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1Sports Medicine Institute International, Palo Alto, California 94300; 2Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas and University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75231; 3US Olympic Committee, Colorado Springs, Colorado 80909; 4Department of Medicine, Stanford University, Palo Alto, California 94305; and 5Australian Institute of Sport, Canberra, ACT, Australia
Submitted 8 September 2003 ; accepted in final form 10 December 2003
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONREFERENCES |
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altitude; athletes; exercise; intermittent hypoxic training; erythropoietin
It has been suggested that the ideal approach to altitude training would enable athletes to optimize the stimuli necessary to achieve central and peripheral changes that improve O2 delivery and utilization while avoiding the detraining effects associated with chronic hypobaric hypoxia (24). This strategy, the "living high-training low" or "Hi-Lo" model, combines living and maintenance training at high altitude (2,500-2,700 m) with intense training sessions at a lower altitude (1,200 m). Significant alterations in red cell volume or soluble transferrin receptor (sTfr; documenting augmented erythropoiesis), Hb concentration ([Hb]), maximum O2 consumption (
O2 max), and 3,000- to 5,000-m running performance at sea level have been shown to occur in athletes ranging from competitive collegians and postcollegians (23) to national- and Olympic-caliber athletes (41) using this approach involving 20-22 h of hypobaric hypoxia per day.
Although the Hi-Lo method of altitude training has been demonstrated to be effective (23, 41), logistically and financially it may be difficult to accomplish for many athletes. Furthermore, at 2,200-2,800 m, the degree of erythropoietic response is highly variable (31). Individually tailored altitudes would be one approach to overcome this limitation, but the higher the altitude, the less practical it is to have a training camp and the less likely it is to have easy access to low-altitude areas conducive to high-intensity training. However, one convenient approach to simulated altitude developed in the former Soviet Union more than 60 years ago (38) is breathing a normobaric hypoxic gas (equivalent to 
5,000 m) at rest for 70 min. This so-called "intermittent hypoxic training" (IHT) comprises 5 min of hypoxia interspersed with 5 min of normoxia and has been proposed as a strategy that would allow a large number of athletes to experience simulated high altitude and individualize exposure with minimal inconvenience.
This investigation tested the hypothesis that short, repeated bursts of normobaric hypoxia at rest provide a sufficient stimulus to accelerate erythropoiesis, increase O2 max, and improve sea-level performance in competitive endurance athletes.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Highly trained male (n = 14) and female (n = 3) distance runners aged 19-34 yr were recruited from collegiate and postcollegiate running teams in the Palo Alto, CA, area (25 m above sea level). All 17 athletes completed the hematologic portion of the protocol (see Study Design), and 15 athletes (14 men and 1 woman) completed the performance measures. Subject characteristics are presented in Table 1. The athletes were competitive in distances from 1,500 m to the marathon, with current 5,000-m or equivalent personal-best times of <14:50 (min:s) for men and <16:50 (min:s) for women. Nine of these athletes competed in the US Track and Field National Championships and/or the US Olympic Trials. Six other athletes competed in the National Collegiate Athletic Association Championships, and one athlete was one of the top California state high school athletes and was heavily recruited to the Stanford University track team. Thus these athletes were highly accomplished and competitive on a US national level. The athletes were on similar training schedules and trained together as a squad throughout the study period. In the 3 mo before and during the period of the study, all athletes were training at their typical volume and intensity and continued a similar training schedule throughout the intervention. Training records before the onset of the protocol were based on athlete report. Training was more closely evaluated from the beginning of the baseline measures to the completion of the study. Training "scores" were based on an estimated fraction of O2 uptake (FO2) associated with various intensities of running and duration and were developed to estimate the overall stress of workouts as popularized by one of the investigators (J. T. Daniels): minutes x FO2. Subjects were asked to divide their training records into five categories: 1) easy jogging, 2) moderately paced runs approximating marathon pace, 3) threshold/tempo runs, 4) intervals, and 5) "anaerobic" repetitions (e.g., 200-m all-out effort). Each category was assigned an estimated FO2 according to previously collected O2 data. For example, a workout consisting of 10 min of warm-up, 30 min of tempo run, and 10 min of cooldown would be calculated as follows: (20 min x 0.70) + (30 min x 0.85) = 39.5. Weekly schedules consisted of two interval sessions, one tempo/threshold session, and one long run. The remainder of the week consisted of easy recovery runs. The athletes were sea-level residents and had not been at altitude >1,500 m for >1 wk during the previous 6 mo. No athlete had exercise-induced asthma or was on medications for reactive airway disease. Voluntary written informed consent approved by the Stanford Institutional Review Board was signed by each athlete before the commencement of the study.
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Study Design
The study was conducted using a matched-pairs, randomized and double-blind design. Subjects were matched by O2 max, 3,000-m run time-trial (3,000TT) performance, gender, and training history and subsequently assigned to the intermittent hypoxic (Hyp) or the placebo normoxic (Norm) group. On the basis of the standard deviation of these athletes for 3,000TT, the subject numbers were adequate to detect a 2% (10.6-s) change in performance [approximately twice the typical error (TE) of measurement in this population] with power = 0.85 at an alpha significance of 0.05. The study was divided into three primary segments: baseline, experimental, and recovery (Fig. 1).
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The baseline segment served as a familiarization period to minimize learning effects, to introduce subjects to laboratory and field testing, and to establish TE (15) of the measurements. The TE of duplicate baseline measurements were 1.2 and 1.1% for 3,000TT performance and O2 max, respectively. All subjects took an oral iron supplement beginning 2 wk before hypoxic exposure at an individualized dosing schedule (50-450 mg/day of elemental iron based on serum ferritin) to ensure adequate iron stores (40). Doses were based on baseline ferritin measures. Iron supplementation was undertaken by placebo and experimental subjects throughout the study. Duplicate, baseline measurements taken during this phase included [Hb], hematocrit (Hct), percent reticulocytes, and mean cell Hb content of reticulocytes (MCHCr), as well as serum concentration of erythropoietin (EPO) and sTfr. The TE for these variables were 4.0, 4.4, 19.2, 2.4, 21.6, and 5.4%, respectively.
The experimental segment consisted of 4 wk of IHT. Subjects came to the laboratory each day for an IHT session administered by a technician who was not part of the experimental team. The Hyp subjects intermittently breathed hypoxic air delivered through a hand-held mask [GO2Altitude Hypoxic Training System (Hypoxicator), Biomedtech] for 70 min five times per week; the Norm subjects breathed normoxic air through the same mask in a randomized, double-blind design. IHT was administered in a ratio of 5:5 (minutes of hypoxic air to minutes of ambient air), and the sessions took place at least 1-2 h before or after exercise training. The temporal and quantitative details of this IHT protocol represent the standard intermittent hypoxic treatment suggested for highly trained athletes according to the manufacturer's instructions and is the protocol most frequently used by competitive athletes to improve performance. The rationale for this protocol is purported to be to provide a hypoxic stimulus severe enough to induce acclimatization, as well as a reperfusion stimulus to induce "oxidative stress." The progressive decrease in fraction of inspired O2 (FIO2) over the 4 wk of the study is to provide a maximal tolerable hypoxic stress by the end of the 4-wk session but allow progressive acclimatization to minimize symptoms and improve tolerance. O2 saturation was measured within the last 5-min "hypoxic" bout using a standard fingertip pulse oximetry clip supplied with the Hypoxicator. The entire protocol is summarized in Fig. 1.
All participants kept diaries of their daily routines, including training volume, duration, and intensity, using a standard form (5). The recovery period required athletes to continue their training routines without an IHT or a normoxia session. After the experimental phase, all subjects performed duplicate performance and hematology tests 1 and 3 wk after the last IHT or placebo session.
Laboratory and Performance Evaluation
Blood parameters. The measured blood parameters included [Hb], Hct, percent reticulocytes, (reticulocyte number x MCHCr) (RetHb), EPO, and sTfr; [Hb], Hct, reticulocyte parameters, and MCHCr were measured using an Advia 120 flow cytometer (Bayer Diagnostics, Tarrytown, NY). The EPO and sTfr concentrations were determined using an automated solid-phase chemiluminescent immunoassay (Diagnostic Products, Los Angeles, CA) and an automated immunonephelometric assay (Dade Behring), respectively, as reported previously (39). Measurements were taken between 8 and 10 AM twice before the onset of IHT or normoxic exposure, after days 1, 2, and 12 of "exposure," within 48 h of the last exposure, and 10 and 26 days after exposure. Ferritin measurements were determined using a photometric assay (Hitachi 911 Biochemistry Analyzer, Roche Diagnostics, Rotkreuz, Switzerland). Periodization of testing is shown in Fig. 1.
Time-trial and laboratory treadmill performance evaluation. The 3,000TT was conducted in Stanford, CA, on the same 400-m outdoor track at 9-10 AM under similar weather conditions (16-18°C, wind 0-4 mph, humidity 75-90%). The first 1,200 m of each time trial was controlled using a pacesetter athlete, who was not part of the study, to better simulate a race situation and to minimize the influence of tactical racing strategies. Laboratory measures were performed at the Sports Medicine Institute International. After a brief warm-up period, subjects ran three separate stages on a treadmill (Fitnex, Custom 36-in. Research Treadmill 2001, Dallas, TX). Two of these stages were 5-min submaximal runs at 0% grade (men at 270 and 320 m/min and women at 230 and 270 m/min). Submaximal economy measures were calculated as O2 x velocity per 1,000 m. The third stage was a progressive O2 max test. The O2 max test consisted of 1 min at 0% grade at the second submaximal speed; thereafter, the grade was increased 1%/min until volitional exhaustion. A 2-min rest period was included between each of the three stages. Submaximal and maximal O2 were measured breath-by-breath and then averaged over 15-s intervals (TrueMax 2400, Parvomedics, Salt Lake City, UT), with the highest four consecutive 15-s values averaged to attain a minute value representative of the exercise bout. Lactate concentrations were determined immediately after the conclusion of each submaximal stage and 2 min after O2 max via fingertip capillary tube collection and analysis (Sport 2300, Yellow Springs Instruments, Yellow Springs, OH). Heart rate was monitored throughout the protocol (Polar, Advantage, Port Washington, NY).
Statistical Analyses
A Kolmogorov-Smirnov test was first performed to ensure that the data satisfied assumptions consistent with a normal distribution. Subsequently, two-factor, repeated-measures ANOVA was used for each of the performance, laboratory, and hematologic measures to compare between groups (IHT vs. Norm) and time (before, during, and after intervention). In the event of significant main effects, Tukey-Kramer multiple-comparison post hoc tests were applied to find the source of difference. Two female placebo subjects were unable to complete the protocol because of injury: one had to abandon the study shortly after commencing, and the other was injured toward the end of the exposure but completed the hematologic measures. As a result, women were excluded from analysis of the laboratory and performance measures to maintain a balanced design. Women were included in hematologic analyses. Significance values were set at P < 0.05. Values are means ± SD.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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O2 saturation levels for the 4 wk of exposure were 89.9 ± 4.2 and 96.8 ± 2.0% (week 1), 86.3 ± 5.2 and 97.4 ± 1.3% (week 2), 85.9 ± 3.6 and 97.0 ± 1.3% (week 3), and 81.4 ± 4.4 and 97.4 ± 0.7% (week 4) for the Hyp and Norm groups, respectively.
Training
Training scores were evaluated using a combination of training intensity and duration to describe the overall "stress" of a work bout. The group mean training scores for the Hyp and Norm groups given as a weekly average were 118 ± 20 and 122 ± 32, respectively. The technique used for calculating scores is given in detail in METHODS. There was no statistically significant difference between training groups.
Performance Measures
No significant differences were found between groups in any parameter (Tables 2 and 3). Neither group improved 3,000TT performance when the best baseline performance and the time trial immediately or within 48 h after the experimental phase were compared, although both groups improved their time-trial performance from the first to the second baseline test, presumably as a result of practice and familiarization with this specific time-trial format (Fig. 2). There were also no significant differences between Hyp and Norm groups at any time before, during, or after the intervention for O2 max or heart rate. Within the Norm group, however, O2 max was significantly greater (P < 0.05) at the 3-wk postexperimental segment of the protocol than at baseline (Fig. 3). Maximal minute ventilation (E) within the Norm group was also significantly greater immediately after the experimental protocol (P < 0.05) than at baseline. Submaximal O2, E, economy, and heart rate were also unchanged from baseline between the Hyp and Norm groups. Lactate measurements during the faster of the two submaximal speeds within the Hyp group were significantly lower in the final test than at baseline. However, 320 m/min appeared to represent a nonsubmaximal effort (lactate >7.0) in several subjects. Therefore, the decision was made to include only 290 m/min as a measure of submaximal effort. There was no significant difference between groups at any time in this parameter.
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Hematology data. There were no significant differences between the Hyp and Norm groups for any hematologic parameters (Fig. 4). EPO in both groups significantly decreased (P < 0.01, F ratio = 20.42), although there was no difference between groups in this response. Within the Hyp group, each of the postintervention EPO measurements was significantly less than at baseline (P < 0.05, 17.4 ± 6.8 vs. 11.0 ± 5.3, 10.8 ± 4.7, and 9.6 ± 3.4 U/l, respectively). The case was similar in the Norm group, where baseline values were significantly greater than values immediately after intervention and 10 days after intervention (P < 0.05, 12.7 ± 3.3 vs. 9.5 ± 2.9 and 9.1 ± 8.9 U/l, respectively). Hb measures within the Hyp group were significantly greater 26 days after intervention than after day 1 of exposure (P < 0.05, 15.3 ± 0.7 vs. 14.7 ± 0.8 g/dl); however, neither of these was significantly different from baseline. Within the Norm group, Hb measures were greater at baseline (15.7 ± 0.9) than at day 1 (14.8 ± 1.3) during the protocol and immediately (14.7 ± 1.1) and 10 days (14.7 ± 1.2) after intervention (P < 0.05). In both groups, percent reticulocytes was greater at day 12 during intervention than 10 days after intervention [P < 0.05, 1.9 ± 0.5 vs. 1.3 ± 0.2% (Hyp) and 1.7 ± 0.3 vs. 1.3 ± 0.2% (Norm)]. Hct within the Norm group at baseline was significantly different from that after day 1 of intervention and immediately after intervention (P < 0.05, 48.1 ± 2.9% vs. 43.8 ± 4.3 and 45.6 ± 3.7%). These observations stress the importance of the inclusion of a placebo-controlled design.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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O2 max, nor does it change their hematologic indexes of erythropoiesis. This observation is reinforced by the use of well-trained national-caliber athletes in a balanced, matched-pairs, double-blind placebo-controlled design. Brief Exposures to Normobaric Hypoxia as a Stimulus for Altered Hematology
The theory behind intermittent normobaric hypoxia is that, by decreasing the O2 concentration of inspired air and, thus, decreasing O2 saturation levels, an increase in the production of EPO and, consequently, red cell mass will be elicited (22, 38). The most salient of the Western studies has demonstrated that at least 120 min of continuous hypoxia or 240 min of intermittent hypoxia at FIO2 of 0.105 (21) is required to increase EPO concentration. Previous studies support and refute the assertion that intermittent hypoxic exposure at rest or during exercise is sufficient to produce changes in hematology associated with increased O2-carrying capacity, although most of these have used much longer (3-5 h/day) exposures to hypoxia. For example, using intermittent hypoxic exposure techniques, some investigators have reported increases in Hct and [Hb] (33); however, measures of true accelerated erythropoiesis have not been shown. Several studies have shown increases in EPO and reticulocyte counts after 10 days of consecutive 12 h/day exposures to 2,000 or 2,700 m of simulated altitude (25), as well as a combination of 17 days of 3-5 h/day at 4,000-5,500 m and low-intensity exercise (6). Several other investigations (1, 10) indicate that short bursts of 84-114 min (4,000 and 3,000 m, respectively) of hypobaric hypoxia elicit an increase in EPO that reaches a maximum 2-3 h after exposure. It is important to emphasize that all our EPO measurements were performed at the same time of day, in the morning, to minimize any circadian variability in EPO concentrations and to parallel previous studies performed with real altitude exposure. However, this strategy could have prevented the detection of a rise in EPO within the first few hours after the IHT exposure that had returned to baseline by the next morning.
Additional studies suggest that exposure to 5,000 m for 3 h/day for 9 days was sufficient to significantly increase red blood cell count, reticulocyte level, and [Hb] (32). Subsequent studies by the same group of investigators support similar findings with longer-term exposure (33). When the number of acute exposures increased to three for 90 min/wk for 3 wk, red blood cell count, reticulocyte level, and [Hb] increased progressively over time. Peak values were seen at the end of the protocol and/or during the subsequent 2 wk. These results (13, 25, 32, 33) should be interpreted with some caution, however, because several of these studies did not have a control group (13, 32, 33), and it has been demonstrated that training alone modulates reticulocyte levels (34). Moreover, other investigators have emphasized that subacute (1-2 wk) exposure to hypobaric hypoxia may increase reticulocyte counts by increasing the release of immature red blood cells from the bone marrow, without a true acceleration of erythropoiesis (14). Our tightly controlled protocol was unable to produce such effects, despite decreased O2 saturation levels as low as 82% for the Hyp subjects during hypoxic exposure. Even sTfr was unaltered, and this is considered a prime and sensitive indicator of the erythroid mass. Our results, therefore, dispute the fundamental theory that erythropoiesis results from IHT regimens that combine 5 min of intermittent hypoxia with 5 min of normoxia for 70 min.
Brief Exposures to Normobaric Hypoxia as a Stimulus for Improved Performance
The primary goal of endurance altitude training for athletes is to enhance performance. Previous studies provide conflicting reports with regard to the assertion that intermittent hypoxic exposure at rest or during exercise improves performance capacity. For example, Casas and colleagues (6) observed significant improvements in O2, pulmonary ventilation, anaerobic threshold, and hematologic measures in athletes combining 17 days of 3-5 h/day at 4,000-5,500 m with low-intensity exercise. Additional investigations by this group showed no difference between passive and active exposure to hypoxia in terms of associated performance benefits (32), implying that hypoxia alone is the primary stimulus for eliciting performance enhancements in athletes exposed to a sufficient stimulus, but neither study included a control group, which is an important limitation for performance assessments. Other carefully controlled investigations have confirmed that supplemental hypoxia administered during training (without sufficient time for "acclimatization") has no additive effect on performance above and beyond training under normoxic conditions (42). Further investigations employing longer periods of hypoxia at rest found no changes in submaximal and maximal O2 after 10 days of consecutive 12 h/day exposures to 2,000 or 2,700 m of simulated altitude, even though EPO and reticulocyte counts increased in both groups (25). Finally, a recent controlled study has reported improved performance in 3,000-m run time after 3 h/day for 14 days at FIO2 of 0.123, without a change in reticulocyte counts (20).
In the present study, there were no changes in laboratory submaximal, maximal, or field 3,000TT performance in the Hyp or placebo control (Norm) group after intermittent hypoxic exposure. This observation is important for several reasons. The inclusion of a placebo control group strongly validates the lack of response seen in the experimental group. Furthermore, the lack of change in performance is consistent with our observation of no evidence of hematologic change. Finally, as the single most critical measure of this and any simulated altitude training method, performance did not improve with use of this protocol. In combination, these data lead to the conclusion that a short burst of normobaric hypoxia is a questionable method of altitude simulation, particularly for improving endurance performance at sea level.
Implications
Previous studies examining the Hi-Lo model, involving 20-22 h of hypobaric hypoxia per day, suggest that individuals with a greater performance enhancement response to altitude training have a more accentuated EPO response initially and throughout the altitude exposure (7). This led to the theory of an EPO "dose" that is required to elicit performance enhancement (22). This dose may be highly individual, with controlled studies in humans demonstrating a more than fourfold difference among subjects in the percent change of EPO in response to sustained (24 h) exposure to simulated altitude of 3,000 m (31). The present study demonstrates clearly that this IHT protocol of short-burst intermittent hypoxic exposure is insufficient to accelerate erythropoiesis. The magnitude (how high), duration (how long per exposure), and frequency (how many exposures per week for how many weeks) of hypoxic exposure necessary to reach a "threshold" for an erythropoietic effect remain uncertain. It remains possible that intermittent hypoxic methods involving more prolonged exposures are efficacious but that the 5-min hypoxic bursts, with 5 min of ambient breathing between each burst, for a total of 70 min, are simply insufficient or ineffective to initiate and sustain the acclimatization process. This may be the case for several reasons based on the understanding of the biological pathways involved in the adaptive response to hypoxia. For example, the principal transcriptional activator of gene expression in hypoxic cells is hypoxia-inducible factor 1 (HIF-1) (35-37, 44). Under normal, well-oxygenated conditions, HIF-1 is hydroxylated via a highly conserved prolyl hydroxylase (the putative cellular "O2 sensor" in peripheral tissues), which then binds to the von Hippel-Lindau factor, targeting the entire complex for rapid degradation via the ubiquitin-proteosome pathway (11, 17-19). This process is so rapid that, in the presence of O2 and iron, HIF-1
has one of the shortest half-lives of any known protein (11, 17, 18, 43). In contrast, under hypoxic conditions, the HIF-1 complex is stable, allowing for transcriptional activation and ultimate stimulation of proteins such as EPO and vascular endothelial growth factor. Moreover, when altitude natives, or even altitude sojourners, return to sea level, EPO is suppressed (7, 12, 14, 23, 30), iron turnover and bone marrow production of erythroid cell lines are dramatically reduced (16, 26, 27), and red cell survival time is markedly decreased (26, 27, 29). This increase in red cell destruction with suppression of EPO levels has been termed "neocytolysis" and has been observed under other conditions of a relative increase in O2 content (3, 4, 28). The rapid ubiquitination and destruction of HIF-1 and neocytolysis (which may be its clinical manifestation) may compromise the ability of short-duration, intermittent hypoxic exposures to induce a sustained increase in the red cell mass.
In conclusion, a 4-wk regimen (5:5-min hypoxia-to-normoxia ratio for 70 min, 5 times/wk for 4 wk) of intermittent normobaric hypoxia is not sufficient to alter 3,000TT performance, O2 max, or indexes of accelerated erythropoiesis in highly trained distance runners.
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FOOTNOTES |
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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.
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REFERENCES |
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O2 max and running performance. J Appl Physiol 39: 262-265, 1975. targeted for VHL-mediated destruction by proline hydroxylation: implications for O2 sensing. Science 292: 464-468, 2001. to the von Hippel-Lindau ubiquitylation complex by O2-regulated prolyl hydroxylation. Science 292: 468-472, 2001.This article has been cited by other articles:
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  P. N. Ainslie, M. Hamlin, J. Hellemans, P. Rasmussen, and S. Ogoh Cerebral hypoperfusion during hypoxic exercise following two different hypoxic exposures: independence from changes in dynamic autoregulation and reactivity Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2008; 295(5): R1613 - R1622. [Abstract] [Full Text] [PDF]
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 M. J. Truijens, F. A. Rodriguez, N. E. Townsend, J. Stray-Gundersen, C. J. Gore, and B. D. Levine The effect of intermittent hypobaric hypoxic exposure and sea level training on submaximal economy in well-trained swimmers and runners J Appl Physiol, February 1, 2008; 104(2): 328 - 337. [Abstract] [Full Text] [PDF]
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F. A. Rodriguez, M. J. Truijens, N. E. Townsend, J. Stray-Gundersen, C. J. Gore, and B. D. Levine Performance of runners and swimmers after four weeks of intermittent hypobaric hypoxic exposure plus sea level training J Appl Physiol, November 1, 2007; 103(5): 1523 - 1535. [Abstract] [Full Text] [PDF]
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M. Neya, T. Enoki, Y. Kumai, T. Sugoh, and T. Kawahara The effects of nightly normobaric hypoxia and high intensity training under intermittent normobaric hypoxia on running economy and hemoglobin mass J Appl Physiol, September 1, 2007; 103(3): 828 - 834. [Abstract] [Full Text] [PDF]
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P. N. Ainslie, A. Barach, K. J. Cummings, C. Murrell, M. Hamlin, and J. Hellemans Cardiorespiratory and cerebrovascular responses to acute poikilocapnic hypoxia following intermittent and continuous exposure to hypoxia in humans J Appl Physiol, May 1, 2007; 102(5): 1953 - 1961. [Abstract] [Full Text] [PDF]
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B. Roels, C. Thomas, D. J. Bentley, J. Mercier, M. Hayot, and G. Millet Effects of intermittent hypoxic training on amino and fatty acid oxidative combustion in human permeabilized muscle fibers J Appl Physiol, January 1, 2007; 102(1): 79 - 86. [Abstract] [Full Text] [PDF]
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C. J. Gore, F. A. Rodriguez, M. J. Truijens, N. E. Townsend, J. Stray-Gundersen, and B. D. Levine Increased serum erythropoietin but not red cell production after 4 wk of intermittent hypobaric hypoxia (4,000-5,500 m) J Appl Physiol, November 1, 2006; 101(5): 1386 - 1393. [Abstract] [Full Text] [PDF]
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 C. Marconi, M. Marzorati, D. Sciuto, A. Ferri, and P. Cerretelli Economy of locomotion in high-altitude Tibetan migrants exposed to normoxia J. Physiol., December 1, 2005; 569(2): 667 - 675. [Abstract] [Full Text] [PDF]
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B. D. Levine and J. Stray-Gundersen Point: Positive effects of intermittent hypoxia (live high:train low) on exercise performance are mediated primarily by augmented red cell volume J Appl Physiol, November 1, 2005; 99(5): 2053 - 2055. [Full Text] [PDF]
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