High-intensity interval training (HIT) is an important component of most elite endurance runners' training programs (43), and its outcomes, in terms of running performance, have been well described (26). Many elite endurance runners also incorporate some form of altitude or hypoxic exposure in their training plan, in the belief that it will improve sea-level performance. Although long-term hypoxic HIT (HHIT) is generally accepted as being a relatively ineffective means of improving cardiorespiratory function and performance (5,20,46), training in hypoxia remains a simple means of increasing or modifying exercise stimulus at the muscular level (17) and to varying training stress and adaptation within the annual training plans of well-trained athletes (28).
Knowledge of the acute physiological, muscular, hematological, autonomic, and immunological responses to HIT is of great importance to coaches to help ensure optimal scheduling of training content and loads, especially for (young) athletes training twice a day. Typically, coaches select training content aimed at either (a) stressing the physiological systems central to performance (e.g., cardiovascular, neuromuscular, or metabolic functions or hematological parameters) and/or (b) controlling the level of acute fatigue or physiological strain (e.g., perceived exertion, homeostasis and immune function changes, neuromuscular constraints) so as to better manage training loads and help prevent injuries and/or overtraining. Typical sea-level HIT sessions consist of repeated short (10–45 seconds) to medium (>1–5 minutes) length intervals at intensities ranging from 90 to 120% of the velocity associated with maximal O2 uptake (νV̇O2max), which enables runners to spend from 25 to 75% of exercise time >90% of V̇O2max (depending on between-effort recovery intensity and duration) (26). Normoxic HIT sessions have also been shown to induce short-term postural control impairment (12), homeostatic perturbation (as assessed via heart rate variability [HRV] analysis ), and immune function depression (13,31). In contrast, short-term muscular performance, such as maximal jump height, was reported to be unaffected (44) or even improved (45) after sea-level HIT.
Little information is however available on the acute responses of the various biological systems involved in performance to HHIT (22,23,31). Acute exposure to hypoxia has been proven to impair performance during intense aerobic exercise by decreasing systemic O2 transport (for a review see ). However, how these hypoxia-induced changes in O2 transport affect the response to HIT is complex, because the influences of reduced O2 availability occur throughout the entire body (i.e., in the brain and in the cardiorespiratory and muscular systems ). During HHIT sessions in competitive runners, running speed has generally to be decreased compared with sea level to make the intervals sustainable (11,22,23,31). This 5–15% lowering in running speed (depending on the severity of hypoxia, the athletes' physiological attributes (37), acclimation level, and interval duration) is likely responsible, among other mechanisms, for reduced heart rate (HR) (22,23,31) and V̇O2 (22,23) during HHIT. Blood lactate responses to running HHIT are less clear with studies reporting either decreased (22) or unchanged (23) values compared with matched sea-level sessions. Niess et al. (31) also reported, while comparing HIT sessions performed at sea level and altitude (1,800 m) matched for blood lactate accumulation, a greater sympathetic activation and immune suppression after the altitude condition. Additionally, acute hypoxia has been reported to exacerbate exercise-induced perturbations of autonomic activity (i.e., premature vagal withdrawal) (9) and motor control (32), as inferred from HRV and postural gait analyses, respectively. However, to the best of our knowledge, the concurrent evaluation of the acute impact of running HHIT on physiological, perceptual, neuromuscular, motor control, hematologic, and autonomic nervous system responses has not yet been assessed in highly trained young endurance athletes.
Therefore, to improve our understanding of the acute physiological strain associated with HHIT running, we sought to compare the rate of perceived exertion (both central and peripheral), cardiorespiratory, blood acidosis, immune, hematological, HRV, sprint and jump performances, and motor control responses to a typical HIT session performed at moderate simulated altitude (2,400 m) with that of a similar HIT session performed in normoxic conditions. Although we expected to observe reduced arterial O2 saturation (SpO2), HR, and V̇O2 for the hypoxic condition, changes in the other aforementioned parameters were difficult to predict given the simultaneous differences in both running speed and O2 availability.
Experimental Approach to the Problem
Runners were required to undergo 3 test sessions over a 2-week period. These sessions were separated by at least 48 hours and were conducted at the same time of the day (±0.5 hours). During the first session, each runner performed a graded maximal running test to determine their V̇O2max and νV̇O2max (sea level). In the 2 subsequent sessions, each runner completed an HIT set comprising 5 × 3-minute runs in a counterbalanced order, in either normoxic (N) or normobaric hypoxic (H) conditions. The normobaric hypoxic condition was set to simulate an altitude of 2,400 m (FiO2 = 15.4%) and was created using a CAT system (Colorado altitude training, Louisville, CO, USA). This system duplicates the lower oxygen pressure found at high altitude by lowering the percentage of O2 in the air. An overview of the experimental schedule is presented in Figure 1. Several variables were measured immediately before and at various times from 3 minutes to 5 hours after each training session to provide measures of the physiological load associated with HIT performed under both normoxic and hypoxic conditions: ratings of perceived exertion were used to subjectively assess exercise intensities; oxygen consumption, and HR for systemic cardiorespiratory stress; HRV measures for autonomic nervous system activity and the body's homeostasis perturbation; acid-base status and blood lactate for anaerobic energy system contribution; hematological parameters for immune system responses and possible changes in erythropoietin (EPO); and lastly, postural sway, sprint speed, and maximal jump height for postural control and neuromuscular performance. The runners refrained from performing any strenuous exercise for 24 hours before each testing session and had their last meal at least 2.5 hours before presenting to the laboratory. Additionally, all runners were provided with a postsession nutrition plan developed by a nutritionist to ensure adequate fluid and nutrient intake between all training sessions.
Eight highly trained young male middle- and long-distance runners took part in the study (Table 1). All runners were postpubertal (as assessed from anthropometric measurements ), healthy, and were not taking any prescribed medications at the time of the project. Their blood pressure levels and electrocardiographic patterns were normal. Each athlete was familiar with the testing procedures and had previously been exposed to hypoxic training sessions. The runners (or their parents) were provided with the procedures and risks associated with participation in the study and gave voluntary written consent to participate in the experiment. The study was approved by the local Review Board for use of Human Subjects as per the JSCR author guidelines.
Maximal Graded Test
The maximal graded exercise test was performed on a motorized treadmill (Woodway PPS Med, Woodway, Waukesha, WI, USA). The test began at an initial speed of 10 km·h−1 and was increased by 1 km·h−1 every minute until the runner stopped because of volitional exhaustion. If the last stage was not fully completed, the peak treadmill speed was calculated using the following formula: peak treadmill speed = Sf + (t/60 × 0.5), where Sf was the last completed speed in km·h−1 and t is the time in seconds of the uncompleted stage (18). The typical within-subject variation in peak treadmill speed from test to test is reported to be 2.5% (41).
High-Intensity Interval Training
All HIT sessions were conducted on a motorized treadmill (Woodway PPS Med, Woodway). Immediately after a standardized 5-minute warm-up run at 50% of νV̇O2max, runners completed an HIT session comprising 5 × 3-minute interval runs at a speed corresponding to either ≈84 or 90% of νV̇O2max for H and N, respectively. Between each interval, runners had a 90-second rest period. Based on pilot tests with our runners, interval-running speed was decreased by ≈6% in H compared with that in N. This was identified as the smallest reduction in running speed possible so as to still enable the runners to complete the H session. This 6% reduction in speed was within the range previously reported in the literature during similar hypoxic sessions in well-trained adult runners (11,22,23,31).
Height (Harpenden, Baty International, Burguess Hill, United Kingdom), body mass (ADE Electronic Column Scales, Hamburg, Germany), and the sum of 7 skinfold sites (triceps, subscapular, biceps, supraspinale, abdominal, thigh, and medial calf; Harpenden skinfold caliper [Baty International]) were measured by an experienced tester.
Perceived Exertion Measures
Participants indicated their rating of central (cardiorespiratory strain, RPEC) and peripheral (legs strain, RPEP) perceived exertion at the end of each interval (6–20 Borg's scale) (24).
During all tests, breath-by-breath respiratory gas exchange was measured using the Oxycon Mobile portable metabolic system (Carefusion GmbH, Hoechberg, Germany) (39). As per the manufacturer's recommendations, the O2 and CO2 analyzers were calibrated using (normoxic) ambient air and calibration gases of known O2 and CO2 concentrations (16 and 5%, respectively) before each test. The HR was monitored continuously with a S810 HR monitor (Polar Electro, Kempele, Finland). Cardiorespiratory values were averaged over 30-second periods during the maximal graded test and over 5-second periods during HIT sessions. Oxygen pulse (O2 pulse, milliliters per beat) was calculated as V̇O2/HR. V̇O2max was defined as the highest V̇O2 values attained in a 30-second period (27). νV̇O2max was defined as the lowest running velocity maintained for at least 1 minute which elicited V̇O2max (3). Time spent above 90% of V̇O2max (t90% V̇O2max) and maximal HR (t90%HRmax) was determined from the V̇O2 and HR values equal to or >90% of V̇O2max and HRmax during HIT sessions (7). SpO2 (Wristox 3100, Nonin Medical Inc., Plymouth, MN, USA) was recorded at the end of each interval.
Heart Rate Variability Measures
Heart rate variability was assessed 25 minutes before, 15 minutes after, and 240 minutes after each HIT session (Figure 1). The runners were required to remain seated for 6 minutes, and beat-by-beat HR was recorded (Figure 1). We chose not to control for respiratory rate because respiratory rate was always in the high frequency range (>0.15 Hz) and vagal-related HRV indices during spontaneous and metronome-guided breathing differed little (4). All R-R series data were extracted using dedicated software (Polar Precision Performance SW 5.20, Polar Electro). Occasional ectopic beats were automatically replaced with interpolated adjacent R-R interval values. For simplicity, only one vagal-related HRV index was calculated during the last 3 minutes of the 6-minute periods, this being the natural logarithm of square root of the mean of the sum of the squares of differences between adjacent normal R-R intervals (natural logarithm of the square root of the mean of the sum of the squares of differences [Ln rMSSD]). Analysis was computed with the accompanying Polar software, which has been shown to provide accurate measurements (33). A coefficient of variation (CV) of 10% is generally reported in young athletes for resting Ln rMSSD (8).
Acid-Base Status and Blood Lactate Measurement
A fingertip blood sample was collected 3 minutes after the end of each test session and analyzed for blood pH, [La]b, bicarbonate ([HCO−3]), and base buffer (BB, which represents the concentration of buffering anions). Blood lactate concentration was measured using a portable automated analyzer (Lactate Pro, Arkray Inc, Kyoto, Japan), whereas the other parameters were analyzed in a blood gas analyzer (Cobas b221, Roche, Mannheim, Germany). The suitability and reproducibility of the Lactate Pro have been previously established throughout the physiological range of 1.0–18.0 mmol·L−1 (38).
Blood samples were obtained by standard venipuncture techniques with the runner seated. Blood samples were collected into 2.0-ml K2 ethylenediaminetetraacetic acid vacuum tubes (Becton-Dickinson, Plymouth, United Kingdom) before exercise and 30 minutes and 4 hours postexercise (Figure 1). The analyses for the full blood count (i.e., neutrophils, monocytes, and lymphocytes) and reticulocytes were performed on a Sysmex XT2000i analyzer (Sysmex Cooperation, Kobe, Japan) within 3 hours of the sample being collected. All parameters were validated before every analysis using 3 internal Sysmex e-check controls. Erythropoietin concentration was determined after centrifugation of the remaining blood and separation of the plasma. The analysis was conducted by an enzyme-linked immunosorbent assay Kit (R and D Systems, Minneapolis, MN, USA) using a Tecan Sunrise plate reader (Tecan Group Ltd, Maennedorf, Switzerland). All blood-derived values were corrected for changes in plasma volume (2). The CVs (%) for repeated measures on the same day were 0.3% for hemoglobin, 0.4% for hematocrit, 1.3% for white blood cells, 12.1% for EPO, 0.1% for pH, and 2.0% for HCO-3, respectively.
Postural Control and Sprint and Jump Performance Measurements
Postural control and vertical jump performance (countermovement jump [CMJ]) were assessed before, 2 minutes after and 20 minutes after HIT sessions (Figure 1). Sprint performance was measured before and 7–8 minutes after HIT. Sprint tests were also repeated ≈5 hours after HIT. For the postural control task, the runners were instructed to stand as still as possible for 30 seconds on a 40- × 60-cm force plate (Kistler 9286AA, Kistler Instrument Corp., Winterthur, Switzerland) with their arms relaxed at their sides and feet together. Once the runners had assumed this position and were ready, they were asked to inform the experimenter to start the test. This task was repeated 4 times on each occasion, with 2 trials performed with eyes open and 2 eyes closed, in a randomized order. After each trial, the runners stepped off the plate for 5–10 seconds. For the eyes-open test, a focus point was placed at eye level on a wall approximately 2 m in front of them. Three-dimensional ground reaction forces were sampled at 500 Hz and filtered (Butterworth low-pass filter, cut-off frequency 10 Hz) using Bioware 3.0 software (Kistler Instrument Corp.). Total sway distance was calculated as the sum of anterior-posterior and mediolateral center of gravity displacement over the 30-second measurement period. For assessing possible changes in jumping performance, the runners performed 3 separate CMJs over a 30-second period on the same force plate described above. The participants were instructed to perform a maximal effort CMJ with hands on their hips and the depth of the countermovement self-selected. Jumping height was calculated from the flight time, and the best jump was selected for further analysis. The typical within-subject variation in jumping height from test to test is <3% in our laboratory. The sprint performance was assessed by a maximal 20-m sprint test with a standing start, using a 100-Hz laser distance measurement device (Laveg LDM 300C, Jenoptik AG, Jena, Germany). The operator of the system aimed the laser beam on the runner's lower back throughout the sprint. The participants repeated the maximal 20-m sprint 3 times on a synthetic track, with a 1-minute recovery interval between each trial. The best 5-m split time and 20-m sprint time were recorded for further analysis. In our laboratory, the reliability of the Laveg laser system for 5- and 20-m time measures has a CV of 3.0 and 1.8%, respectively.
Data are presented as means and SDs. The distribution of each variable was examined with the Shapiro-Wilk normality test. Homogeneity of variance was verified by a Levene test. Data were assessed for clinical significance using an approach based on the magnitudes of differences (16). After log transformation, between-condition differences in cardiorespiratory, SpO2, and RPE values; and between-condition differences in the changes in blood acidosis, hematological parameters, Ln rMSSD, jump and sprint performance, and postural control were expressed as a standardized difference or Cohen's d (±90% confidence limits) using pooled SD. Threshold values for Cohen's d statistics were >0.2–0.5 (small), >0.5–0.8 (moderate), and >0.8 (large). To compare changes between conditions, the chance that the true (unknown) changes for H were greater (i.e., greater than the smallest practically important difference, or the smallest worthwhile [difference] change [0.2 multiplied by the between-subject SD, based on Cohen's d principle]), similar or lower were calculated. Quantitative chances of greater or lower values were assessed qualitatively as follows: <1%, almost certainly not; 1–5%, very unlikely; 5–25%, unlikely; 25–75%, possible; 75–95%, likely 95–99, very likely; >99%, almost certain. If the chances of having higher or lower values were both >5%, the true difference was assessed as unclear (16). In addition, the SD representing individual responses (the square root of the difference in the variances in the observed parameters in each experimental condition, expressed as a CV) was used as a measure of individual responses to HIT in both conditions. A positive value indicates a larger SD in the H condition, which is consistent with the presence of individual responses; a negative value indicates the opposite.
Running speed, cardiorespiratory, SpO2, and RPE responses to HIT in both conditions are presented in Table 2. Compared with N, H was associated with similar V̇E, but at least likely lower V̇O2, HR, and SpO2. t90% V̇O2max and t90% HRmax were also very likely and likely lower for H. Conversely, both RPEC and RPEP were very likely higher for H. The difference in central vs. peripheral ratings of perceived exertion was however similar for both conditions (i.e., slightly greater for RPEP). Changes in cardiorespiratory, SpO2 and RPE responses between HIT intervals, for each condition, are illustrated in Figure 2. V̇E, HR, RPEC, and RPEP increased progressively in both conditions. V̇O2 increased with interval repetitions in N, whereas it remained stable during H. There were however no within-condition changes in SpO2.
Changes in blood pH, [La]b, HCO−3, and BB are presented in Table 3. Changes in all these parameters were at least possibly greater for H compared with those for N.
Changes in differential leukocyte counts, EPO, and Ln rMSSD are presented in Table 4. Changes in neutrophils and monocytes were likely lower for H compared with those for N, although there was no difference for lymphocytes. There was no clear difference in the changes in EPO and Ln rMSSD.
Sprint, jump, and postural control data and their respective changes are provided in Table 5. Although there were no between-condition differences in the changes in CMJ, improvements in sprint times and impairment in postural control were greater after N compared with after H.
This study examined for the first time the responses of several biological systems in young highly trained runners to a typical HIT session performed in both normoxia and normobaric hypoxia (simulated altitude of 2,400 m). The present results confirm that in hypoxic conditions, typical HIT sessions are associated with reduced cardiovascular responses compared with normoxic sessions (as evidenced by shorter time spent near V̇O2max and HRmax), despite greater ratings of perceived exertion and slightly higher blood acidosis. Our findings also show that HHIT sessions have a similar impact on cardiac autonomic activity and plasma EPO concentration, while affecting cellular immune function to a lesser extent. The influence of a hypoxic HIT session on neuromuscular and motor control impact is also likely lower compared with a normoxic session.
In this study, the decrease in running speed at the simulated altitude of 2,400 m was applied to compensate for the reduced O2 availability thereby allowing the runners to be able to perform the intervals. We acknowledge that the isolated effect of hypoxic exposure per se could not be investigated and that the speed reduction could abolish potential differences in the physiological strain associated with each running condition. Nevertheless, this was done to allow examination of the acute physiological responses to an HHIT session as typically performed by runners in real world situations, which increases the practical application of the present results. This reduction in running speed led to lower V̇O2 and HR levels, which is in accordance with the findings of previous studies on competitive runners (21,23,31). This is however the first time that the (shorter) time spent above 90% of V̇O2max and HRmax (believed to be good criteria to assess the cardiorespiratory impact of a given exercise ) has been reported during HHIT (Table 2). The unchanged O2 pulse indicates that the reduction in HR matched that of V̇O2; the matching of cardiac output to pulmonary diffusing capacity being thought to be necessary to optimize gas exchanges (36). Because training at (and maintaining) high V̇O2 and cardiac output levels is believed to be a determining factor in improving maximal cardiovascular function (26), it is not surprising that HHIT, has repeatedly failed to substantially improve V̇O2max in well-trained athletes (for reviews see [5,20,46]). It is however worth noting that large interindividual variability in the cardiorespiratory responses to HIT was observed (e.g., CV of −6 and 528% for V̇O2 and t90% V̇O2max, respectively), despite the tight individualization of running speed (i.e., fixed percentage of νV̇O2max). The magnitude of most of the CVs (i.e., individual responses, Table 2) is in line with that of previous studies on cardiorespiratory responses to HIT at sea level (7) and confirms that factors other than νV̇O2max should also be considered when selecting optimal running speeds during HIT (e.g., O2 kinetics (27) or ability to recover between-efforts and anaerobic capacity ). In addition to the aforementioned factors, interindividual differences in the sensitivity to the hypoxic stimuli during HHIT are likely to further increase the variability in the responses observed (10,37).
Despite a reduced running speed, we found that the acid-base status was slightly more affected after HHIT; for example, substantially greater increases and decreases in arterialized blood lactate and bicarbonate were observed, respectively (Table 3). This is in contrast to the findings of previous studies, which reported either reduced (22) or unchanged (23,31) blood lactate concentrations during HHIT compared with HIT performed at sea level. Differences in interval intensity or duration, which are likely to affect anaerobic contribution during HIT running (6,44), might partly explain these inconsistencies. We also observed higher central and peripheral RPEs in H compared with those in N (Figure 2). This confirms that hypoxia itself (independent of exercise-related stress) might affect perceived exertion (24). In fact, central fatigue is likely elicited by low brain oxygenation (1), as possibly evidenced in this study by the lower SpO2 levels. It is also worth noting that in this study the experimental conditions were not blinded to the athletes; therefore, a possible placebo effect on RPE data during H cannot be excluded.
In this study, the increase in plasma EPO concentration was slightly greater in H than in N 30 minutes post HIT; it was however similar 240 minutes after the session (Table 4). Although we are not aware of any comparable data on acute plasma EPO responses to HIT in highly trained young runners, the present data confirm that a single exercise bout (for a total exposure time of <30 minutes as in this study) is likely insufficient to induce substantial changes in EPO concentration (30), and that longer continuous hypoxic exposures at rest (30) or during exercise (42) may be necessary. Although restricted to acute responses to HHIT, these data therefore support the numerous studies that did not report changes in hematological variables (and therefore no improvement in O2 carrying capacity via increases in red cell volume or hemoglobin mass) after HHIT training (for reviews see [5,20,28,46]).
Regarding the impact of HIT on differential leukocyte counts, we found the H condition to be associated with a lower increase compared with N (especially for neutrophils, both 20 minutes and 4 hours postexercise, Table 4). This is in contrast with the general belief that hypoxic training might compromise the immune system to a greater extent than sea-level training does (25), and with the exacerbated immunological stress response described previously in runners after comparable HHIT sessions (31). Immune function is partly regulated by changes in sympathoadrenal activity and is itself related to exercise intensity and hypoxic severity (i.e., the degree of homeostasis perturbation) (25). In this study, although data for epinephrine or norepinephrine were not available, we used noninvasive HRV measures to assess the degree of autonomic nervous system and homeostasis perturbation (15). As expected, Ln rMSSD values were depressed immediately after exercise, but they returned to pre-exercise values within 4 hours (Table 4) for both conditions, suggesting similar levels of homeostasis perturbation. Therefore, despite the higher blood acidosis after HHIT, it is possible that the reduced running speed compensated for the increased hypoxic-related stress on cardiac autonomic function (9,14), leading, in turn, to similar homeostasis changes (i.e., Ln rMSSD). As for the cardiorespiratory variables, large interindividual variations in the differential leukocyte count response were observed (e.g., inferred from high SD for the mean between-condition difference in the changes for neutrophils [Cohen's d]: −0.6 ± 0.8). Again, although this remains behind the scope of this study, our data confirm that physiological (10) and immunological (30) responses to altitude are highly individual. From a practical point of view, the present data suggest that, despite a small to moderate postexercise increase in blood acidosis, the HHIT sessions examined were associated with similar to lower autonomic and immune perturbations than in normoxic HIT sessions.
It is well established that endurance performance does not only depend on energy supply but that neuromuscular functions also plays an important role (34). Examining the acute impact of HIT on motor control and neuromuscular performance is therefore of interest to assess the level of strain that such training sessions are likely to put on these systems. In this study, irrespective of the environmental condition, HIT did not affect jumping ability (Table 5), whereas greater impairments in postural control and improvements in sprinting times were observed after HIT in N. The unaffected CMJ height obtained after HIT and improved sprinting performance (after N) are in line with the findings of previous studies that have reported no changes (44) or an increase (45) in jumping performance after HIT in endurance runners. The ability to sustain an adequate (or improve) muscular performance and to tolerate fatigue during HIT seems to be typical for middle distance runners and is likely related to their high percentage of slow twitch fibers (45). Because of the reduced running speed during H, which probably decreased muscular and neural stress compared with that during N (e.g., although not measured here, lower electromyographic activity has been previously observed in hypoxia ), a probable postactivation potentiation effect (45) was less likely, possibly explaining, in turn, the lack of improvement in sprint times. These present data therefore lend support to the belief that reduced mechanical and neuromuscular stimuli in hypoxia (via a reduced running speed) may lead to a gradual weakening in important neuromuscular determinants of endurance performance (40). Finally, a tendency for a lower impairment in postural control in H (especially eyes open, Table 5) was also observed. This finding is somewhat surprising because exposure to hypoxia has previously been reported to impair postural control (32). It is however possible that in this study the lower running speed during the H session influenced postural control more than exposure to hypoxia. Taken together, our results suggest that HHIT sessions, irrespective of environmental conditions, only put a limited strain on the neuromuscular system. The fact that all neuromuscular performance variables returned to baseline values within 20 minutes suggests that such sessions may be suitable for twice-daily training schedules (at least on the neuromuscular side), as commonly practiced by elite runners.
Many elite endurance runners incorporate some form of altitude or hypoxic exposure in their training, in the belief that it will improve sea-level performance. The present results in highly trained young middle- and long-distance runners show that compared with sea-level sessions, HIT sessions performed at a simulated altitude of 2,400 m are associated with reduced cardiovascular responses and immune, neuromuscular, and motor control impact, while being perceived as being substantially harder. These particular physiological responses suggest that this type of hypoxic HIT training can be of interest to a coach willing to vary training stimuli during high-volume training periods and for athletes training twice a day. The present results confirm that prescribing HHIT sessions following a typical model (26) may not be optimal to concurrently stress and train both the cardiorespiratory and neuromuscular determinants of endurance performance in well-trained athletes (for reviews see [20,40,46]). Both the long-term and acute physiological and neuromuscular responses to other types of hypoxic training sessions, performed at slightly lower intensities (e.g., second ventilatory threshold [11,28]) or with longer between-effort recovery times to minimize running speed reduction (28), still need to be investigated to draw more definitive conclusions on the potential efficiency of HHIT training.
The authors declare no conflict of interest. The authors thank the runners for their enthusiastic participation, Marc Quod for initiating the present study, the coaches Carlos Cavalheiro and Malcolm Geluk for their support and Mohamed Ibrahim Elzain Elgingo, Anoosh Merzoian, and Roula Mattar and Matthieu Sailly for their help in data collection.
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