythropoietin (Epo)
concentration after 30 h at altitude compared with
nonresponders. After 14 days at altitude, Epo was still elevated in
responders but was not significantly different from sea-level values in
nonresponders. The Epo response led to a significant increase in total
red cell volume and
O2 max in responders; in contrast, nonresponders did not show a difference in total red cell
volume or O2 max
after altitude training. Nonresponders demonstrated a significant
slowing of interval-training velocity at altitude and thus achieved a
smaller O2 consumption during those intervals, compared with responders. The acute increases in Epo
and O2 max
were significantly higher in the prospective cohort of responders,
compared with nonresponders, to altitude training. In conclusion, after
a 28-day altitude training camp, a significant improvement in 5,000-m
run performance is, in part, dependent on
1) living at a high enough altitude
to achieve a large acute increase in Epo, sufficient to increase the
total red cell volume and
O2 max, and
2) training at a low enough altitude
to maintain interval training velocity and
O2 flux near sea-level values.
athletes; hypoxia; erythropoietin; exercise
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INTRODUCTION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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ALTITUDE TRAINING is frequently used by competitive
endurance athletes in an attempt to improve sea-level athletic
performance (7). Despite several controlled studies demonstrating no
group improvement in sea-level performance after living and training at
altitude (2, 13), numerous anecdotal accounts exist describing a wide
variance in performance after a traditional altitude training camp.
Previously, we have demonstrated that a portion of the variability in
sea-level performance after altitude training can be accounted for by a
high prevalence of iron deficiency among trained athletes (22).
However, subsequently, even when high-dose iron supplementation was
initiated 6 wk before exposure to moderate-altitude living and
low-altitude training (live high-train low), the individual variation
in improvements in 5,000-m run time remained substantial despite a mean
improvement in group performance (14.1 ± 36.0 s, range 112 s slower
to 55 s faster) (13, 23). Although a portion of this variability may be
due to nonphysiological factors influencing exercise performance,
maximal O2 uptake
(O2 max), a
physiological marker that is a strong correlate of endurance exercise
performance, also showed an overall mean improvement (2.5 ml · min
1 · kg1)
with a similarly wide variability after altitude exposure (range 
3.2 to +8.7 ml · min1 · kg1).
In an effort to explain the substantial interindividual variability in the adaptive response to an altitude training camp, we retrospectively examined data from 39 athletes who lived at an altitude of 2,500 m and trained between altitudes of 1,200 and 3,000 m for 4 wk during the summers of 1994, 1995, and 1996. This examination attempted to determine which characteristics of acclimatization or training were different between athletes who responded to altitude training with a significant improvement in performance vs. athletes who were "nonresponders" to altitude training. Specifically, we hypothesized that the difference between responders and nonresponders to altitude training would be manifested through 1) an altitude-acclimatization pathway, dependent on the hematologic adaptation to altitude exposure, and 2) a training-response pathway, dependent on the maintenance of interval-training velocity and O2 flux at altitude comparable to sea-level training values. A portion of these factors were then examined in a separate cohort of 22 elite athletes in a prospective fashion to confirm the relationships established in the retrospective analysis.
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METHODS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Retrospective Analysis
Subjects. Thirty-nine distance runners (27 men, 12 women, age 21.6 ± 2.9 yr) were recruited from collegiate track and cross-country teams, local running clubs, and USA Track and Field development teams. All 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 min 30 s for men and <18 min 30 s for women. All were sea-level residents and could not have been to an altitude above 1,500 m for a period exceeding 1 wk in the previous 10 mo. All subjects gave their written informed consent to a protocol approved by the Institutional Review Board of the University of Texas Southwestern Medical Center at Dallas.
Study design.
An outline of the study design, including a detailed description of the
project phases, methods used, and measurements completed, has been
published elsewhere (13). A graphic depiction of the basic study time line is shown in Fig. 1.
Briefly, all athletes completed 6 wk of supervised sea-level training,
during which time familiarization with laboratory testing procedures
and iron maintenance or replacement therapy were initiated for all
subjects (22). At the conclusion of the 6-wk sea-level control period, laboratory and performance testing were completed, and all athletes were transported by van to Deer Valley, UT (2,500 m). All athletes lived at this altitude for a period of 28 days. Training followed three
separate paradigms: 1) all training
at a moderate altitude (2,500-3,000 m), designated
"high-high" (n = 13; 9 men, 4 women); 2) all training at a low
altitude (1,200-1,400 m), designated "high-low"
(n = 13; 9 men, 4 women); or
3) low-intensity "base" training at moderate altitude, with high-intensity "interval" training at low altitude, designated "high-high-low"
(n = 13; 9 men, 4 women).
Moderate-altitude training took place on trails and roads in the
Wasatch and Uinta mountain ranges. Low-altitude training occurred
nearby (~30-min drive) in Salt Lake City, UT. The training program
during the altitude training camp was designed to match the training
program completed at sea level. Training was conducted according to an
individualized template based on a 4-wk mesocycle, intended to provide
increasing volume and intensity during the first 3 wk, with a slight
taper in week 4 before laboratory and
performance testing. When the subjects returned to sea level after the
altitude training camp, plasma and blood volume were measured on the
second day, a 5,000-m time trial was completed on the third day, and an
incremental test of
O2 max was measured on the fourth day after return from altitude.
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Evaluation of performance. The primary outcome measure of this study was running performance, measured both on a track and in the laboratory on a treadmill.
TRACK EVALUATION. 5,000-m Time trial. Multiple 5,000-m time trials at select time points were conducted on a 400-m track. All time trials were performed at sea level in Dallas, TX, between 0700 and 0800, with temperature 22-26°C, humidity 80-100%, and wind velocity 0-10 km/h. To avoid the influence of racing strategies, all starts were staggered by at least 2 min. TREADMILL EVALUATION.O2 max. The primary
treadmill evaluation measure was an incremental exercise test that used
a modified Astrand-Saltin protocol (20). 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.
O2 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 highest 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. Additionally,
to verify that O2 max
was achieved, on a separate day a supramaximal treadmill run was
performed with the measurement of
O2. The highest value
obtained on either test was considered to be
O2 max.
Maximal steady state (MSS). MSS was estimated from the ventilatory
threshold according to standard criteria and methods (3) as follows. By
using breath-by-breath data from the incremental test of
O2 max, 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. ventilation (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.
OTHER LABORATORY MEASURES.
Blood compartments. Plasma volume, blood volume, and volume of red cell
mass, or the total red cell volume, were measured at each testing time
point at sea level. Plasma volume was measured by using the Evans blue
dye indicator-dilution technique (17). Briefly, after the subjects
rested quitely for least 30 min in the supine position, a known
quantity of Evans blue dye was injected through a catheter placed in a
peripheral vein, 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 (model DU 600, Beckman). Hematocrit was measured by
microcapillary centrifugation, and blood volume was estimated by
dividing plasma volume by 1 minus hematocrit, by using appropriate
corrections for trapped plasma and peripheral sampling (17). Total red
cell volume was defined as blood volume minus plasma volume.
Erythropoietin (Epo) and hemoglobin concentration. Plasma Epo
concentration and hemoglobin concentration were measured at sea level,
before the altitude training camp, after 30 h and 14 days of
exposure to 2,500 m, and on return to sea level. All blood samples were
obtained between 0600 and 0700 while the subjects were in a fasted,
resting state. Epo concentration was determined by an
125I radioimmunoassay, by using a
commercially available kit (model DSL-1100, Diagnostic Systems
Laboratories) and a Cobra auto-gamma counter. Hemoglobin concentration
was determined by using an Instrumentation Laboratories CO-oximeter.
Pulmonary diffusing capacity for CO
(DLCO).
A CO-rebreathing method (19) was used to measure
DLCO during
rest and steady-state exercise (16.1 km/h, 0% grade). Measures
completed during exercise were calculated in absolute terms as well as
normalized to O2 max.
Arterial oxygen saturation (SaO2)
during exercise at simulated altitude. A
submaximal, steady-state treadmill exercise bout was performed pre- and
postaltitude in a hypobaric chamber, at a simulated altitude of 2,700 m. SaO2 was estimated by using pulse oximetry (Ohmeda 3700), with values accepted only when the pulse was
within 2 beats/min of electrocardiogram recordings of heart rate.
SaO2 during sleep at sea level and
altitude. Pulse oximetry was used to determine
SaO2 during sleep (measured between 0200 and 0300), both prealtitude and after 30 h at altitude.
Evaluation of Training. training logs. Each runner kept a detailed training log book that included duration and intensity of each workout, along with resting and training heart rate (Polar). Logs also included description of well-being, fluid intake, body weight, and quantity and quality of sleep, and the logs 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 and compare training among the groups, we used the method of Banister and Wenger (4) for the calculation of 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. 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, running velocity andO2 were measured during typical base and interval training under all training conditions: sea
level (Dallas, TX; 150 m) and low (Salt Lake City, UT; 1,250 m) or
moderate altitude (Deer Valley and/or Bonanza Flats, UT; 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 ventilation with a
polarographic electrode to measure expired oxygen fraction. This device
assumes a respiratory exchange ratio of 1.0, which may underestimate
O2 at very high work rates
(14). Testing sessions were conducted on measured trails, allowing the
calculation of mean running velocity. The standard interval training
session was composed of four to six repetitions of 1,000-m runs.
Prospective Analysis
A prospective analysis of data collected in the summer of 1997 was completed to confirm our stated hypotheses and any relationships established through the retrospective analysis. The prospective analysis examined responses of 22 elite distance runners (14 men, 8 women, age 24.8 ± 2.5 yr) who completed 4 wk of altitude training after the high-high-low model, in the same Deer Valley and Salt Lake City, UT, setting. In this prospective group, the measures completed were 1) Epo and hemoglobin concentrations at four time points (2 days prealtitude, 18 h at altitude, 20 days at altitude, and 18 h after return to sea level), 2)O2 max (2-4
days prealtitude and 4-48 h postaltitude), and
3) 3,000-m time trial performance (1 day prealtitude and 3 days postaltitude).
Statistics
To examine the individual variability in response to 4 wk of altitude exposure and training, athletes were divided into groups classified as responders and nonresponders to altitude training. For the retrospective analysis, this grouping (Fig. 2) was based on the change in sea level 5,000-m time before and after the altitude training camp as follows: nonresponders,
0-s improvement in 5,000-m time
(n = 15, 9 men, 6 women; 7 high-high,
4 high-high-low, 4 high-low), responders, 
14.1-s improvement in
5,000-m time (n = 17, 13 men, 4 women;
3 high-high, 6 high-high-low, 8 high-low). An improvement of
>14.1 s for the responder classification was chosen on the basis
of the mean improvement in the high-low group and high-high-low group
athletes (14.1 ± 36.0 s). Because these two altitude training
strategies (high-low and high-high-low) have been clearly demonstrated
to produce significant performance improvements (13, 23), it was
rationalized that an improvement greater than the mean observed in
those two groups would be indicative of a strong responder to altitude
training. The seven subjects (3 high-high, 3 high-high-low, 1 high-low)
with a 5,000-m time improvement between 0 and 14.1 s were excluded from
the analysis, to establish distinct group differences. For the
prospective analysis, responders and nonresponders were classified in a
similar fashion to the retrospective analysis, on the basis of
individual improvement in 3,000-m time trial performance after altitude
training [i.e., 0-s improvement = nonresponder; the mean
improvement (5.8 s) = responder].
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Because it not known whether certain physiological variables, such as
Epo concentration, blood volume, and total red cell volume, have a
Gaussian distribution, these variables were first analyzed by using the
D'Agostino D statistic for normality
testing. No significant departures from normality were found. However, to be statistically conservative, we tested the above dependent variables by using both nonparametric (Wilcoxon matched pairs and
Kruskal-Wallis) and parametric (Student's
t) tests. Data for the above
variables are presented in Table 2 both nonparametrically as medians
with the full range of observed values and parametrically as means ± SD. All other dependent measures were analyzed by
using Student's t-tests. For all
comparisons, the 
for statistical significance was set at
P 0.05.
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RESULTS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Retrospective Analysis
Subject characteristics for the group of responders and nonresponders examined in the retrospective analysis are shown in Table 1. Despite the post hoc group classifications, no prealtitude differences were observed in anthropometric, hematologic, treadmill, or running performance measures between groups.
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Measures of Acclimatization
Epo concentration, blood volume, and total red cell volume are presented in Table 2. There were no divergent statistical results on the basis of whether parametric or nonparametric tests were used. Epo concentration increased significantly in both groups after 30 h at 2,500 m. However, the responders had a significantly larger increase in mean Epo concentration compared with the nonresponders, both in absolute terms (6.5 ± 3.3 vs. 4.7 ± 3.0 mU/ml; P 0.05) and when expressed as a
percentage of sea-level baseline (152.0 ± 5.7 vs. 134.3 ± 10.3%; P 0.05; Fig.
3). After 14 days at altitude, responders
still had a significantly higher mean Epo concentration than at
prealtitude; however, there was no significant difference between the
mean Epo concentration prealtitude and after 14 days in the
nonresponders. Both groups demonstrated a significant increase in
hemoglobin concentration and hematocrit from before to after the
altitude training camp. A significant 8% increase in the total red
cell volume was observed in the responders, with no change in the
nonresponders after 4 wk at altitude (Fig.
4A).
Mean blood volume was significantly lower in the nonresponders after 4 wk at altitude, but it was not different in the responders.
O2 max was
significantly increased by 7% in the responders postaltitude, with no
change in the nonresponders (Table 3).
Between groups, O2 max
was also significantly higher postaltitude in the responders vs. the
nonresponders (69.2 ± 6.8 vs. 64.4 ± 4.7 ml · min1 · kg1;
P 0.05) despite no prealtitude
difference. The postaltitude measure of MSS
O2 was also significantly
higher in the responders vs. the nonresponders (59.0 ± 9.1 vs. 52.4 ± 4.9 ml · min1 · kg1;
P 0.05), despite no prealtitude
difference. However, the MSS occurred at the same
percentage of O2 max
between groups both pre- and postaltitude, suggesting that this
difference was primarily due to an increase in
O2 max and
was not due to a fundamental shift in the factors that regulate the
ventilatory threshold. Gender differences within groups were present in
variables that classically differ between male and female
athletes, such as
O2 max, hemoglobin,
hematocrit, and total red cell volume. However, no difference between
genders in the response of these variables to altitude or training was
found in either the group of responders or nonresponders.
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Training Response Measures
No significant difference was found between groups for either TRIMPS, training duration, or estimated total mileage, during the sea-level training phase or the altitude training camp (Fig. 5). Interval training velocity at altitude significantly declined by almost 9% within the group of nonresponders but was not significantly different within responders (Fig. 4B). At altitude, nonresponders ran their intervals at a significantly slower pace than did responders, despite maintaining similar training velocities between groups at sea level. Both groups demonstrated a significant reduction in intervalO2 at altitude, as measured
by the K2 device. However, the responders were able to maintain a
significantly higher O2 during altitude interval training compared with nonresponders, despite
no difference between groups in sea-level interval
O2 measures. As
with measures of acclimatization, no gender difference within groups of
responders and nonresponders was found in any training response
measure.
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Additional Measures
Fourteen of the 17 responders and 11 of the 15 nonresponders completed a steady-state run at a simulated altitude of 2,700 m, both before and after the altitude training camp. No difference was found between groups in pulse oximetry measures of SaO2, either before (responders 80.3 ± 3.5%, nonresponders 80.4 ± 3.8%) or after the altitude training camp (responders 84.7 ± 4.7%, nonresponders 83.5 ± 3.7%). The increase in SaO2 from before to after the altitude training camp was significant in both groups, demonstrating a similar degree of ventilatory acclimatization in both responders and nonresponders. Measures of sleeping SaO2 (both at sea level and altitude) and measures of DLCO completed at rest and during exercise (expressed both in absolute terms and normalized toO2 max) were
not significantly different between responders and nonresponders.
Prospective Analysis
After 4 wk of high-high-low altitude training, 22 elite distance runners demonstrated a significant improvement in 3,000-m run time of 5.8 ± 9.2 s (P 0.05). With use
of the same criteria to assign responder and nonresponder
classifications as done in the retrospective analysis [i.e.,
responders > the group mean improvement (5.8 s) in 3,000-m time;
nonresponders 0-s improvement in 3,000-m time], nine subjects
(5 men, 4 women) were assigned to the responder group while five
subjects (all men) were classified as nonresponders. In this
prospective analysis, mean Epo concentration significantly increased in
the responders from prealtitude to 18 h at 2,500 m (8.8 ± 2.6 vs.
18.3 ± 5.8 mU/ml; P 0.05),
whereas the nonresponders did not demonstrate a significant difference (10.1 ± 2.7 vs. 14.9 ± 3.9 mU/ml;
P = 0.11).
O2 max was
significantly increased in the responders after altitude training
[change in O2 max
(
O2 max) 3.4 ± 2.1 ml · min1 · kg1;
P 0.05] but was not different
in the nonresponder group
(O2 max 0.1 ± 2.1 ml · min1 · kg1).
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DISCUSSION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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The principal new observations from the present study
are that the individual variability in the response to altitude
training may be accounted for by two mechanistic pathways: an
altitude-acclimatization effect, i.e., an increase in
O2-carrying capacity and
O2 max, and a
training effect, i.e., maintenance of training velocity and
O2 flux near sea-level values,
facilitating improvements in O2 max and race
performance. These findings extend our previous observations in
endurance athletes, regarding appropriate altitude training strategies
(13, 23).
High-Altitude Acclimatization Pathway
Acclimatization to high altitude includes a number of physiological and hematologic adaptations that theoretically should improve O2 transport to skeletal muscle during exercise (12). Performance enhancement in the group of responders was, in part, due to a series of robust acclimatization responses to high altitude: a greater acute and sustained increase in Epo
increase in total red cell volume increase in
O2 max significant improvement in 5,000-m run time (Fig.
4A). Why the responder group
demonstrated a more augmented Epo response at 2,500 m is not readily
clear and is likely dependent on several factors. At a moderate
altitude (2,315 m) similar to the one used in this study, Gunga et al. (10) found a wide variation in Epo response after 48 h. In their study
of 29 mountaineers, they reported median increase in Epo was 10.1 mU/ml, with increases at the 25th and 75th percentiles of 5.8 and 16.3 mU/ml, respectively. For comparison, after 30 h at 2,500 m,
the 39 endurance athletes in the retrospective analysis had a median
increase in Epo of 5.9 mU/ml, with increases at the 25th and 75th
percentiles of 4.1 and 8.2 mU/ml. Although the Epo concentration after
acute exposure to altitude within subjects is likely proportional to
the severity of the hypoxic stress (8, 16), the present data also
confirm a wide variability of Epo response to a fixed altitude among
subjects. These individual differences in the magnitude of Epo response
at a common altitude could be influenced by several factors such as
individual differences in hypoxic ventilatory drive,
O2 half-saturation pressure of
hemoglobin, or sensitivity to hypoxia at the point of Epo release, and
many of these factors may be genetically inherited traits
(21).
Several studies that have examined the time course of Epo response to
moderate altitude note a maximal Epo increase at 2 days postascent (1,
16). It could be argued that our acute altitude measure of Epo
concentration (30 h after arrival) occurred before this hormone reached
a peak level in the blood. If, for example, the Epo concentration of
nonresponders did not peak until a much later time than did that of the
responders, the timing of this measure could possibly account for the
significant difference between groups. We do not believe this is the
case because after 14 days at 2,500 m, Epo concentrations were still
significantly elevated over sea-level values in the responders but had
returned to near sea-level values in the nonresponders (Fig. 3).
Moreover, Epo was measured at the same time points in both groups. This observation, combined with the subsequent differences between responders and nonresponders in total red cell volume and
O2 max, leads us to
believe that the differences in Epo concentration are true
physiological differences and are not dependent on sampling time points
or individual differences in the achievement of a peak Epo response.
A key observation emphasizing the importance not only of Epo production but also of erythropoiesis as the primary mechanism for this altitude-related effect is the finding that nonresponders, despite a significant acute increase in Epo concentration after 30 h at 2,500 m, did not display an increase in the total red cell volume. Previously, we have demonstrated that athletes with low serum ferritin levels do not increase total red cell volume after 4 wk at altitude, despite an acute increase in Epo (22, 24). However, all athletes in this investigation received vigorous oral iron supplementation (as high as 400 mg of elemental iron/day in some athletes) during the 6 wk before altitude exposure, and there was no difference in prealtitude serum ferritin measures between groups (nonresponders 29.1 ± 15.5 mU/ml, responders 33.3 ± 18.6 mU/ml). Therefore, we conclude that the difference in total red cell volume in this study is not summarily explained by frank iron deficiency. Additionally, it is interesting to note that nonresponders had a classic normalization of Epo concentration back to sea-level values after 4 wk at 2,500 m, despite failing to augment O2-carrying capacity through an increased total red cell volume. Ultimately, whether the difference in the increase in total red cell volume between groups is due to a contrasting individual amount of Epo release to a given hypoxic stimulus or due to the same proportional Epo release to different hypoxic stimuli is difficult to determine. Responders could have had greater diffusion limitations during rest, greater ventilation-perfusion mismatch, or a blunted hypoxic drive. However, we did not observe any group differences in the decrease in SaO2 either during sleep or exercise at altitude nor differences in DLCO or magnitude of ventilatory acclimatization between groups.
Another possible difference between responders and nonresponders is the sensitivity of the bone marrow stem cells to a given concentration of Epo, as well as individual differences in the rate of Epo catabolism. No data collected in this study allow comment on this point; however, there was a significant difference in the Epo concentration between groups of responders and nonresponders. Thus the simplest explanation of the present data is that the erythropoietic difference between groups is found in the kidney, where the magnitude of Epo release was different for similar levels of desaturation. Regardless of the specific mechanism, however, we propose that, for nonresponders, a greater hypoxic stimulus may be necessary to induce a sufficiently large release in Epo and augment red cell production.
Both nonresponders and responders demonstrated a significant and
surprisingly similar increase in hemoglobin concentration after
altitude exposure. However, in the nonresponders, the hemoglobin increase was due primarily to a significant decrease in plasma volume
with no change in the total red cell volume. In contrast, the
responders increased hemoglobin concentration via an increased total
red cell volume and reduced plasma volume, thereby maintaining a
constant blood volume. One published model relating the effect of the
combination of changes in blood volume and hemoglobin
concentration on
O2 max (26) accurately
predicts a 248 ml/min change in O2 max in the
responders (actual
O2 max = 245 ml/min) and only a 91 ml/min change in the nonresponder group
(actual O2 max = 57 ml/min). These hematologic acclimatization differences
between responders and nonresponders reinforce the concept that changes in hemoglobin concentration alone are insufficient in predicting resultant changes in
O2 max and physical
performance after an altitude training camp.
An altitude-acclimatization pathway for predicting responders and
nonresponders to altitude training was also confirmed in the
prospective analysis. Although the data collection in the prospective
analysis was not as extensive (total red cell volume, interval-training
velocity, and interval-training
O2 were not measured), the
differences in the change in acute Epo concentration and
O2 max between
responders and nonresponders are comparable to, and equally compelling
as, the differences discovered in a retrospective manner. Unlike the
retrospective analysis, the group of nonresponders did not demonstrate
a significant increase in mean Epo concentration from prealtitude to
acute altitude. Because of the limited number of subjects
(n = 5) in the nonresponder group, we
likely did not have enough statistical power to demonstrate a
significant difference in mean Epo concentration from sea level to
acute altitude with our observed treatment effect
(P value of 0.11). However, a
between-groups comparison of the change in Epo from prealtitude to
acute altitude shows a similar trend (change in Epo: nonresponders 4.8 ± 5.1 mU/ml; responders 9.5 ± 6.2 mU/ml, P = 0.12), and a power analysis of the
Epo data gives an estimate of three additional subjects necessary for
this relationship to achieve statistical significance (with a power of
0.80 and an alpha of 0.05). Therefore, we believe that this
prospectively derived data confirm the relationships established in our
retrospective analysis.
Training-Response Pathway
A well-known consequence of acute exposure to altitude is a reduction in maximal aerobic power and exercise performance. Highly trained athletes appear to be even more susceptible to a reduction inO2 max at altitude,
because of the large reduction in SaO2 (5) secondary to pulmonary gas-exchange limitations at high work rates
(6, 11). The reduction in SaO2 is
believed to cause a 1% reduction in
O2 max for every 1%
drop in SaO2 below 92% (18), a
threshold that many highly trained athletes are below during maximal
exercise, even at sea level (5, 6, 11, 18). Therefore, because of this
reduction in O2 transport, some
elite athletes are not able to maintain the high work rates or training
velocities at altitude necessary to maintain competitive fitness (20).
This concept is reflected in the nonresponders, who demonstrated a 9%
reduction in interval-training velocity and a significantly lower
O2 during interval training
(Fig. 4B). We propose that the
reduction in interval-training intensity contributed to the
nonresponders' reductions in 5,000-m performance after altitude
training, despite maintaining
O2 max at precamp levels (15).
It is important to note that not all athletes trained at the same
altitude, because more than two-thirds of all athletes performed interval-training sessions at a "low" altitude of 1,250 m (see Table 1). Certainly, training at a lower altitude allows for faster
running speeds and higher O2
values to be maintained, compared with training at moderate altitudes.
Because it is known a priori that a high-low strategy results in a
significant improvement in performance compared with traditional
high-high-altitude training, the responder classification should be
(and was) biased toward the athletes who performed their interval
training at low altitude. However, over one-half of the nonresponders
performed their interval training at a low altitude of 1,250 m, whereas
three athletes who performed all of their training at moderate altitude
demonstrated the necessary improvements in performance to be classified
as responders. These examples demonstrate that, for some
athletes, the low altitude of 1,250 m may still be "high"
enough to impair training, and in fact
O2 max has been shown
to be significantly reduced in many endurance athletes at mild,
simulated altitudes between 580 and 1,000 m (5, 9, 25). In contrast,
some athletes with an excellent ability to tolerate hypoxic exercise were able to maintain running speed and
O2 flux even at a moderate altitude (2,700 m); these are examples that emphasize the varying degree of hypoxic exercise tolerance that exists among the athletic population, which has a direct effect on the training response at
altitude.
Implications for Performance
We speculate that these findings could be applied in a manner that would serve to minimize the number of athletes who do not respond to an altitude training camp with an increase in performance. By screening the erythropoietic and training velocity response to acute altitude, either shortly after arrival at altitude or in a laboratory setting (e.g., a hypobaric chamber), adjustments could be made in the altitude(s) where living and interval training take place, or perhaps individual assignment of appropriate living and training altitudes could be made before an altitude training camp. A screening procedure of this type may also identify athletes who could use the classic form of altitude training (high-high) and still experience performance gains, thereby minimizing the inconvenience of traveling to a low-altitude site several days per week, while expanding the number of available altitude training sites. Similarly, athletes who apparently will not respond adequately to altitude, regardless of an individual prescription of living and training altitudes, might also be determined. This type of athlete would likely be better served by staying at an appropriate sea-level training site, sparing the expense and inconvenience of relocating to an altitude training camp for 3-4 wk. However, more research is needed in this area.In conclusion, these data demonstrate that athletes who respond to
altitude training with a significantly large improvement in performance
1) have a significantly larger acute
increase in Epo concentration and total red cell volume compared with
athletes who do not improve and 2)
are able to maintain interval-training velocity at low or moderate
altitude near sea-level speeds while maintaining a significantly higher
O2 during interval training compared with athletes who are nonresponders to altitude training. We
propose that the number of nonresponders to altitude training may be
minimized by the individual assignment of living and training altitudes, on the basis of screening of the erythropoietic and training-velocity response to acute altitude exposure.
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ACKNOWLEDGEMENTS |
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This work was supported by US Olympic Committee Grants S94-049-A-TF, SST96-ATH-003, and SST97-ATH-007 and by USA Track and Field Grants 596500 and 59967.
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FOOTNOTES |
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Address for reprint requests: B. D. Levine, Institute for Exercise and Environmental Medicine, 7232 Greenville Ave., Dallas, TX 75231 (E-mail: levineb{at}wpmail.phscare.org).
Received 6 October 1997; accepted in final form 28 May 1998.
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Top
Abstract
Introduction
Methods
Results
Discussion
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