Journal of Applied Physiology AJP: Endocrinology and Metabolism
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J Appl Physiol 104: 328-337, 2008. First published November 29, 2007; doi:10.1152/japplphysiol.01324.2006
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The effect of intermittent hypobaric hypoxic exposure and sea level training on submaximal economy in well-trained swimmers and runners

Martin J. Truijens,4 Ferran A. Rodríguez,2 Nathan E. Townsend,3 James Stray-Gundersen,1 Christopher J. Gore,5,6 and Benjamin D. Levine1

1Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas and University of Texas Southwestern Medical Center at Dallas, Dallas, Texas; 2Institut Nacional d'Educació Física de Catalunya, Universitat de Barcelona, Spain; 3New South Wales Institute of Sport, Sydney, Australia; 4Faculty of Human Movement Sciences, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands; 5Australian Institute of Sport, Canberra; and 6Exercise Physiology Laboratory, School of Education, Flinders University, Adelaide, Australia

Submitted 21 November 2006 ; accepted in final form 19 November 2007


    ABSTRACT
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
To evaluate the effect of intermittent hypobaric hypoxia combined with sea level training on exercise economy, 23 well-trained athletes (13 swimmers, 10 runners) were assigned to either hypobaric hypoxia (simulated altitude of 4,000–5,500 m) or normobaric normoxia (0–500 m) in a randomized, double-blind design. Both groups rested in a hypobaric chamber 3 h/day, 5 days/wk for 4 wk. Submaximal economy was measured twice before (Pre) and after (Post) the treatment period using sport-specific protocols. Economy was estimated both from the relationship between oxygen uptake (VO2) and speed, and from the absolute VO2 at each speed using sport-specific protocols. VO2 was measured during the last 60 s of each (3–4 min) stage using Douglas bags. Ventilation (VE), heart rate (HR), and capillary lactate concentration ([La]) were measured during each stage. Velocity at maximal VO2 (velocity at vO2max) was used as a functional indicator of changes in economy. The average VO2 for a given speed of the Pre values was used for Post test comparison using a two-way, repeated-measures ANOVA. Typical error of measurement of VO2 was 4.7% (95% confidence limits 3.6–7.1), 3.6% (2.8–5.4), and 4.2% (3.2–6.9) for speeds 1, 2, and 3, respectively. There was no change in economy within or between groups (ANOVA interaction P = 0.28, P = 0.23, and P = 0.93 for speeds 1, 2, and 3). No differences in submaximal HR, [La], VE, or velocity at VO2max were found between groups. It is concluded that 4 wk of intermittent hypobaric hypoxia did not improve submaximal economy in this group of well-trained athletes.

altitude; running; swimming


THE APPLICATION of severe (~4,000- to 5,500-m altitude or its equivalent) hypobaric or normobaric hypoxia at rest for short periods of time (1.5–5 h/day for 2–3 wk), so-called "intermittent hypoxic exposure" (IHE), has been proposed as a time-efficient variant (39) of the "live high-train low" (LHTL) altitude training strategy (5, 15, 45). The ultimate goal of this method is to induce sufficient altitude acclimatization to improve both altitude and sea level performance. At present there is intense controversy regarding the physiological mechanisms that may underlie the observed improvements in sea level performance that have been associated with these and other altitude training approaches (9, 26). Both accelerated erythropoiesis (25, 42, 45, 50) as well as enhancements in submaximal economy (8, 12, 21, 22, 43) have been proposed as mechanisms contributing to the improvement.

Whether exercise economy (defined as a reduced oxygen uptake during submaximal exercise) changes after acclimatization to high altitude is controversial. Although the majority of early data in the literature suggested that economy did not change (23, 29, 36, 51), a few recent studies have raised the possibility of small, but physiologically important, improvements after a mountaineering expedition (13) or short-term normobaric hypoxia (8, 21, 22, 32, 43). Furthermore, cross-sectional studies of high-altitude natives have suggested that they may have improved energy efficiency compared with sea level natives (18, 30). However, such cross-sectional analysis is confounded by inevitable differences between populations in nutrition, body composition, physical fitness, and socioeconomic factors that may complicate data interpretation. Moreover, reports of improved economy in high-altitude natives are inconsistent (3, 6, 18, 49), and longitudinal studies in athletes also do not consistently observe improved economy even within the same laboratory and experimental paradigm (5, 8, 43, 46). A recent exhaustive review and report of data from multiple different laboratories has cast doubt on the concept that full-time acclimatization to natural altitude may improve exercise economy (27), although relatively large measurement error may obscure small but real differences. Whether shorter duration exposures to high altitude interspersed with periods of sea level normoxia could have a different effect from more sustained altitude exposure is less clear, and this question has never been addressed in a randomized, double-blind design.

Therefore the purpose of this study was to test the hypothesis that resting exposure to severe intermittent hypobaric hypoxia improves whole body submaximal economy in competitive athletes. Using matched pairs of subjects in a double-blind, randomized design, the present study brought together representative researchers who have argued opposite sides of this contentious debate (9, 26) to investigate the effects of hypobaric IHE (3 h/day, 5 days/wk, for 4 wk) combined with sea level training on whole body submaximal economy and related variables such as velocity at maximal oxygen uptake (velocity at VO2max), which is a performance-based expression of changes in economy for endurance athletes. To enhance the external validity of the study and improve generalization of the results, a very inefficient form of human locomotion, swimming, and a relatively efficient form of human locomotion, running, were examined.


    METHODS
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects

Twenty-eight athletes (13 runners and 15 swimmers; age 22.5 ± 8.1 yr, body mass 67.0 ± 11.9 kg) of both sexes (17 men and 11 women) were recruited from mostly local and regional high school, collegiate, and masters swimming and running teams [see Table 1; for further details with regard to subject characteristics, the reader is referred to Rodriguez et al. (40)]. Three male subjects were excluded from the study before the intervention period due to incompatibility with their training and working schedules; two other male subjects dropped out within the first 2 wk of the intervention. Thus twenty-three subjects, 12 men and 11 women, successfully completed the intervention protocol and testing and were used for data analysis. However, two subjects were unable to complete the second set of posttesting for logistical reasons.


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Table 1. Subject characteristics and performance level

 
All subjects were sea level residents and gave their voluntary written informed consent to a protocol approved by the Institutional Review Boards of the University of Texas Southwestern Medical Center and Presbyterian Hospital of Dallas.

Study Design

To obtain familiarization with all testing equipment and determine test-retest reliability, all baseline measurements were conducted twice by each subject (Pre1 was conducted ~3 wk and Pre2 ~2 wk before the start of the intervention). Subjects were matched for sport, sex, time trial performance, and training history into pairs and assigned to either the placebo control (Normoxia: 0–500 m) or the experimental (Hypoxia: 4,000–5,500 m) group by balanced, stratified randomization. By this technique, within each matched pair, there was a 50–50 chance of being assigned to the control or experimental group. All measurements were repeated twice after the intervention period (Post1 was conducted within the 1st week and Post2 in the 3rd week after the intervention). This way both the immediate effects of IHE as well as the off (recovery) response of these effects could be evaluated.

Hypobaric Chamber Exposure

The hypobaric chamber located at the Institute for Exercise and Environmental Medicine, Dallas, Texas, consists of two halves that can be operated independently and controlled for simulated altitude and rate of ascent/descent. Four chamber runs per day were scheduled to accommodate the living and training schedules of all subjects.

All subjects rested in the chamber for 3 h/day, 5 days/wk (from Monday to Friday), for four consecutive weeks. The Hypoxia group was exposed to a barometric pressure corresponding to a simulated altitude from 4,000 up to 5,500 m according to the following schedule: 4,000 m (chamber sessions 1–2), 4,500 m (sessions 3–4), 5,000 m (sessions 5–6), and 5,500 (sessions 7–20). In the first 7 min of each chamber session, the chamber was repeatedly compressed and decompressed to no higher than 3,500 m for both groups in an attempt to blind the subjects to their treatment with the Normoxia group spending the remaining 2 h 53 min at a pressure equivalent to 500 m. Moreover, no member of the research team was aware of the blinding code until all the data were analyzed.

At the end of the study each subject was asked to guess which intervention they received and to indicate the certainty of that guess (certain; not sure; no idea) to determine the effectiveness of the double-blind design.

To avoid iron depletion during the experiment, all subjects received oral liquid iron supplementation (Feo-Sol, 9 mg elemental iron/ml) with the dose (ranging from 5 to 15 ml, 1–3 times/day) adjusted based on their preintervention plasma ferritin concentration. Iron supplementation started 2 wk before the start of the intervention.

Training

Individualized training plans were developed by the athlete and his or her coach. Training corresponded to the competitive season for the swimmers and the postcompetitive season for the runners. Careful matching of subjects resulted in matched pairs that were mostly members of the same team. This way, substantial differences in training programs between groups could be minimized. Besides, each athlete kept a detailed training log that included duration, volume, and intensity of each workout (estimated using a 20-point Borg scale), so that differences in training programs could be identified.

Evaluation of Performance

Running and swimming performance at sea level was measured both in the field (time trials on the track or in the swimming pool) and in the laboratory (VO2max testing on a treadmill or in a swimming flume). A detailed description of the measurement methods is reported elsewhere (40).

Laboratory Testing

To evaluate the possibility of an erythropoietic effect of IHE, hemoglobin mass (Hbmass), red blood cell volume (RCV), erythropoietin (EPO), and soluble transferrin receptor concentrations, as well as several hematological indexes, were measured both before and after the intervention period. A detailed description of the measurement methods and the results of these studies are reported elsewhere (10).

Submaximal Economy

Submaximal economy was determined using two separate methods. To allow for a group comparison irrespective of sport, economy was evaluated as the oxygen uptake (l/min) at a certain speed. However, to allow for an estimation of overall economy and make predictions of velocity at VO2max, economy was also determined as the slope of the linear regression between oxygen uptake and speed according to a sport-specific protocol described in detail below.

During this test oxygen uptake was measured simultaneously with the Douglas bag technique and an online system for breath-by-breath measurements. Vinyl Douglas bags (~200-liter capacity) were considered as the criterion for all oxygen uptake measurements. Breath-by-breath data served as back up and were used for identification of steady states and plateaus. The online system for breath-by-breath measurements consisted of four, one-way valves (Hans Rudolph, 2700 series, Hans Rudolph, Kansas City, MO) to direct flow, two sample lines for measuring gas fractions, and a turbine flowmeter (VMM, Interface Associates) for measuring ventilation. Breath-by-breath data were stored on a computer and analyzed using customized software. The Douglas bag gas fractions were analyzed by one of two mass spectrometers (Marquette MGA 1100) that were calibrated twice a day with two of four alpha standard (Puritan Bennett, Pleasanton, CA; ±0.02% accuracy) gases and confirmed before each test. The two mass spectrometers were used for both Douglas bags and the breath-by-breath system, with one system dedicated to measuring the runners and one for the swimmers. Ventilatory volume was measured with one of two 120-liter Tissot spirometers, one dedicated to the measures for running and the other for swimming. In addition, heart rate was monitored continuously (Polar CIC, Port Washington NY).

Running.   Submaximal economy during flat treadmill running was estimated from the relationship between VO2 and treadmill speed during three, 4-min submaximal runs at 8, 10, and 12 mph for men, and 8, 9, and 10 mph for women (2 female runners, 1 from each group, ran at 7, 8, and 9 mph) at intensities ranging from 40 to 80% VO2max. VO2 at each level was measured from a 1-min Douglas bag obtained from the third to fourth minute. Running economy was defined as the slope of the linear regression relating VO2 to treadmill speed. Pulmonary ventilation (VE), heart rate, and capillary lactate were measured during each stage.

Swimming.   Swimming economy was determined by measuring oxygen uptake at three, 3-min submaximal swimming speeds (1.1, 1.2 and 1.3 m/s for men, and 1.0, 1.1 and 1.2 m/s for women) at intensities ranging from 40 to 80% VO2max, ensuring that subjects swam within the range of aerobic performance and were able to maintain normal swimming technique even at the lowest velocity. During this test the swimmers wore a specially designed respiratory valve that fixed the inspiratory and expiratory tubes vertically parallel. The valves in the inspiratory and expiratory tubing were placed in an extension of the mouthpiece ensuring a minimal "dead space" of 30 ml (47). Each of the three submaximal swims was used to obtain a measure of the metabolic power output (Pmet) that is required to swim at a certain velocity, according to the following equation (48)

Formula 1(1)
where Pmet is metabolic power output (W), RER is respiratory exchange ratio, and Formula 1O2 is oxygen uptake at minute 2 to 3. Swimming economy was then calculated from the estimated Pmet corresponding to each speed related to velocity cubed (for additional details, see Ref. 48). Formula 1E and heart rate were measured during each stage, and capillary blood lactate was measured after the fastest submaximal speed only.

Velocity at Formula 1O2max

Velocity at Formula 1O2max was calculated by identifying the speed that would elicit Formula 1O2max, on the basis of the economy regression equation and Formula 1O2max [for a detailed description of the assessment of Formula 1O2max, the reader is referred to Rodriguez et al. (40)].

Statistics

Duplicate baseline measurements were used to calculate the typical error of measurement (TEM = SD of differences/

Formula 1
), expressed as a coefficient of variation. For statistical comparison the "Best" Pre test score was used for all effort dependent performance markers, and the "Average" Pre test score was used for all other parameters. Data analysis was complicated by the fact that two subjects were unable to complete the Post2 tests for logistical reasons. Therefore the change from preintervention to the first week after the intervention (Pre to Post1) was used as the primary statistical comparison with the most statistical power to determine the effectiveness of the intermittent hypoxia exposure. Because of the small subject number, the investigators elected not to use a general linear model, or impute data for these missing values at the Post2 time point in the primary comparison. To assess the effect of persistence of the primary effect over time, a comparison among all time points (Pre, Post1, and Post2) was performed with the two placebo subjects having missing data substituted by means of the mean substitution method to retain statistical power. A two-way, repeated-measures ANOVA with main effects of time (Pre, Post1; or Pre, Post1, Post2) and treatment (Hypoxia vs. Normoxia) was used for analysis using SigmaStat 3.0 (SPSS); in addition, a three-way ANOVA (time vs. treatment vs. sport) was used to assess the effect of swimming vs. running on the response to IHE. Where a significant effect was obtained, a post hoc pairwise multiple comparison analysis was performed with the Tukey test to identify differences.

Unless otherwise specified, data are presented as means ± SD.


    RESULTS
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects and Chamber Exposure

The subject characteristics are contained in Table 1. No changes in body mass or percent body fat were observed over the time span of the study. Subjects completed 94% of the chamber sessions with an average number of sessions missed of 1.1 ± 1.5 of 20, with no difference between groups (P = 0.46). By the end of the study, 91% of all subjects were able to guess correctly in which group they were included. However, only 50% were certain about their guess (chi square P = 0.84 by Fisher's exact test for the difference between groups).

Training

Training was closely matched among the groups as determined from the training log information regarding distance, duration, and estimated intensity of the training.

The training logs also made clear that the swimmers started a progressive taper period toward the end of the intervention period that continued in the period between the first and second Post test. This period aimed at performance improvement and was characterized by a marked decrease in training distance (Hypoxia –24%, Normoxia –22% from the average training distance of intervention period to the second Post test).

Reliability of Measurements

Repeated baseline measures of submaximal economy, HR, and ventilatory values are shown in Table 2; TEM is indicated as well. At the start of the intervention period there were no significant differences between the groups in any of these variables (see Table 2). TEM values for submaximal Formula 1O2 for running were ≤3.0%, which is similar to that reported by others in whose laboratories changes in running economy have been observed after IHE (11). TEM values for swimming were somewhat higher, with all values ≤5.5%. However, no standards for TEM of submaximal Formula 1O2 in swimming could be found in the literature. Considering the relationship between power output and speed in swimming (PO ~ v3) and the accuracy of the swimming flume, the values reported in this study seem to be well within the limits of acceptability.


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Table 2. Reliability of measurements from double baseline measures (Pre1, Pre2)

 
Submaximal Economy

There was no significant change in submaximal economy between groups from Pre to Post1 or from Post1 to Post2 (ANOVA interaction P = 0.28, P = 0.23, and P = 0.93 for submaximal level 1, 2, and 3, respectively) (see Table 3 and Fig. 1). This result was found irrespective of the method used to determine submaximal economy [P = 0.21 for the "slope method" (see also Fig. 2) ] or type of sport (3-way ANOVA interaction P = 0.53). All individual relationships between submaximal Formula 1O2 and swimming velocity cubed, as well as between submaximal Formula 1O2 and running speed, were highly linear [swimming: r2 = 0.97 (±0.04); running: r2 = 1.00 (±0.0)].


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Table 3. Submaximal performance indexes, Formula 1O2max, and derived variables before and after the intervention

 

Figure 1
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Fig. 1. Individual and mean data for oxygen uptake in l/min for submaximal work load 1, 2, and 3 for hypobaric hypoxia (Hypo) (A, B, C) and normoxia (Norm) (D, E, F). Open symbols, swimmers; filled symbols, runners.

 

Figure 2
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Fig. 2. Individual and mean economy slopes for Hypo (A1 and A2) and Norm (B1 and B2) before the intervention period (Pre) and after the intervention period [postintervention test 1 (Post1) and test 2 (Post2)]. Gray lines are individual linear regression lines. Gray symbols are individual data points. For each subject similar line structures and symbols were used Pre and Post. Moreover, similar symbols and line structures were used for matched pairs of subjects. Black solid line, average linear regression line. Black symbols and error bars, mean data points and SD. Formula 1O2, oxygen uptake; Po, power output.

 
There were no significant differences within or between groups in submaximal heart rate or capillary lactate concentration at any of the submaximal speeds considered (see Table 3). Formula 1E increased in both groups (Hypoxia 6.5% and 5.2%, Normoxia 5.2% and 5.7% for Pre vs. Post1 and Post2 comparison, respectively). No differences between groups were found at Pre, Post1, and Post2 (P = 0.72, P = 0.84, and P = 0.87, respectively).

Velocity at Formula 1O2max

Velocity at Formula 1O2max did not change significantly within (P = 0.44) or between groups (P = 0.38).

Brief Summary of Results Published Elsewhere in Companion Manuscripts

Time-trial performance did not improve in either the Hypoxia or Normoxia group [F1–19 = 1.66, P = 0.20, Hypoxia +2.6% (0.9–4.3); Normoxia +1.3% (0.3–2.2)]. Also, we could not detect a significant difference between groups for a change in Formula 1O2max [Hypoxia +0.01 l/min (–0.10 to 0.12); Normoxia –0.07 l/min (–0.15 to 0.00)], maximal Formula 1E, maximal HR, or Formula 1O2 at ventilatory threshold at any time point after the intervention (group x test interaction P = 0.31, 0.24, 0.26, 0.12, respectively) (40).

Gore et al. (10) reported that despite a significant increase in serum EPO concentration in the Hypoxia group 3 h following the hypoxic exposure, no changes indicative of accelerated erythropoiesis could be observed at any time. The mean change in RCV from Pre to Post for the Hypoxia group was 2.3% (95% confidence limits = –4.8 to 9.5%) and for the Normoxia group was –0.2% (–5.7 to 5.3%). The corresponding changes in Hbmass were 1.0% (–1.3 to 3.3%) for Hypoxia and –0.3% (–2.6 to 3.1%) for Normoxia. No changes in soluble transferrin receptor concentrations or reticulocyte parameters measured with flow cytometry were observed in either group.


    DISCUSSION
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
The present study showed that short-term hypobaric IHE (4,000–5,500 m, 3 h/day, 5 days/wk, for 4 wk) did not improve submaximal economy in well-trained runners and swimmers when measured at sea level. This conclusion is strengthened by the carefully matched groups containing well-trained athletes and the randomized, double-blind, placebo-controlled nature of the intervention.

Previous Work on IHE in Athletes

The few studies on IHE in athletes reported in the literature show conflicting evidence for the effects of IHE on submaximal economy. For example, Katayama et al. (21) reported improved running economy and lower HRs during submaximal exercise after an IHE protocol consisting of 90 min/day, 3 days/wk for 3 wk at ~4,500 m. Moreover, it was calculated that the improvement in submaximal running economy accounted for 37% of the observed improvement in 3,000-m run time (~1.3%). Unfortunately, in this study economy was calculated from non-steady-state Formula 1O2 measurements; therefore another study was conducted by the same research group. Again, it was reported that intermittent exposure [12.3% O2 (~4,200 m) for 3 h daily for 14 consecutive days] led to an improvement in submaximal running economy (22). These findings are consistent with the LHTL (hypoxic exposure 9–12 h/day) studies conducted by Gore et al. (8), involving 23 nights exposure to 3,000-m simulated altitude, and Saunders et al. (43), 20 nights exposure to 2,000- to 3,100-m simulated altitude.

In contrast to these investigations, the results of the present study did not demonstrate improved economy after IHE, which is in accordance with the LHTL studies of Levine and Stray-Gundersen (25), Stray-Gunderson et al. (45), and Piehl Aulin et al. (35), as well as other studies by the same group of Australian investigators (5, 46). Moreover, using a substantially different protocol of IHE, 5:5-min hypoxic:normoxic ratio for 70 min, 5 times/wk, for 4 wk, Julian et al. (20) were unable to demonstrate any effect on submaximal economy. What could be the explanation for these discrepancies?

As noted elsewhere (27) in one of the Katayama studies (21), the average oxygen requirements for a given work rate before altitude exposure were very high in the hypoxic group. After exposure, the hypoxia group had more typical and appropriate values for these work loads, which were virtually identical to those of the control group both before and after the intervention. Unfortunately, we can only speculate about the reasons for the unusually high submaximal Formula 1O2 values observed in the hypoxic group before the intervention. However, it is possible that the hypoxic group contained less well-trained subjects who became trained over the course of the intervention period, possibly stimulated by their training camp exposure. It also is well known that training itself can lead to improvements in economy (7) in part due to the change in relative work rates after training and might explain the observed changes in economy. The same argument, however, cannot be made regarding the study conducted by Gore et al. (8), because the small (3–4%) reduction in submaximal Formula 1O2 at the same absolute work loads occurred in the face of a 4–7% reduction in Formula 1O2max. Recently, the same research group published another study in which training was carefully controlled (43). Submaximal Formula 1O2 was reduced by ~3% at each of 14, 16, and 18 km/h after 3 wk of living high (2,000–3,000 m)-training low (600 m); when the absolute Formula 1O2 was averaged across all three running speeds, this change (3.4%) was statistically significant. When this approach was also applied to the data of the present study, the results remained the same, i.e., no change in economy was observed [combined Formula 1O2 (l/min) for speeds 1, 2, and 3: 2.70 (±0.61), 2.77 (±0.66), and 2.74 (±0.66) for Pre, Post1, and Post2, respectively; ANOVA interaction P = 0.30]. Overall, it appears that the magnitude of the reduction in Formula 1O2 at a given work load after various hypoxia exposures, if present, is small (~3%) and inconsistent (5, 8, 13, 20, 21, 25) and may be confounded by other effects such as training (7, 34).

In the present study, not only was there no reduction in oxygen uptake observed during submaximal exercise, but no secondary indications of improved economy were found based on changes in [La–], RER, or ventilatory equivalents (Formula 1E/Formula 1O2 and Formula 1E/Formula 1CO2). These results are in accordance with Katayama et al. (21, 22) and the LHTL studies of Gore et al. (8) and Saunders et al. (43). In contrast, in a study with six elite climbers, Casas et al. (4) reported a right shift of the lactate-work load curve and improvements in ventilatory threshold after an IHE protocol of 3–5 h/day at 4,000–5,500 m for 17 consecutive days. However, these results should be interpreted with caution, since only six subjects participated in the study and no control group was included. Moreover, in this study each hour of hypoxic exposure was combined with 15 min of nonspecific low-intensity cycling exercise.

One key difference between the present study and some of the previous studies of the effects of IHE on exercise economy that might contribute to the differences in results could be the method of application of the hypoxic stimulus. For example, both Katayama et al. (21, 22) and Gore and colleagues (8, 43) used normobaric hypoxia, whereas in the present study the hypoxic stimulus was created by lowering the barometric pressure. Detailed animal studies have demonstrated a greater degree of hypoxemia and pulmonary hypertension, as well as exaggerated increases in lung lymph flow, in sheep exposed to hypobaric compared with normobaric hypoxia (24). More recently, in humans Savourey et al. (44) observed a greater breathing frequency, a lower tidal volume, and lower minute ventilation in hypobaric hypoxia compared with normobaric hypoxia, suggesting an increase of dead space ventilation, leading to greater hypoxemia, hypocapnia, blood alkalosis, and a lower arterial oxygen saturation. These results suggest that, if anything, hypobaric hypoxia would increase the severity of the hypoxic stimulus compared with normobaric hypoxia and therefore should enhance rather than reduce the effects of a hypoxic intervention. However, it is unclear how these differences would translate to differences in whole body economy under sea level conditions. The mechanisms behind these differences need further investigation.

Mechanisms of Improvement in Economy With Altitude Exposure

One of the challenges in interpreting studies of IHE on economy is the lack of obvious biological stimulus to skeletal muscle substrate utilization during exercise under normoxic conditions when the athletes are exposed to short periods of systemic hypoxia at rest. Under resting conditions, the metabolic rate of skeletal muscle is quite low, and the vasodilator reserve is quite large, with careful matching of oxygen delivery to metabolic demand (37, 41).

Since exercise economy is defined by the amount of energy that is necessary to perform at a certain absolute work load, for improvements in economy to occur alterations in energy metabolism must be hypothesized.

Carbohydrates are a more efficient fuel, in terms of the generation of ATP per mole O2 consumed (17), than fats. Some studies have shown an increased preference for carbohydrates over fats in oxidative phosphorylation with full-time altitude acclimatization involving living and exercising as well as resting at high altitude (1, 18, 38). However, interpretation of these studies and indeed all studies of economy at altitude are complicated by the critical importance of relative exercise intensity in determining substrate utilization. For example, it is widely appreciated that the relative importance of carbohydrates increases progressively with exercise intensity (2). In most altitude studies, however, measurements were conducted at the same absolute work load at sea level, acute hypoxia, and after acclimatization (1, 38, 53). This approach is generally taken to ensure that the metabolic demand of exercise remains the same under all conditions. However, since Formula 1O2max decreases at altitude, acclimated and control groups were compared at different percentages of their Formula 1O2max. Therefore, the increased reliance on carbohydrates during exercise reported with altitude acclimatization could well be related to the higher relative exercise intensity and might not be a specific effect of acclimatization (28). Both McClelland et al. (31), working with a whole animal model involving Wistar rats, as well as Ou and Leiter (33) using homogenized muscle, have demonstrated quite convincingly that neither substrate utilization nor muscle glycolytic function is altered by very-high-altitude exposure.

Despite the conflicting results at the level of metabolic substrates, there is substantial consistency in data collected at a regional muscle or systemic level (27), albeit some of the groups studied exhibited mean changes in economy that were approximately >10%, which were not statistically significant. In general, submaximal whole body Formula 1O2 is unchanged after chronic exposure to altitudes up to 4,300 m (28, 52). At higher altitudes, the data seem a bit more divided. Green et al. (14) found improved economy and mechanical efficiency in five untrained mountaineers retested at sea level after a 3-wk expedition to Mt. Denali (6,189 m) and related these changes to a downregulation in muscle Na+-K+-ATPase (12). However, most other studies reported no change in submaximal Formula 1O2 after altitude acclimatization when measured at sea level (16, 23), and changes in Na+-K+ ATPase have not been observed at lower altitudes (19). Moreover, there seems to be no clear evidence for higher work efficiency in high-altitude natives compared with sea level natives (3, 30) although such comparisons are often complicated by the marked racial, cultural, and socioeconomic differences between the studied populations (27).

Limitations of the Present Study

A limitation of the present study that could have disguised a change in economy was that no measurements were conducted within the first 24–48 h after the intervention. However, other investigators who have reported changes in economy following altitude exposure have made measurements well within this time frame (5, 8, 22, 43). Nevertheless, it is unlikely that any change in economy that is so evanescent that it disappears by 72 h would be of much benefit for sea level performance of competitive athletes.

Since the primary hypothesis of the present study centered on sea level performance and subjects performed no exercise under hypoxic conditions, no measurements were conducted at altitude and thus no conclusion can be drawn regarding the effects of IHE on economy at altitude.

Last, although statistically nonsignificant, we realize that some of the differences in training volume between groups could be interpreted as important. The primary reason for this impression is the low statistical power due to substantial missing data for the training logs. However, we should emphasize that as a result of the balanced randomization design, matched subjects were usually members of the same team and therefore trained according to virtually identical training schedules. Therefore, we feel confident that the training logs with sufficient detail for analysis were indeed representative, and the training was quite similar between groups.

Conclusions

We conclude that 3 h of hypobaric hypoxia equivalent to an altitude of 4,000–5,500 m for 5 days/wk for 4 wk is insufficient to alter submaximal exercise economy in a diverse group of well-trained athletes.


    GRANTS
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
This project was supported by the United States Olympic Committee, the Australian Institute of Sport, American College of Sports Medicine, Institut Nacional d'Educacio Fisica de Catalunya Barcelona-UB/GenCat, Ditmerfonds, and IEEM.


    ACKNOWLEDGMENTS
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
This project involved the coordinated support and effort of many people and several organizations. We thank the athletes who participated in the project; Dean Palmer and Sarah Witkowski for efforts in preparation of this study; Dak Quarles for excellent technical support; Dean Palmer, Sarah Witkowski, Emily Martini, and the summer students Alicia Jones, Chris Salamasick, and Chip Bond, for their great support during the experiments. Particular thanks goes to the hypobaric chamber staff (Leo Murray, Tami Poli, Adam Mottley, Virginia Adams, Linda Lautenschlager, and Wayne Plunkett) for taking care of the athletes during the chamber sessions. Furthermore, we thank the biochemistry laboratories at Institute for Exercise and Environmental Medicine (IEEM) (Michael Lisby and Jun Yi) for efforts in analyzing the large amount of blood samples that came from this study.


    FOOTNOTES
 

Address for reprint requests and other correspondence: B. D. Levine, Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, 7232 Greenville Ave., 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.


    REFERENCES
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 METHODS
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 ACKNOWLEDGMENTS
 REFERENCES
 

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