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1 Norwegian University of Sport and Physical Education, 0806 Oslo, Norway; 2 Indiana University, Bloomington, Indiana 47405; and 3 The Institute of Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, and the University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75231
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Acclimatization to moderate high altitude
accompanied by training at low altitude (living high-training low) has
been shown to improve sea level endurance performance in accomplished,
but not elite, runners. Whether elite athletes, who may be closer to
the maximal structural and functional adaptive capacity of the
respiratory (i.e., oxygen transport from environment to mitochondria) system, may achieve similar performance gains is unclear. To answer this question, we studied 14 elite men and 8 elite women before and
after 27 days of living at 2,500 m while performing high-intensity training at 1,250 m. The altitude sojourn began 1 wk after the USA
Track and Field National Championships, when the athletes were close to
their season's fitness peak. Sea level 3,000-m time trial performance
was significantly improved by 1.1% (95% confidence limits
0.3-1.9%). One-third of the athletes achieved personal best times
for the distance after the altitude training camp. The improvement in
running performance was accompanied by a 3% improvement in maximal
oxygen uptake (72.1 ± 1.5 to 74.4 ± 1.5 ml · kg
1 · min1).
Circulating erythropoietin levels were near double initial sea level
values 20 h after ascent (8.5 ± 0.5 to 16.2 ± 1.0 IU/ml). Soluble transferrin receptor levels were significantly elevated on the 19th day at altitude, confirming a stimulation of erythropoiesis (2.1 ± 0.7 to 2.5 ± 0.6 µg/ml). Hb concentration measured
at sea level increased 1 g/dl over the course of the camp (13.3 ± 0.2 to 14.3 ± 0.2 g/dl). We conclude that 4 wk of acclimatization to moderate altitude, accompanied by high-intensity training at low
altitude, improves sea level endurance performance even in elite
runners. Both the mechanism and magnitude of the effect appear similar
to that observed in less accomplished runners, even for athletes who
may have achieved near maximal oxygen transport capacity for humans.
endurance performance; hypoxia; erythropoietin; symmorphosis; maximal oxygen uptake; running; athletics
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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WE HAVE PREVIOUSLY
SHOWN that 4 wk of acclimatization to moderate altitude (2,500 m)
combined with training at low altitude (1,250 m) (HiLo) is superior to
an equivalent training camp at sea level (24). This form
of altitude training produced a 1.4% improvement in group sea level
endurance performance in collegiate and recent postcollegiate runners
(age 20 ± 2 yr). The mechanism for the improvement in performance
with this approach appears to be twofold: an increase in red cell mass
as a function of the hematological adaptation to moderate altitude,
which produces an increase in maximal oxygen uptake
(
O2 max), plus the maintenance of sea
level oxygen flux during low-altitude training, which preserves
skeletal muscle structure and function and facilitates an improvement
in sea level running performance.
However, despite numerous anecdotal reports of the success of altitude
training for world class athletes, some recent reports have suggested
that HiLo, or any form of altitude training, may not be advantageous
for elite compared with collegiate level athletes (1, 2,
14). The concept of symmorphosis, as elaborated by Hoppeler and
Weibel (17), argues that, for any system, such as the
respiratory chain for oxygen transport, the maximal capacity of each
parameter is adjusted quantitatively to match the structural and
functional limits of the demands placed on the system as a whole. Thus,
for the "elite athletes" of the animal kingdom, each step of the
pathway of oxygen from the atmosphere to the mitochondria has evolved
toward optimal function and maximal aerobic power, allowing little room
for further adaptive improvement. Therefore, for elite human athletes,
small, short-term improvements in one step of the oxygen cascade may be
met by functional limits in other steps, minimizing the potential
performance benefit of altitude training. However, elite human athletes
living and training at sea level are unable to develop similar levels
of circulating hemoglobin/red cell mass as "high-endurance" animal
species who have the ability to autotransfuse by splenic contraction
(23, 25). Thus raising circulating hemoglobin levels
conceivably has the greatest potential for improving elite endurance
performance in humans. In addition, the interaction between convective
and diffusive components of oxygen transport, as described by Wagner (35), would predict an increase in
O2 max with increasing circulating
hemoglobin and red cell mass. In support of these concepts, transfusion
studies (5, 10, 37) and those administering recombinant
erythropoietin (3, 4) suggest that an increase in red cell
mass by itself will increase the O2 max
for all endurance athletes, regardless of performance level.
Thus the present study was designed to investigate the effect of the HiLo paradigm on elite runners who were likely to be much closer to their ultimate performance potential than the athletes previously studied with this approach. The study was timed such that the athletes would be in the best shape of the year [i.e., after they had just completed the spring track season culminating with the National Collegiate Athletic Association (NCAA) championships and the USA Track and Field National Championships]. We hypothesized that the combination of acclimatization to 2,500 m and high-intensity training at 1,250 m would improve sea level performance in elite middle- and long-distance runners.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
Twenty-six distance runners (17 men and 9 women) were recruited. Athletes were required to be competitive at a national level in an event from the 1,500 m to the marathon. Twenty-four of the 26 athletes were ranked in the US top 50 for their event in 1997. The athletes included two 1996 Olympians, and 50% of the athletes had competed in the 1996 US Olympic Trials. All but four athletes competed in the 1997 NCAA Championships or the 1997 USA Track and Field Championships or both. Three of those four athletes were attempting to run qualifying times up to the day of the meet. Exclusion criteria included altitude residence (>1,000 m) or recent illness or injuries preventing normal training and racing. The subjects gave their written consent to the study, which had received approval from the Institutional Review Board of the University of Texas Southwestern Medical Center.Protocol
The study protocol was a modification of one previously developed by the authors for collegiate runners (24). Briefly, the athletes were assessed at sea level in the week before and the week after 27 days of living at 2,500 m (see Fig. 1). The NCAA Championships were held at sea level 3 wk before the altitude sojourn, and the USA Track and Field Championships ended 1 wk before the altitude sojourn. Individualized training plans were developed by the athlete and his or her coach. Plans were discussed with the investigators and conformed to a training template presented by the investigators (24). Athletes were required to perform high-intensity, high-velocity training at 1,250 m. All other training took place between 1,250 and 3,000 m with most of the training occurring between 2,000 and 2,800 m. This modification of the HiLo model, termed "HiHiLo," (living at moderate altitude, low-intensity base training at moderate altitude, high-intensity interval training at low altitude), has been demonstrated in pilot work to provide identical improvement inO2 max and 5,000-m time as the original
HiLo model (34). All athletes received oral liquid iron
supplementation (Feo-Sol, 9 mg elemental iron/ml) with dose adjusted on
the basis of plasma ferritin concentration (range: 5-45 ml/day).
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Assessments
Performance. Sea level performance was assessed by 3,000-m time trial races on a 400-m all-weather track (Indiana University, Bloomington, IN) the day before and 3 days after the altitude sojourn. The time trials were run in men's and women's heats in the early evening (1900 to 2000). Athletes were instructed to achieve the best time possible on each time trial. Experienced pace setters (athletes not otherwise involved in the project) were utilized to set a fast, competitive pace for the first 1,600 m of the 3,000 m race to ensure physiological rather than tactical performance. The pace setter or "rabbit" ran the same preselected race pace in both the prealtitude and postaltitude time trials. Temperatures ranged from 25 to 27°C, relative humidity ranged between 50 and 75%, and there was no wind. Time was recorded for each subject to the nearest 0.1 s.
Treadmill assessment. After a 15-min warm-up, the athlete ran to volitional exhaustion performing a protocol with constant velocity and increase in grade of 2% every 2 min. Inspired ventilation was measured by a dual-thermistor flow probe (Torrent 1200, Hector Engineering), and expired gas concentrations were measured in a 5-liter mixing chamber by mass spectrometer (Marquette RMS M-100, Milwaukee, WI). Heart rate was recorded at the end of each minute by telemetry (Polar). Percent arterial oxyhemoglobin saturation was measured by ear oximetry (Hewlett-Packard 47201A). Data were collected and displayed with the use of a data acquisition control system (Workbench for Windows 2.0, Strawberry Tree) sampling at 40 Hz. Values for arterial oxygen saturation, oxygen uptake, and minute ventilation were averaged over each minute of exercise.
Hematology assessment.
Venous blood was drawn into tubes containing EDTA, with the subject in
the supine position, between 0600 and 0700 on four occasions: 3 days
before the altitude sojourn, after the first night at altitude (20 h),
after 19 days at altitude, and 20 h after return to sea level.
Whole blood was assayed in duplicate for hemoglobin concentration
(Radiometer OSM-3) and hematocrit (spun capillary tubes). Plasma was
then obtained by centrifugation and stored frozen (
80°C) until
assayed. Plasma was assayed by RIA with commercial kits and a gamma
counter (ISODATA 20-20) for ferritin (DSL, Webster, TX),
erythropoietin (DSL), and soluble transferrin receptor concentrations (Orion).
Statistics
Data are presented in the tables as means ± SD. SPSS 6.1 was utilized for statistical calculations. Performance andO2 max were compared by paired
t-test. The hematologic data were compared by one-way ANOVA.
Gender differences were tested by using a two-way ANOVA (altitude × gender). Significance was set at P 
0.05. When a
significant effect was obtained, post hoc analysis was performed with
the Student-Newman-Keuls test to identify differences.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
Fourteen men (25 ± 3 yr, 179 ± 5 cm, 63.6 ± 5.2 kg) and eight women (24 ± 3 yr, 168 ± 5 cm, 53.3 ± 4.9 kg) successfully completed the protocol for a total of 22 complete subjects. Four subjects (three men and one woman) suffered injury (n = 2) or illness (n = 2) during the sojourn that prevented normal training or racing and were not included in the analysis. There were no gender differences with respect to the response to the altitude sojourn; therefore, data for men and women are considered together.Performance
Group 3,000-m performance at sea level was significantly improved after the HiLo treatment (Table 1 and Fig. 2). Men and women improved to similar extents, reducing time trial time by 5.8 s (95% confidence limits 1.8-9.8 s) or 1.1% (95% confidence limits 0.3-1.9%). Three athletes improved their sea level 3,000-m time by as much as 23 s, whereas one athlete ran 18 s slower.
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Maximal Exercise
O2 max was significantly increased
by 3% after the altitude camp (see Fig.
3). Maximal ventilation was also
significantly increased after the altitude camp (Table
2). There was a significant relationship
between the change in O2 max and the
change in maximal minute ventilation (r = 0.67, P = 0.0006). Moreover, there was a less robust but
still statistically significant relationship between the change in
O2 max and the change in 3,000-m running time (r = 0.48, P = 0.02).
Maximal heart rate was unchanged. Arterial oxygen saturation was
reduced to 89 ± 4% during maximal exercise but was unaffected by
the altitude camp. Time to exhaustion on the treadmill was not
significantly different.
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Hematology Assessments
Hemoglobin concentration increased on acute ascent to altitude, remained elevated during the camp, and was significantly elevated on return to sea level (see Table 3). Hematocrit was significantly elevated when measured on the 19th day at altitude and remained significantly elevated on return to sea level. Plasma ferritin concentrations were not significantly altered from the initial value. However, despite oral iron supplementation, there was a trend (P = 0.07) for subsequent values to be lower than the initial value. Plasma erythropoietin concentration doubled after one night at 2,500 m and was not different from baseline after 19 days at the camp. Then plasma erythropoietin levels decreased significantly on return to sea level. Soluble transferrin receptor concentrations were significantly elevated (25%) after 19 days at altitude, consistent with active erythropoiesis (3, 5), and returned to baseline on return to sea level.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The major finding of this study is that, in this group of elite runners, sea level 3,000-m running performance improved significantly in response to a 27-day camp utilizing the HiLo paradigm. In fact, nine athletes recorded personal records at the distance after the HiLo camp, despite having prepared for and competed in national championship events just before the sojourn. The mechanism of the improvement appears to be similar to that previously described in carefully controlled studies of collegiate-level athletes (24) with a stimulation of erythropoiesis leading to an apparent increase in oxygen delivery to peripheral tissues as evidenced by 1) a near doubling of plasma erythropoietin concentration and a 43% reduction in serum ferritin concentration despite oral iron supplementation on acute exposure to altitude, 2) a rise in soluble transferrin receptor concentration with chronic exposure to altitude, and 3) an increase in hemoglobin concentration and hematocrit on return to sea level with a decrease in plasma erythropoietin concentration below original sea level baseline.
Limitations
We must acknowledge that our study suffers from a major limitation shared by most research conducted in elite athletes: namely, the absence of a concurrent control group performing a similar training camp at sea level. Such a control group would be optimal to ensure that the athletes did not improve merely from the result of a training camp per se, rather than living high-training low. A number of lines of evidence, however, suggest that the study design employed in this experiment was sufficient to account for most of this effect. First, in our previous studies (24), which included many years of piloting work, we determined that for collegiate athletes at least 2 wk of controlled training were necessary to overcome the "training camp effect." For example, in one preliminary study of a sea level training camp, six male runners increased theirO2 max from 68 ± 1.5 to 70 ± 1.4 ml · kg1 · min1
after 2 wk of supervised training, but did not increase further after
an additional 2 wk of training (70 ± 1.8 ml · kg1 · min1) (Levine
and Stray-Gundersen, unpublished observations). Thus, for all the 52 male and female athletes studied in our previously published reports
(24, 34), after a 2-wk "lead-in" phase of supervised
training there was no significant increase in
O2 max with an additional 4 wk of
structured training at sea level (64 ± 0.8 to 64 ± 0.8 ml · kg1 · min1). Moreover,
after these 6 wk of sea level training by collegiate athletes in these
studies, there was no further improvement obtained even by an
outstanding training camp environment at sea level for an additional 4 wk (24). In the present study, we considered that the
months of preparation by these elite athletes for their national
championships were at least equivalent to the 2 wk of training applied
to collegiate athletes a number of weeks after their competitive season
for the purpose of minimizing the training camp effect. Additionally,
on review of each athlete's training program leading up to the
championships, all had peaked appropriately for this event. As far as
could be determined from inspection of training logs and individual
meetings with each athlete over the course of the study, no one had a
change in training that could explain an improved performance.
We suspect, but cannot prove, that the athletes were equally motivated to give their best performance in precamp as well as postcamp time performance tests. We can say, however, that these athletes were all extremely competitive, and it was our clinical impression that motivation was high during all study races. Moreover, all the time trials were paced by an experienced pace setter who maintained the same running speed for 4 of 7.5 laps in both the pre- and postcamp trials. Finally, athletes were pushed to exhaustion in all treadmill tests, and there was no evidence from respiratory exchange ratio or heart rate that the athletes gave a better effort on the second test than the first (for example, maximal heart rate was 192 on the first test and 191 on the second test).
We also cannot exclude the possibility that the use of iron supplements to ensure adequate iron availability for erythropoiesis with altitude exposure (24) could have resulted in an increase in hemoglobin concentration independent of an altitude effect. We suspect this possibility is unlikely, however, for the following reasons. 1) None of the athletes in this study was anemic or had small red blood cells typical of iron deficiency anemia. All had normal hemoglobin concentration and hematocrit, and all had normal red cell size and distribution. 2) Despite oral iron supplementation, the iron requirements of altitude exposure were such that bone marrow iron stores as measured by serum ferritin did not increase over the course of the training camp. In fact, ferritin decreased with each longitudinal measurement (Table 3), suggesting that bone marrow iron stores were more rather than less depleted at the end of the altitude camp. 3) The baseline erythropoietin concentrations were normal and low, arguing against a physiologically significant anemia; anemia is the most potent stimulus to synthesis of erythropoietin (20). Thus the available evidence would argue against simple treatment of iron deficiency as the mechanism of the increase in hemoglobin and hematocrit in this study.
Finally, because of time constraints associated with performing the
study in elite athletes during peak competition periods, the subjects
were not as completely characterized, nor were the details of the
training program as rigorously controlled to the same extent as in
previous work (24). However, the same basic training
template was used for the protocol, and key parameters were measured in
both populations, including erythropoietin and hemoglobin
concentrations, O2 max, and time trial
performance, that allowed comparison to our previous studies.
When the results from carefully controlled, comprehensively assessed
studies on collegiate runners are compared with the results of the
present study (see Table 4), the results
are remarkably similar in both direction and magnitude of the effect.
In addition, when similar parameters were measured, the results suggest
that the same mechanism produced the effect, i.e., an increase in
erythropoietin leading to an increase in hemoglobin concentration,
increased O2 max, and increased
performance. Therefore, we believe that the compromises made in this
study to evaluate elite athletes during a time of peak fitness did not
compromise the validity of the results.
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The Unique Model of Elite Athletes
Elite athletes of the animal kingdom provide a unique model of the concept of symmorphosis, whereby the structural design of all components comprising a system is matched quantitatively to functional demand (17). For example, foxes, dogs, and horses have ~2.5 times the mass-specific rate of oxygen consumption compared with sedentary species of the same body size, such as the agouti, goat, or steer. For such animals, the mechanism of this large adaptive range of oxygen consumption appears due to a large mitochondrial volume, matched by a large muscle capillary volume and vascular conductance in skeletal muscle; a higher hemoglobin concentration; and a large maximal stroke volume. The redundancy in the pulmonary system of nonathletic species, manifested by excess ventilatory and diffusing capacity, is nearly eliminated in the athletic species, confirming the principle of symmorphosis. In other words, comparative studies suggest that such "athletes" are operating at or close to the upper limit of their structural capacity for convective transport of oxygen atO2 max.
If this analysis is also relevant for humans, it could be argued that
elite human athletes would have a smaller adaptive capacity for
increasing oxygen transport than less accomplished athletes, such as
those originally reported using the HiLo approach. Although the
amount of published data examining truly elite athletes undergoing altitude training is limited, at least one small study of world-class Australian cyclists, before and after a 31-day altitude camp (2,690 m),
recently reported no changes in hemoglobin mass nor sea level O2 max despite an improvement in
performance (14). The authors suggested that the outcome
was, at least in part, due to limited adaptive reserve in such athletes
(14), particularly in the lung, which is essentially
static to training. For example, elite endurance athletes display
pulmonary gas-exchange limitations at sea level of a greater magnitude
and prevalence than lesser trained individuals, part of which is
accounted for by limitations in ventilation (8). However,
in the present study, we observed an increase in maximal ventilation
that was commensurate with the increase in
O2 max. We cannot determine from the data in this experiment whether the increase in maximal ventilation was
simply a consequence of the increased
O2 max or rather the cause of the
increased O2 max as a function of
increased ventilatory work. An increase in ventilation during exercise
that persists for a period of time after return to sea level would be
an expected result of ventilatory acclimatization to high altitude and
suggests that, at least in these athletes, flow limitation did not
restrict maximal ventilation to a major degree. We speculate that if
the initial increase in O2 max was, at
least in part, required to support an increase in ventilatory work from altitude acclimatization, then the restoration of normal respiratory control over time after return to sea level would allow the increased oxygen transport capacity to be directed to working skeletal muscle, thus providing an explanation for the oft-cited observation
(9) that many athletes achieve their best performances
after a period of reacclimatization to sea level. Further study will be
necessary to confirm or exclude this hypothesis.
A more detailed analysis of human vs. nonhuman athletes suggests, in
fact, that the most likely avenue for elite human athletes to improve
oxygen transport would be to raise their red cell mass and circulating
hemoglobin concentration. In human athletes, red cell mass is the one
component of the oxygen cascade that does not increase to the level
observed in "elite athletes" of the animal kingdom. Humans do not
clearly autotransfuse by splenic contraction at the onset of exercise
like horses (25) and dogs (23). This effect
raises exercise hematocrit well into the 50s in those species. Thus,
when the oxygen-carrying capacity of the blood is increased in elite
athletes, either by acute red blood cell infusion (5, 10,
37) or by chronic administration of recombinant human
erythropoietin (3, 4),
O2 max increases. The results shown in
the present study are in the same direction as and half the magnitude
of the results obtained by either an acute (transfusion) or chronic
increase in red cell mass (exogenous rhEPO administration). At least
one uncontrolled study has suggested altitude-induced improvements in
O2 max in undeniably elite athletes
(7). One of these subjects (JR) went on to set a world
record after living at altitude and training intermittently at sea level.
Some investigators, failing to observe an increase in hemoglobin/myoglobin mass after brief periods of time in normobaric hypoxic environments (8-10 h/night for 10 days to 3 wk), have questioned the erythropoietic effect of moderate altitude exposure (1, 2). However, the evidence in favor of such an altitude-mediated erythropoiesis is quite compelling. Cross-sectional studies in the Peruvian Andes (19, 28, 32) as well as in the Colorado Rockies (36) have demonstrated clearly that there is an elevated red cell mass in natives of high altitude that is proportional to the oxyhemoglobin saturation (19, 36).
Moreover, when sea level natives ascend acutely to altitude, there is an increase in iron turnover by more than twofold that begins within the first few hours of exposure and peaks by ~2-3 wk (12, 18, 28). Direct examination of the bone marrow during acute high-altitude exposure has documented a dramatic increase in nucleated red blood cells, virtually doubling by 7 days, indicative of accelerated erythropoiesis (18, 28). Although most of these data are from altitudes higher than the 2,500 m studied in the present experiment, our elite endurance athletes spent significant time exercising at low-moderate altitudes, which causes further arterial desaturation (8), suggesting that athletes may have a greater stimulation of erythropoiesis for the same altitude than a more sedentary population.
As in the present study with elite athletes, previous studies have also shown that both iron turnover (18, 28) as well as erythropoietin concentrations (6, 15, 20, 24, 30) return to sea level values relatively rapidly during chronic altitude exposure. Nevertheless, the red cell mass continues to increase for up to 8 mo of chronic altitude exposure, at least at altitudes above 4,000 m (28), suggesting that this level of stimulated erythropoiesis is elevated for the absolute level of the arterial oxygen content. Thus when altitude natives or altitude sojourners return to sea level, there is a suppression of erythropoietin (6, 12, 15, 20, 24, 30), a reduction in iron turnover and bone marrow production of erythroid cell lines (18, 28), and a decrease in red cell survival time (28, 29). The change in the ratio of hemoglobin concentration to erythropoietin concentration over the time course of the present study (decrease with acute exposure, increase during chronic exposure, and further increase on return to sea level) is further evidence for the stimulation of erythropoiesis on ascent and deceleration of the erythropoiesis on return to sea level in these athletes following the living high-training low model of altitude training.
Many other factors exist, however, that may compromise the ability of small studies to document clearly an increase in red cell mass with moderate altitude exposure, and that may have led to divergent results with different groups of elite athletes. Duration of altitude exposure, in terms of both time/day at altitude and number of weeks, may play an important effect: studies employing 8-10 h hypoxia/day have not been effective (1, 2), whereas those employing 16 h hypoxia/day have shown an increased in hemoglobin/myoglobin mass using the same methods (31). Inflammatory cytokines (e.g., IL-1) also may limit the increase in erythropoietin in response to hypoxia (11, 13, 21), suggesting that the presence of injury or infection could impair the erythropoietic response to altitude.
There is also a marked individual variability in the response to altitude training. We have previously reported that, even with the optimal method of HiLo or HiHiLo training, only slightly more than 50% of athletes will be robust responders (i.e., improvement by more than the group mean) to altitude, in part because of a prominent and sustained increase in erythropoietin at altitude leading to an increase in red cell mass (6). Although the genetic mechanisms responsible for determining the erythropoietic response to hypoxia in humans have not been entirely worked out, animal models suggest that this response may be transcriptionally regulated (26). Moreover, at least some individuals have genetic polymorphisms in the erythropoietin gene (33) or the erythropoietin receptor (27) that may profoundly influence the erythropoietic response to hypoxia (22). It is possible, therefore, particularly in studies with relatively small sample sizes, that the presence of significant numbers of nonresponders could bias the study outcome in favor of no detectable response.
Practical Implications for Performance of Elite Athletes
In previous work examining collegiate athletes (6, 24), we identified a 1.4% improvement in 5,000-m performance, a 2.5 ± 2.4 ml · kg1 · min1 improvement
in O2 max, and a 1.1 ± 0.7 g/dl
increase in hemoglobin concentration after 4 wk at 2,500 m. In this
study, we obtained a 1.1% improvement in 3,000 m performance, a
2.3 ± 2.6 ml · kg1 · min1 improvement
in O2 max, and a 1.0 ± 1.1 g/dl in hemoglobin concentration in elite runners. When all the
athletes who have completed a HiLo or HiHiLo camp in our studies are
examined together, there is no influence of performance ability on the
response to such altitude training (Fig.
4).
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Figure 4 also demonstrates that, although substantial individual variability remains within all athletes, the variation is smaller for the elite subjects. Thus the coefficient of variation for the collegiate athletes was 3.3%, whereas that for the elite athletes was just over half as great, or 1.9%. Because of this reduced variability, the percent improvement, expressed as a fraction of the variation within the elite population, is 0.58, well within the criteria of 0.5-0.7 recently recommended for the identification of a "worthwhile" enhancement of performance for elite athletes (16). Although a 1.1% improvement in performance may not seem like a large effect, at an elite level in sports, races are won or lost by small fractions of a percent. Thus the benefit of a HiLo or HiHiLo altitude training camp has the potential to substantially improve race outcome for individual elite athletes.
In conclusion, despite having prepared for and competed in national championship events, elite runners improved sea level running performance by 1.1% (95% confidence limits 0.3-1.9%) after 27 days of living at moderate altitude (2,500 m) and performing high-intensity training at low altitude (1,250 m). Data collected indicate that the magnitude and mechanism of the effect are similar to those obtained in collegiate runners undergoing the same experimental paradigm. The mechanism involves expansion of the red cell mass and an increase in circulating hemoglobin levels, accompanied by maintenance of oxygen flux to working muscle. Thus the HiLo training approach is effective in improving sea level running performance ranging from 50 to 90% of the world record in events lasting from ~7 to 20 min. We believe that this paradigm can be used to enhance sea level performances that are dependent on high levels of oxygen transport.
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ACKNOWLEDGEMENTS |
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This project involved the coordinated support and effort of many people and several organizations. We thank the athletes who participated in the project. We also thank all the people who helped to bring about this experiment, including the speakers, the Department of Health Science, Indiana University, the track coaching staff at Indiana University, and the staff and volunteers of USA Track and Field and the US Olympic Committee. Particular thanks go to Drs. Harmon Brown, David Martin, Jay T. Kearney, and Martha Ludwig for tireless support and perseverance. A special note of gratitude and appreciation goes to Greg Harger for all of his work on this project.
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FOOTNOTES |
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Address for reprint requests and other correspondence: B. D. Levine, Institute for Exercise and Environmental Medicine, 7232 Greenville Ave., Suite 435, Dallas, TX 75231 (E-mail: benjaminlevine{at}texashealth.org).
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. Section 1734 solely to indicate this fact.
Received 20 July 2000; accepted in final form 17 May 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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