Many endurance athletes aim to improve performance at sea level by staying for several weeks at altitude. The studies concerning the improvement of performance at sea level after a sojourn at altitude are contradictory (2). Indeed, it is likely that this is because of the difficulty in determining an optimal altitude for both hematological adaptations and training load (13), because the altitude necessary for a consequent stimulation of the hematopoiesis does not allow for realization of intensive interval training. Discontinuous hypoxic exposure in the form of “living high, training low” is currently a popular practice among athletes (12). This strategy allows exposure to hypoxia with concurrent maintenance of training intensity at or near sea level (12).
Whereas long-term exposure to severe hypoxia can progress to muscle cell deterioration (9) and to a relative detraining state with respect to the lower training intensity maintained in hypoxia, short-term exposures may be of sufficient amplitude to initiate adaptive responses by providing periods of recovery that avoid the negative effects of oxygen (O2) deprivation. This so-called intermittent, periodic, or episodic hypoxia might preserve the training intensities close to those of competition, and improve performance more so than continuous hypoxia. However, to date, only the effects of a continuous hypoxic training of several minutes or a few hours have been studied (16,21,22,27–29). Moreover, many of these studies didn't include a control group exercising in normoxia.
Rodriguez et al. (22) stated that a single hypoxic (4000–5000 m) exposure of 90 min, 3× wk−1 for three consecutive weeks, resulted in a significant increase in hematocrit (Hct), red blood cells (RBC), reticulocytes (RET), hemoglobin (Hb) concentration ([Hb]), and ventilatory threshold. Therefore, these authors suggest that a continuous exposure of 90 min represents the minimal stimulus to trigger an acute secretion of erythropoietin (EPO) (hypobaric chamber at 540 hPa to 504 hPa). However, no significant differences were found in cycling exercise time or V̇O2max, and no normoxic control group was included.
Intermittent hypoxic training refers to the discontinuous use of normobaric or hypobaric hypoxia, in an attempt to reproduce some of the physiological adaptations of altitude acclimatization (e.g., improved O2 delivery and utilization (8,12,23)), with the ultimate goal of improving sea-level athletic performance. In general, intermittent hypoxic training can be divided into two different strategies: (a) providing hypoxia at rest, with the primary goal being to stimulate altitude acclimatization (e.g., enhanced O2-carrying transport system (8,23)); or (b) providing hypoxia during exercise, with the primary goal being an ability to enhance the muscle-tissue adaptations (e.g., muscle mass, fiber size) mediated by the decrease in O2 tension (20). Each approach has many different possible application strategies, with the essential variable among them being the dose of hypoxia necessary to achieve the positive effect.
Interval training is used extensively by endurance athletes (25). Such training typically employs sustained exercise bouts alternated with periods of reduced intensity or complete rest. Although such training is a basic element in athletic conditioning, and is associated with improvements in physical performance capacity (14,25), little is known about the rate at which physical changes occur in response to such training under circumstances of hypoxic exposure. The effects and optimal characteristics of interval training carried out in hypoxia also remain unclear. Hendriksen and Meeuwsen (10) found that 9 d after a 10-d intermittent hypoxic training period (60–70% of the heart rate reserve in a hypobaric chamber, 2500 m, 105 min·d−1), maximal power output and mean and peak anaerobic power had improved. However, no significant differences were observed 9 d after the same training performed at sea level. In contrast, Truijens et al. (28) found that 5 wk of intermittent hypoxic training in a swimming flume (three high-intensity interval training sessions per week at 2500 m) improved sea-level performance (100- and 400-m freestyle time trials) and V̇O2max, but that there was no additive effect of hypoxic training. Naturally, the physical activity by itself generates peripheral and central cardiovascular adaptations. Thus, it is possible that the combination of these two forms of training (interval training exercise and hypoxic stimulus) could induce a positive additive effect. Therefore, an “intermittent hypoxic interval training” can be characterized by 1) the exercise bouts in normoxia, to develop the neuromuscular adaptations related to the high intensity (i.e., high mechanical power in cycling); and 2) the recovery bouts (short duration, 2–15 min) in hypoxia to stimulate the hematopoiesis.
The use of such an artificial technique to simulate a hypoxic exposure poses ethical problems (doping) that cannot be concealed. The present study provides objective elements to help understand the benefits associated with the use of a simulated hypoxic exposure. The purpose of this study was 1) to elucidate the influence of intermittent hypoxic interval training and to test the hypothesis that the effects of the intermittent hypoxic interval training would lead to a greater improvement in aerobic performance than normoxic or continuous hypoxic interval training; and 2) to determine whether a short intermittent hypoxic exposure (∼79 or ∼114 min·wk−1) is sufficient to obtain an (additional) effect on the hematological variables and the performance.
Thirty-three healthy male endurance-trained athletes (cyclists and triathletes) gave their written informed consent to participate in this study, which was approved by the institutional ethics committee (Nîmes, France). All subjects were sea-level residents, familiarized with the tests and equipment used in the experiment, and none of them exhibited signs or symptoms of any pathology. In addition, none had a history of recent travel to altitude (e.g., 3 wk before the training period). The subjects were initially randomized into three groups. The three groups comprised an intermittent hypoxic training group (IHT; N = 11), an intermittent hypoxic interval training group (IHIT; N = 11), and a normoxic group (Nor; N = 11). The groups were of comparable training status in terms of the average power output and average oxygen consumption measured during a laboratory time trial (TT) before the experimental training period. The experiment took place in the preseason. It was assumed that at this time of the season, the athletes had not reached a plateau of training. Subject characteristics for each group are presented in Table 1. Unfortunately, four athletes (1 IHIT and 3 Nor) withdrew from the study because of illness or injury.
Figure 1 represents an overview of the experimental design.
For 7 wk (W1–W7), the subjects performed two interval training sessions per week. Each training session consisted of a 15-min warm-up, followed by an interval training session and a cool-down of 10 min. The warm-up, recovery bouts, and cool-down were controlled and maintained during the training period at 50% of respective V̇O2max measured in normoxia for Nor and IHIT and in hypoxic conditions for IHT. The interval training was progressive in nature, but aimed to improve peak power output (PPO) and V̇O2max. The interval training consisted of 6–8 reps of 2–3 min duration at 100% PPO during the first 4 wk, then progressively increased to 5 reps of 5–6 min at 90% of PPO, then 4 reps of 8 min at 90% of PPO in the last week of training (Table 2). The subjects trained on their own bicycles, fixed on an electromagnetic resistant home trainer (Elite Travel, Milan, Italy); therefore, the laboratory training was quite similar to a normal cycle training.
Each training session was performed in either normoxic (PIO2 of 160 mm Hg) or hypoxic (PIO2 of 100 mm Hg, simulated altitude of ∼3000 m) conditions for the Nor and the IHT group, respectively. The IHIT group performed the warm-up, the cool-down, and the recovery from each interval in hypoxia, whereas the high-intensity exercise bouts were in normoxic conditions. The average duration of the hypoxic stimulus per week during the training period was 114.9 and 79.4 min for the IHT and IHIT group, respectively. The subjects did not perform supplementary interval training outside the two supervised interval training sessions per week.
Before the training period (pretraining = W0) and at the eighth week (posttraining = W8), a medical examination and determination of physical characteristics was completed (Fig. 1). Each subject's percent body fat was estimated from his total mass and the sum of four skinfold measurements (triceps, biceps, subscapular, and suprailiac) (5). The subjects also performed a submaximal constant-load test, followed by an incremental exercise test to exhaustion. On a second day, a laboratory TT was performed. The laboratory TT was also repeated the fourth week of training (midtraining = W4). The incremental test and submaximal constant-load test were performed in either normoxic (Nor and IHIT groups) or hypoxic (IHT group) conditions. In contrast, the TT was performed only in normoxia. In conjunction with the performance tests, blood samples were taken at W0, W3, and W8.
Iron supplementation (Oligo-essentiels, Laboratoires Richelet, Paris, France) of 3 mL·d−1, was initiated 2 wk before the beginning of the experiment, and continued during training to prevent low-iron states, which could limit the erythropoiesis. After every training session and test, the rating of perceived exertion (RPE) was recorded using the modified Borg scale (3). A physician was in attendance at all times, and was responsible for the safety of the subjects during the study.
Most studies examining the effect of altitude on exercise performance at sea level have used much higher altitudes, and therefore more severe hypoxia, than reported in the present study—generally >4000 m. In contrast, the majority of occupational and recreational exposures occur at more moderate altitudes, between 2000 and 3000 m. A review of many research studies suggests that the appropriate training altitude ranges between 2000 and 3000 m (4). Therefore, the level of induced hypoxia of 3000 m was suggested to be sufficient for erythropoietic stimulation (6), while still well tolerated by the subjects even during the sudden transitions from normoxia to hypoxia. The hypoxic gas mixture was delivered continuously by a system that enriches the inspired air by adding nitrogen (Altitrainer 200®, SMTEC, Geneva, Switzerland). This device allows the production of large quantities of a hypoxic gas mixture (up to 200 L·min−1), with an easily adjustable O2 fraction over a large range, and a short response time (between 15 and 45 s). A display is permanently in place to follow the oxygen content of the mixture. This can be expressed either by the equivalent altitude (∼3000 m) or by the oxygen partial pressure (PIO2 ∼100 mm Hg), taking into account the barometric pressure. Air inhaled from outside the machine is mixed with a fixed quantity of nitrogen coming from a bottle, and then mechanically mixed before being stocked in a buffer tank of 30 L. The first safety check is ensured by the mixer's mechanical limit, which cannot exceed a certain nitrogen fraction (FIO2 = 9.7%). The user inhales the mixture contained in the tank through a Hans Rudolph two-way respiratory valve. An O2 probe, a second safety check plunged in the buffer tank, measures the PO2. This probe, aided by a microprocessor, allows the PO2 of the inhaled mixture or the equivalent altitude to be displayed, and cannot decrease less than 66 mm Hg (5500 m). The respiratory mask could be removed at all times, and so the subjects found themselves immediately in normoxic conditions. A breath-by-breath analyzer can be placed in series to measure the gas exchanges.
The subjects completed three different performance tests before (W0) and after (W8) the training period. Only the cycle time trial test was also performed at W4 (midtraining). All tests were consistent in terms of time of day, and were performed on two consecutive days.
1) Submaximal constant-load test.
This test consisted of 8 min of cycling at 150 W for the IHIT and Nor group in normoxic condition, and at 100 W for the IHT group in hypoxic condition. The pedaling rate was fixed between 90 and 95 rpm. This test was performed for assessing the influence of the intermittent hypoxic training on energy expenditure (EE, J·s−1, W·L−1) and V̇O2·W−1 (mL·min−1·kg−1·W−1).
2) Incremental test to exhaustion.
The subjects performed an incremental test to exhaustion for determination of maximal oxygen uptake (V̇O2max; L·min−1), the peak power output (PPO; W), maximal heart rate (HRmax; bpm). The test began at an initial power output of 100 W, and the workload was increased by 50 W every 3 min until the respiratory exchange ratio (RER) was equal to 1.0; thereafter, an increase of 25 W was applied every minute until exhaustion. Exhaustion was reached when two out of three of the following criteria were obtained: (a) the heart rate (HR) approaching the maximal theoretical HR (220 − age), (b) V̇O2 obtained a plateau even with an increase in intensity, and (c) RER > 1.1. Breath-by-breath data were reduced to 30-s averages, and V̇O2max was determined as the highest 30-s V̇O2 average. PPO was defined as the highest mechanical power maintained during 1 min. The groups IHIT and Nor performed this test in normoxia, the group IHT in hypoxia.
3) Cycle time trial.
The time trial consisted of producing the highest mean power output for a period of 10 min in normoxia. Subjects were instructed to perform the trial at an even pace, but to attempt to obtain the best average performance. This test was performed for assessing the influence of the intermittent hypoxic training on endurance in normoxia by determining: the mechanical power output (average power over the 10-min TT; W), the average oxygen consumption (V̇O2avg; L·min−1), and average heart rate (HRavg; bpm). Subjects were informed of the elapsed time but received no feedback on power output or performance. The duration of 10 min for the TT was chosen so that the test could be administered easily. At the same time, the test was considered to be long enough to elicit a considerable aerobic contribution for energy provision (30).
All the tests were performed on a bicycle equipped with an SRM® Road Professional Powermeter (Schoberer Rad Messtechnik, Jülich, Welldorf, Germany). The saddle height on the cycle ergometer measured during the first test was kept identical for the remaining tests. Power output and pedaling cadence were recorded with an acquisition frequency of 1.0 s. The 30-s average values were stored. The calibration procedure and technical aspects concerning the SRM crank system have been described in detail by Jones and Passfield (11). Briefly, the procedure consists of establishing a baseline or zero-offset setting by pedaling the SRM crankset in a reverse direction, unloaded. The zero offset is the amount of strain being generated by the Powermeter itself, without any force being applied on the pedals. Before setting off, the cranks should be spun backwards a few times to activate and calibrate the Powermeter. The resultant values should not deviate more than ±10 Hz, if no force is exerted on the pedals. The SRM® Road Professional Powermeter is constructed with four strain gauges within the crank, and has been shown to be highly accurate in power measurement. The 95% limit of agreement is 2.1 W, which is equivalent to 1.8% (11).
At pre- and posttraining, gas exchange was measured during exercise by a CPX analyzer (Medicals graphics, St. Paul, MN) during the incremental test to exhaustion and the submaximal constant-load test, and by the K4b2 (Cosmed, Rome, Italy) during the TT. The discrepancies between these two metabolic systems have been shown to be nonsignificant (15). At W0 and W8, a comparison was made between the two analyzers during a submaximal exercise (150 W; below ventilatory threshold (VT)) in three subjects by altering the analyzers every 2 min for 20 min. The difference between the average V̇O2 values of these two analyzers was less than 2%. The K4b2 setup was used to calculate the ventilatory variables with the accurate FIO2 rather than with the default version. The aforementioned variables were measured breath by breath, and averaged every 30 s. Before each test, the system was calibrated using ambient air, whose partial O2 composition was assumed to be 20.93%, and a gas of known CO2 (5%) and O2 (16%) concentration. The calibration of the turbine flowmeter of the K4b2 was performed with a 3-L syringe (Quinton Instruments, Seattle, WA).
During the different tests and training sessions, HR was constantly monitored using a HR monitor (S810, Polar, Kempele, Finland). EE was calculated in the submaximal constant-load test from the average values of V̇O2 and V̇CO2 (17).
Blood samples at rest were obtained by venapuncture by a physician on three occasions: W0, W3, and W8. These samples were analyzed, following standard procedures, in the 2 h following the drawing, by the Pentra 120 Retic (abx, Montpellier, France) for several parameters: red blood cell (RBC; 106 mm−3), Hb (g·dL−1), Hct (%), red blood disc (RBD; 103 mm−3), and reticulocytes (RET; % and 106 mm−3). EPO levels were measured in the specific radioimmunoassay (RIA) for EPO (EPO-Trac125I RIA kit INCSTAR, Stillwater, MN). In the EPO-Trac RIA, the minimum detectable EPO concentration is 4.4 mU·mL−1, and cross-reactivity with other serum proteins is <0.001%. Sample values were reproducible, with an intraassay coefficient of variation (CV) of 4.8%, and an interassay coefficient of variation of 6.7%. The blood samples were placed on ice and centrifuged at 4°C with a centrifugation force of 900 × g for 10 min, and the plasma was stored at −80°C until the EPO assay was performed. All samples were assayed in triplicate, and all samples obtained from a subject during the course of an exposure were measured in one RIA assay kit, eliminating the problem of interassay variation.
The training characteristics outside the protocol were recorded daily using a computerized training diary from the beginning until the end of the training period. This training diary recorded the type of activity (cycling, swimming, conditioning, etc.) and intensity. The training intensity was divided into five intensity levels (18). All sessions were individually timed, and each exercise categorized, according to these intensity levels. To calculate the average intensity of each session, the distance performed was multiplied by its corresponding multiplying factor (2, 4, 6, 10, and 16, respectively) (18), and the sum was divided by the overall distance of the session. Since subjects trained in different activities, it would not have been sensible to compare hourly volume. Therefore, the parameters recorded were the number and average intensity of the sessions, calculated by the method of Mujika et al. (18), but also, for practical use, as a percentage of maximal heart rate (%HRmax).
All values are reported as mean ± standard deviation (SD). The influence of the three training methods on the measured variables was, after analysis of the normality and the homogeneity of variance of the tested samples, analyzed using a two-way analysis of variance (ANOVA) (three groups (IHIT, IHT, Nor) × time) with repeated measures on the second factor; for example, two (incremental test to exhaustion and submaximal constant-load test) or three (cycle time trial) measures. The reliability of the cycle time trial was also assessed as the typical (standard) error of measurement expressed as a coefficient of variation (CV; percent of the mean) between trials. Significant effects were subsequently analyzed using the Bonferroni post hoc test. All analyses were completed using SigmaStat 2.3 (Jandel Corporation, San Rafael, CA), and statistical power was calculated for each analysis. Statistical significance was accepted at P < 0.05. The sample size or minimum number of subjects required to detect a significant difference between the three groups was between 8 and 25 for the parameters measured during TT, and between 20 and 30 for the measured parameters in the two other performance tests and for the blood parameters.
Cycle Time Trial
Before the training period there were no significant differences between the groups in terms of average power output (Pavg) or V̇O2avg. The IHIT, IHT, and Nor groups improved their performance (P < 0.05) 5.2 ± 3.9, 3.7 ± 5.9, and 5.0 ± 3.4% during the first 4 wk of training (W1–W4), respectively. The Pavg values were 298 ± 39, 304 ± 30, and 282 ± 18 W at W0; and 313 ± 42, 316 ± 43, and 296 ± 23 W at W4 for the IHIT, IHT, and Nor groups, respectively. During the following 3 wk of the training period, from W4 to W8, no significant improvement was observed in the three groups (1.1 ± 5.6%, 1.1 ± 4.8%, and 3.4 ± 3.5% for the groups IHIT, IHT, and Nor, respectively). The Pavg values at W8 were 316 ± 33, 319 ± 34, and 310 ± 30 W, for the groups IHIT, IHT, and Nor, respectively. No effect between the three groups (IHIT, IHT, and Nor), and thus no effect specific to the training methods, was observed (P = 0.57). CV was 10, 11, and 10% for the three completed time trials, respectively. The other physiological variables (e.g., V̇O2avg and HRavg) measured during the cycle time trial are presented in Table 3.
Submaximal Constant-Load Test
There were no significant differences in the physiological variables measured in the submaximal test, either between W0 and W8 or between groups. EE values, calculated in normoxia at W0 and W8, are represented in Table 4.
Incremental Test to Exhaustion
The measured variables obtained from the incremental test are presented in Table 5. There was no significant difference in initial PPO measured in normoxia between the IHIT and Nor groups. V̇O2max (L·min−1) increased (P < 0.05, power = 0.70) in the IHIT group between W0 and W8. Group IHT showed no changes for the measured parameters.
The hematological variables measured during the training period are represented in Table 6. No significant differences between groups or weeks have been observed during the training period.
No differences between the three groups were observed in terms of training outside the protocol, which was mainly of low intensity, without any other interval training session. The number and average intensity of sessions were similar. The average intensity during the 7-wk training period was similar: 3.7 ± 0.6, 3.3 ± 0.5, and 3.6 ± 0.6 for the IHIT, IHT, and Nor groups, respectively. Also, the HRavg and %HRmax during the 7-wk training period showed no significant differences, and were 141.0 ± 32.9 bpm and 73.0 ± 10.5%, 138.2 ± 23.5 bpm and 70.5 ± 10.8%, and 136.4 ± 26.0 bpm and 74.8 ± 20.1% for the IHIT, IHT, and Nor groups, respectively. The detail of the training data outside the protocol during the 7 wk is presented in Table 7.
To our knowledge, the present study is the first of its kind, measuring the effects of high-intensity interval training in three groups of well-trained athletes exposed to different environmental conditions, and providing novel results about the interaction between hypoxia and normoxia in the same endurance training session. The present study showed that interval training significantly improved endurance performance, as quantified by average power output during a 10-min cycle time trial. However, this improvement was not further enhanced by performing such training under hypoxic or intermittent hypoxic conditions. Therefore, the initial hypothesis—that intermittent hypoxic interval training improves sea-level performance more than intermittent hypoxic or normoxic training—was rejected. Moreover, the hypoxic exposure needs to exceed 114 min·wk−1 to obtain an effect on the hematological variables and the performance. This aside, endurance performance greatly improved during the first 4 wk of training, without any further significant improvement in the three following weeks. This suggests that 4 wk of interval training in normoxia, 2× wk−1, is sufficient to obtain significant improvements in endurance performance. Furthermore, only the IHIT group improved V̇O2max during the training period, without any corresponding change in EE or in any of the hematological variables measured.
The three groups significantly improved endurance performance over the period of the study. This confirms the major effects of interval training reported previously in the literature (14,25). The main part of the improvement took place during the first 4 wk (∼4–6%). The subjects were all well-trained cyclists or triathletes, and had been familiarized with this type of test, so it is likely that the learning effect was negligible. All the individuals were retested on the same equipment, at the same location, and by the same operators, so that no additional error due to differences in the calibration or functioning of the equipment, localization, or in the ability of the operators could surface. Also, the fact that the CV was identical between the three different trials shows that the 10-min TT was a reliable measure of performance.
Of interest is that only the V̇O2max of the IHIT group increased during the training period. It is well known that for very well-trained athletes, endurance performance may be independent of V̇O2max, and that other submaximal variables may influence performance to a greater extent (1). As Fulco et al. (8) have mentioned, it should be noted that small, statistically nonsignificant training-induced improvements (often reported as “no change”) can result in a significant increase in endurance performance. Moreover, in well-trained athletes, where it is difficult to induce an increase in V̇O2max, a small improvement in performance may make the difference between winning and losing (13). In the literature, an increase in V̇O2max due to hypoxia is generally associated with an increase in red blood cell count (RBC) (23). In the present study no differences in hematological parameters existed between the three groups. So, the increase in V̇O2max of the IHIT group in the present study cannot be explained by a difference in the blood variables, as no changes in these parameters were observed. However, altitude training can improve V̇O2max at sea level for certain athletes, but the individual responses can be very different; therefore, a significant group-level improvement does not always arise (23). Also, a possible inhibition of EPO secretion, related to the metabolic acidosis caused by intense physical training, has been suggested (7,24). Although the lack of increase may be due to the short hypoxic exposure time (∼114 min·wk−1), Eckardt et al. (6) demonstrated that EPO levels during hypoxia were significantly elevated after 114 min at 3000 m. Mean values increased from 16.0 to 22.5 mU·mL−1, or a rise in EPO levels corresponding to 1.8-fold.
It is of interest to observe that average training intensity was identical, as was the progress in endurance performance between the three groups. Training intensity was reported as the key factor in performance improvement (19). The greatest improvements in aerobic power occur when the greatest challenge to aerobic power occurs (e.g., according to intensity). Moreover, Mujika et al. (19) reported that improvement in performance correlated significantly with the mean intensity of training.
One can speculate that exposure to an hypoxic environment, as presented in the present study, would stimulate hematopoiesis, which results in an increase in Hct, Hb concentration, and proportion of RET. This response also supports the maintenance of the arterial O2 load and the increase of the O2 transport capacity, and thus of the aerobic performance after return to sea level. These adaptations are induced by EPO, which is synthesized and released primarily by the kidneys.
Since the three groups improved their performance during the normoxic cycle time trial to the same extent, it seems that the exposure to the hypoxic stimulus (∼114 min·wk−1) was not sufficient to obtain an additional effect, regardless of the method of exposure tested. These results show that significant improvement in performance was a result of normoxic interval training. Therefore, the hypothesis that the effects of intermittent hypoxic interval training would lead to a larger improvement in performance than that seen after normoxic or all-round hypoxic interval training was rejected.
The present results are in accordance with those of Truijens et al. (28), who found that 5 wk of high-intensity training in a flume improved sea-level performance in well-trained swimmers, but that there was no significant additive effect of hypoxic training (15.3% oxygen equivalent to a simulated altitude of 2500 m). Terrados et al. (27) investigated the effect of intermittent hypoxic training in eight elite cyclists, randomly assigned to either hypobaric hypoxia (2300 m) or normoxia, who trained for 3–4 wk, 4–5 sessions per week, each session consisting of cycling for 60–90 min continuously and 45–60 min intermittently, and found no difference between groups either for work capacity or for maximal power output. Similarly, Vallier et al. (29) found no significant differences in V̇O2max or maximal power output in five elite triathletes following intermittent hypoxic training. For 3 wk these subjects modified their usual training schedule (approximately 30 h·wk−1), replacing three sessions of bicycling exercise with three sessions on a cycle ergometer in a hypobaric chamber simulating an altitude of 4000 m. However, Vallier et al. (29) did not include a control group. Therefore, from this study it is not possible to compare the relative affects of the exercise or the exercise/hypoxic intervention.
On the contrary, Rodriguez et al. (21) showed that performance at sea level can be improved after passive intermittent hypobaric hypoxic exposure (3 h·d−1 for 10 d) between 4000 and 5500 m. In contrast, the hypoxic group, which combined passive exposure with low-intensity exercise in hypoxic conditions, did not show any changes. However, a limitation of that study was that no normoxic control group was included. Even low-intensity training during an intermittent hypoxic exposure (2 h·d−1 for 10 d) in a hypobaric chamber significantly improved V̇O2max, power, and performance at sea level, as shown by Meeuwsen et al. (16). Rodriguez et al. (22) stated that a single hypoxic (4000–5000 m) exposure of 90 min activates the secretion of EPO. The most important result of the latter study was the significant increase in Hct, RBC, RET, [Hb], and ventilatory threshold at the end of three consecutive weeks with three hypoxic intermittent session of 90 min·wk−1. These authors suggest that an exposure of 90 min represents the minimal stimulus to trigger an acute secretion of EPO (hypobaric chamber at 540 hPa to 504 hPa). However, no normoxic control group was included.
In summary, an additive effect of intermittent hypoxia in combination with endurance training in well-trained athletes has not been unequivocally demonstrated (28). Several other investigators (26) have speculated that benefits from hypoxic training are likely to be anaerobic in nature. One could suggest that in the present study, an increase in the anaerobic capacity could be an additive underlying mechanism of the improvement in performance. However, further experiments are needed to reveal the mechanisms surrounding these adaptations.
Intermittent hypoxic interval training, even after 7 wk, does not seem to be a sufficient stimulus to provoke an increase in hematological O2 transport or a greater increase in performance than normoxic training of a similar type would provoke.
The results of this study allow a better determination of the intermittent hypoxic interval training method. Apparently, the hypoxic exposure needs to exceed 114 min·wk−1 to obtain an effect on the hematological variables and the performance. On the other hand, the duration of an intense training period does not have to exceed 3 or 4 wk, because of the achieved plateau in performance. This study shows that hypoxic exposure did not provide any more beneficial effects than those provided by the interval training.
The authors wish to acknowledge the support of Mr. F. Mansuy and Mr. P. Salame of the Centre Régional d'Education Physique et Sportive (CREPS), Montpellier, France. This study was supported by the International Olympic Committee and by the French Ministry of Sport.
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