To date, altitude training has mainly been used by individual “endurance” athletes with the primary goal of further improving exercise performance upon return to sea level. Several paradigms—“live high–train high” (residing and training at altitude) and, more recently, “live high–train low” (LHTL) (sleeping at altitude but training near sea level) approaches (30,31)—have subsequently been introduced to reach this goal. To date and despite ongoing debate on its efficiency in elite endurance athletes or on the nature of its underlying mechanisms (17,24), LHTL is widely recognized as the “gold-standard” altitude training method (23) for athletic performance enhancement. Its success belongs to the erythropoietic effect of chronic hypoxia initiated by continuously residing at natural/terrestrial (hypobaric hypoxia) or simulated (normobaric hypoxia) altitude, with the possibility of maintaining high training intensity and rates of oxygen flux at sea level (43).
An emerging concept is that positive gains associated with the LHTL method may rely on the magnitude of hypoxia-induced increase in hemoglobin mass (Hbmass) (24). Reportedly, LHTL was found to be less efficient in (endurance) athletes with high preintervention Hbmass (16). Because team-sport (28,41) athletes are generally characterized by moderate Hbmass (24) and/or maximal oxygen uptake (V˙O2max), one may speculate on substantial gains in Hbmass after LHTL. Because aerobic metabolism dominates energy delivery in most team sports (e.g., soccer, rugby, or field hockey), it is likely that LHTL would benefit some team-sport athletes (13). Although positive short-term benefits on Hbmass have been reported after only 13–19 d of exposure in Australian Football League (AFL) (28), soccer (41), or water-polo (12) players, the level of evidence of the usefulness of LHTL in improving sport-specific performance in team-sport athletes is still limited (2).
Team sports share a common feature—high-intensity intermittent exercise patterns, where the ability to repeatedly perform maximal or near-maximal bouts with incomplete recoveries [i.e., repeated-sprint ability (RSA)] for sustained periods is important for match outcome. In field hockey, for instance, although the distances covered by high-intensity running (∼8%) and sprinting (∼1%) only represent a small percentage of the total match duration, both decrease from the first half to the second half, which may increase chances to evade an opponent and create scoring opportunities (26). In order to better resist fatigue in the most intense periods of a game or toward match end, innovative hypoxic training methods have recently been tailored for team-sport use (2,13,29). In this vein, we have recently updated the panorama of the different hypoxic methods currently available to add repeated-sprint training in hypoxia (RSH) (30) as a new form of “live low–train high” regimen. Briefly, RSH, which includes maximal-intensity efforts under moderately hypoxic conditions, has proved superior to repeated-sprint training in normoxia (RSN) in enhancing peripheral adaptations (9,33,38) and thereby to RSA (8,9,11). With physical performance only acutely (within days) assessed after the RSH intervention, however, the long-term (few weeks) deacclimatization effects (if any) of this hypoxic method are currently unknown. Although all available RSH studies have so far been conducted in a laboratory environment, only two have adopted a running mode (i.e., nonmotorized treadmill [5,11]), yet none of them have used overground sprints, which would considerably increase the ecological validity of literature findings.
Evaluating the combination of altitude training methods and its effects on the magnitude and time course of several aspects of match-related performance and adaptive physiological response is an integral part of the role of research scientists. The capacity of team-sport athletes to repeatedly perform high-intensity actions depends not only on their Hbmass but also on skeletal muscle tissue adaptations and the efficiency of their neuromuscular system. Theoretically, for team-sport athletes and coaches looking to elicit concurrent aerobic and anaerobic adaptations to improve sea-level performance, “live high–train low and high” [LHTLH; i.e., 2–3 wk of sleeping at 2500–3000 m with training at sea level, except for a few (two to three) hypoxic training sessions per week], suggested as early as 2010 (30,31), is an attractive combination. However, it is currently unknown whether combining LHTL and RSH in a cohort of team-sport athletes would produce larger performance gains than would concurrent LHTL and RSN.
Using a randomized, double-blind, controlled design, this study aimed to investigate the immediate (few days) and prolonged (3 wk) effects of the “traditional” LHTL approach, combined with either RSH or RSN (both compared with controls), on team-sport-specific sea-level performance and Hbmass in elite field hockey players. We hypothesized that, combined with traditional “LHTL” exposure, RSH (LHTL + RSH, namely, LHTLH) versus RSN (LHTL + RSN, namely, LHTL) provides similar hematological adaptations but larger sport-specific physical performance gains, persisting at least 3 wk postintervention.
Thirty-six lowland elite male field hockey players (mean ± SD: age, 25.3 ± 4.6 yr; height, 178.4 ± 6.0 cm; body weight, 75.8 ± 7.9 kg; estimated V˙O2max, 52.1 ± 1.9 mL·min−1·kg−1 ) were recruited from among Belgium, Spanish, and Dutch first division clubs (nine of the participants were national team members of their respective countries) to participate in this study. The experiment was approved by the Anti-Doping Lab Qatar institutional review board (agreement SCH-ADL-070) and conformed to current Declaration of Helsinki guidelines. Subjects gave their written informed consent after having been informed in detail of all experimental procedures and possible risks [e.g., severe intensity nature of the proposed exercise, acute mountain sickness (AMS), including headache, dizziness, tiredness, shortness of breath, and nausea, in isolation or in combination], associated with the experiments. Exclusion criteria for participation were acclimatization or exposure to hypoxia of more than 2000 m for more than 48 h during a period of 6 months before the study and any history of altitude-related sickness and health risk that could compromise the subject’s safety during training and/or hypoxia exposure. During the study, one subject from the control group (see “Study Design”) was excluded after the lead-in period due to insufficient fitness level (i.e., incapacity to satisfy the criterion score for physical performance tests; see “Pre, Post-1, and Post-2 Testing Sessions”), whereas three others (control group, n = 1; experimental groups, n = 2) were excluded due to illness or injury.
The experimental design (Fig. 1) consisted of the following: a 2-wk lead-in period (from middle of December to beginning of January) at sea level where training sessions were supervised and load quantified; a 1-wk preintervention period at sea level where baseline testing (Pre) was performed; a 14-d hypoxic intervention period; and, finally, a 3-wk postintervention period at sea level with training sessions supervised and load quantified, where Post-1 (2–3 d) and Post-2 (22–23 d) test sessions were performed.
Each of the three test sessions (Pre, Post-1, and Post-2) was 48 h in duration and involved the 32 players on the same sea-level testing site (Belgium). At this occasion, physical performance and Hbmass were evaluated in invariant order under similar temperate conditions (±2 h). After the completion of Pre, subjects were randomly assigned to one of the three following groups according to their initial fitness level and playing position (Table 1): 14 d of “LHTL” altitude training (>14 h·d−1 and simulated altitude of 2500–3000 m) during which players trained (i.e., regular field hockey practice) at sea level with the addition of six repeated-sprint training sessions either in normobaric hypoxia simulating an altitude of 3000 m (LHTL + RSH, namely, LHTLH; n = 11) or in normoxia (LHTL + RSN, namely, LHTL; n = 12) and “live low–train low” (LLTL) training (n = 9). LLTL players resided at sea level yet under comfort conditions similar to those in the two experimental groups. Although LLTL players were not enrolled in training camp (Qatar, January 2014, normal environmental conditions), they followed the same training/competition routine (i.e., without the completion of any additional repeated-sprint training session) as LHTLH or LHTL players. All subjects were familiar with the testing procedures as part of their regular physical performance assessment implemented in their clubs. Although not recorded, particular attention was paid to food intake, hydration, and sleep habits during the experiment, such that players from all three groups were provided with similar diets and bedtime schedules, which were based on club guidelines and experience gained from previous training camps.
To evaluate physical performance, subjects performed a test battery at sea level on a well-ventilated indoor synthetic ground (Taraflex®) gymnasium at a constant temperature of ∼22°C. Pre, Post-1, and Post-2 testing sessions were performed in the exact same sequence as follows: (i) jump tests; (ii) after 10 min of rest, repeated sprints; and (iii) after an additional 15 min of recovery, and Yo-Yo Intermittent Recovery Level 2 (YYIR2). Due to the extreme intensity of the tests, subjects were asked to arrive at the testing sessions in a rested and hydrated state (at least 3 h after a meal and having avoided strenuous training in the preceding 24 h). In all cases, subjects were asked to reproduce their last meals, avoiding alcohol and caffeine intakes during the 24 h before each test scheduled in the same time slot. Tap water was provided ad libitum. For all tests, subjects were vigorously encouraged during all efforts. Before the test battery, a standardized 15-min warm-up, including athletic and acceleration drills, was supervised by two investigators.
Living hypoxic exposure
The sleeping and recreational hypoxic facilities were fully furnished normobaric hypoxic rooms with O2 filtration (CAT system; Colorado Altitude Training, Louisville, Colorado, USA). Three days before the start of the study, all rooms were controlled and calibrated by qualified engineers. Furthermore, all investigators, except for the main investigator, were blinded to group assignment. In all rooms, air pumps were constantly turned on. O2 fraction in each room was continuously monitored from independent O2 probes connected to a control panel located in a room where access was restricted to the main investigator only. The two intervention groups were exposed to normobaric hypoxia equivalent to 2500 m [fraction of inspired oxygen (FiO2), 15.1%; blood pressure, 768.0 mm Hg; partial pressure of inspired oxygen (PiO2), 108.3 mm Hg] for the first 24 h of the intervention period (day 1). Thereafter, O2 fraction was further decreased to the equivalent of 2800 m (FiO2, 14.5% ± 0.1%; blood pressure, 766.8 ± 1.1 mm Hg; PiO2, 104.5 ± 0.6 mm Hg; days 2–5) and 3000 m (FiO2, 14.2% ± 0.1%; blood pressure, 765.3 ± 1.5 mm Hg; PiO2, 101.7 ± 0.8 mm Hg; days 6–14). Subjects were strictly confined (as verified by the main investigator) to their rooms from 2200 to 0700, from 0800 to 1000, and again from 1300 to 1600 during these 2 wk. However, they were encouraged to spend more time in their rooms, if desired. Concentrations of ferritin (143.6 ± 68.9 μg·L−1; range, 45–279 μg·L−1) and soluble transferrin receptor (254.7 ± 33.3 mg·dL−1; range, 202–330 mg·dL−1) measured during the lead-in period indicated that none of our subjects were iron deficient at the time of study entry.
Daily physiological measures and questionnaires
During the intervention period, arterial oxyhemoglobin saturation (SPO2) and HR were recorded in a blind manner, using fingertip pulse oximeters (GO2™ Achieve 9570-A; Nonin, Plymouth, MN, USA), every morning upon waking up. Afterward, participants had to fill three different questionnaires: (1) the Lake Louise score questionnaire, which included five simple questions (scale from 0 to 3) that were sensitive to quantifying AMS severity (34). Overall Lake Louise score was determined by summing all scores; (2) the Daily Analysis of Life Demands for Athletes (DALDA) questionnaire (36), which was used to monitor psychological status (i.e., mood state); parts A and B of the DALDA questionnaire represent the sources and manifestations of stress (general fatigue and feelings) in the form of signs and symptoms, respectively. For both parts, the number of items marked as “worse than normal” (i.e., a scores) was tallied and reported; and (3) the 15-item Groningen Sleep Quality Scale (GSQS), which was used to evaluate high-altitude sleep disturbance (42). Finally, subjects (in minimal clothing) were weighted with a digital balance (±0.1 kg; Seca, Hamburg, Germany) before breakfast. All aforementioned variables were averaged over the 14-d training camp for subsequent analysis.
Field hockey training sessions
During the entire study (from the start of the lead-in period to Post-2), each field hockey training session and match was monitored. Players’ training loads [arbitrary units (a.u.)] were calculated as total training/competition duration (min) × session RPE (Borg’s scale from 6 to 20), collected within 10 min of completing each training session. On days with two training sessions, daily training load was taken as the sum of the sessions performed. On average, tested players practiced ∼7.0–9.0 h·wk−1 (three to four field hockey sessions + two to three fitness sessions + one to two matches) during the season (i.e., within the 3 months preceding the lead-in period).
Supervised training protocol
In addition to their usual field hockey practice, players of the two intervention groups completed six specific repeated-sprint training sessions during the 14-d intervention period with at least 36 h recovery in between. Sessions were completed on synthetic grass inside a mobile inflatable simulated hypoxic equipment (Altitude Technology Solutions Pty Ltd, Brisbane, Queensland, Australia), as recently described (14). Briefly, it comprised a polyvinyl chloride inflatable running lane tunnel (length, 45 m; width, 1.8 m; height, 2.5 m) and a state-of-the-art hypoxic trailer (a 55-kW screw compressor), generating more than 3000 L of hypoxic air per minute, with FiO2 between 21% and 10% (a simulated altitude of up to 5100 m). FiO2 was continuously measured (every 5 s) by two sensors located at 15 and 30 m in the tunnel and displayed on the control panel, which was managed only by the main investigator. Air input flow was sufficient for safe, comfortable, and stable training conditions, with temperature and humidity maintained at ∼25°C and ∼55% relative humidity, respectively. For RSH, ambient air was mixed with nitrogen (from pressurized tanks) to reduce FiO2 to ∼14.5% in order to simulate an altitude of 3000 m. In order to blind subjects to altitude, the system was also run for RSN with normoxic airflow (FiO2, 21.0%) into the tunnel. For motivational reasons and reinforcement of the subjects’ blinding to group classification, all players were assigned to different teammates during each of the six training sessions.
Specific training sessions
Each session lasted ∼50 min, including a 15-min warm-up, repeated-sprint training routine, and a 10-min recovery phase (i.e., a total of 300 min for the six sessions during the 14-d training camp). Specifically, the repeated-sprint training routine included four sets of 5 × 5-s maximal sprints interspersed with 25 s of recovery with 5 min of passive recovery between sets, finally ending with a 10-min cooling-down period (Fig. 1B). Subjects were constantly reminded to exert “all-out” effort in trying to reach peak acceleration and to maintain the highest possible running speed for every 5-s sprint bout. Up to six subjects trained simultaneously in the inflatable marquee. Commercially available energy drinks and bottled water were provided ad libitum during training to ensure appropriate hydration.
This research was run in a double-blind controlled manner. With the exception of the control group, subjects in both the LHTLH group and the LHTL group were told (based on the head coach’s request to increase team motivation) that they were both residing in and training under hypoxic conditions but had no accurate information about the simulated altitude levels inside the rooms and inflatable marquee. The efficacy of the blinding process was evaluated upon experiment termination (i.e., immediately after Post-2) by administering Likert scales (100 m marks from 0 to 4000 m), where each participant had to indicate (separately) which simulated altitude he believed he had been living at and training in for the first and second weeks of the altitude camp (i.e., scores for weeks 1 and 2 were then averaged to report only one value for the total duration of the camp).
Pre, Post-1, and Post-2 Testing Sessions
Players performed the following vertical jump tests with their hands kept on the hips to eliminate any influence of arm swing: (i) squat jump (SJ) starting from a static semisquatting position (∼90° of flexion) maintained for ∼1 s and without any preliminary movement; (ii) countermovement jump (CMJ) starting from a standing position, squatting down to ∼90° angle, and extending the knee in one continuous movement; and (iii) one set of multirebound jumps (MRJ) with rebounds to the highest possible point six times. For SJ and CMJ, subjects were asked to perform two maximal trials, and the highest jump was recorded. During MRJ, they were instructed to keep their knees as stiff as possible (“ankle jumps”) and to have as brief a contact time as possible. Jump heights were calculated by recording flight times (SJ, CMJ, and MRJ) and ground contact (MRJ) with an optical measuring apparatus (Optojump; Microgate, Bolzano, Italy).
The subjects underwent an RSA test consisting of eight 20-m sprints departing every 20 s. The sprints were performed back and forth to allow for passive recovery during the short rest period. Players had to complete the distance in a straight line as fast as possible. Three seconds before the start of each sprint, they were asked to assume the ready position and to await the start signal with a 3-s countdown (3, 2, 1, “go”). Each sprint was initiated from a standing position, 50 cm behind the photocell gate, which started a digital timer. Sprint times were measured to the nearest 0.01 s using photocells connected to an electronic timer (Polifemo Radio Light; Microgate), whose height was adjusted according to the height of the subject’s hip. The two photocells were placed at 0- and 20-m distance intervals. During the first sprint, subjects were required to achieve at least 95% of their criterion score (i.e., defined as the best of three single 20-m sprints interspersed with 2 min of recovery; data not presented) as a check on pacing. All of the subjects satisfied this criterion score. Two scores were calculated during the RSA test: cumulated sprint time and percentage of sprint decrement calculated as follows: [(cumulated sprint time)/(best sprint time × 8) − 1] × 100 (15). A similar RSA test (i.e., 6 × 30 m departing on 25 s) in highly trained field hockey players was found to be very reliable, as evidenced by a typical error of 0.7% for the total sprint time (39).
Specific aerobic capacity
To assess high-intensity intermittent running performance, subjects performed an incremental running test up to exhaustion (YYIR2) (1). Briefly, the test consisted in repeated 20-m shuttle runs at increasing speeds (starting at 13 km·h−1) controlled by audio beeps interspersed by 10 s of active recovery. When the subject failed to reach the finish line in time twice, the distance covered was then recorded and represented the test result. HR (Polar Electro, Kempele, Finland; 5 s on average) was measured, with the highest value retained as HRmax. During the YYIR2 test, none of the subjects reported an HRmax <95% of their age-predicted HRmax (i.e., traditional 220 − age formula), indicating maximal exhaustion. This test is reproducible and is a sensitive tool for assessing aerobic capacity in team-sport players (20).
Hbmass was measured in duplicate at each time point by using a slightly modified version (40) of the optimized CO rebreathing method described by Schmidt and Prommer (37). Briefly, subjects spent 5 min in sitting position before three capillary blood samples (35 μL) were taken from the earlobe and analyzed immediately for baseline carboxyhemoglobin values (ABL 800flex; Radiometer A/S, Copenhagen, Denmark). Subjects then rebreathed for 2 min a gas mixture of 100 mL of pure CO (Multigas SA, Domdidier, Switzerland) and 3.5 L of oxygen in a closed-circuit system (glass spirometer; Blood Tec GbR, Bayreuth, Germany). During the rebreathing period, a CO gas analyzer (Dräger PAC 7000; Dräger Safety, Lübeck, Germany) was used to check for possible CO leakage at the nose, mouthpiece, and spirometer system. On minutes 6 and 8 after the start of CO rebreathing, two final capillary blood samples were taken from the earlobe and averaged as a 7-min postcarboxyhemoglobin value. Directly before and 2 min after rebreathing, the same CO gas detector as described above was used to quantify end-tidal CO concentration (in parts permillion). Hbmass was calculated from the mean change in carboxyhemoglobin before and after CO rebreathing, as described previously by Steiner and Wehrlin (40). Both measurements were performed on two consecutive days (12-h to 24-h time lag between measures), and the results were averaged. In our mobile laboratory, the typical error was 1.6% for CO rebreathing method and 1.1% for mean duplicate Hbmass measurement over all measurement time points.
All data in the text and figures are presented as mean ± SD. Relative changes (%) in performance are expressed with 95% confidence intervals (95% CI). LHTLH and LHTL room and inflatable marquee exposures were compared with paired t-test. One-way ANOVA was used to test differences in training load, questionnaires, and physiological measures between groups. Two-way ANOVA with repeated measures [Time (Pre vs Post-1 vs Post-2) × Condition (LHTLH vs LHTL vs LLTL)] was used to compare physical performance and Hbmass data. ANOVA assumptions were verified before all statistical analyses. Pairwise differences were identified using the Holm–Sidak post hoc analysis procedure adjusted for multiple comparisons. Pearson’s product–moment correlation analysis was employed to determine correlations between Pre and Post-1 and/or Post-2 changes between Hbmass and physical performance tests. The null hypothesis was rejected at P < 0.05. All statistical calculations were performed using Sigmaplot 11.0 software (Systat Software, San Jose, CA).
Hypoxic dose and efficacy of the blinding procedure
Mean daily room confinement (14.5 ± 0.8 and 14.4 ± 0.7 h·d−1; P = 0.52), total RSH/RSN exposure (3.9 ± 0.7 and 3.7 ± 1.1 h; P = 0.51), and total hypoxic dose (202.5 ± 4.5 and 201.2 ± 3.0 h; P = 0.75) were similar between LHTLH and LHTL. Participants from both experimental groups were not able to correctly identify the simulated altitude they were residing at [2591 ± 767 m (range, 200–3700 m) and 2491 ± 658 m (range, 1500–3500 m) for LHTLH and LHTL, respectively] and training in [2445 ± 771 m (range, 1000–4000 m) and 2648 ± 761 m (range, 1000–3750 m) for LHTLH and LHTL, respectively]. Overall, this indicates that the blinding process was successful and that subjects were unaware of the hypoxic group classification.
Morning HR, SPO2 and questionnaires
No difference (P = 0.74) in the mean values of wake-up HR was found between groups during the experimental period (60 ± 8, 60 ± 3, and 59 ± 7 bpm for LHTLH, LHTL, and LLTL, respectively). Mean SPO2 for LLTL (97.2 ± 0.7%) was higher (P < 0.001) than those for both intervention groups, and LHTLH showed lower SPO2 than LHTL during hypoxic exposition (92.3 ± 0.9% and 93.2 ± 0.9%, respectively; P < 0.05). No change in mean body weight was observed between groups (P = 0.87) during the study.
The mean Lake Louise score was 1.0 ± 0.9 for LHTLH, 1.2 ± 0.8 for LHTL, and 1.4 ± 0.7 for LLTL, and no difference (P = 0.54) was found between groups. Part A (0.6 ± 0.5, 0.7 ± 0.8, and 0.9 ± 0.7 for LHTLH, LHTL, and LLTL, respectively; P = 0.41) and part B (1.2 ± 1.3, 2.1 ± 1.7, and 2.6 ± 2.1 for LHTLH, LHTL, and LLTL, respectively; P = 0.14) of the DALDA questionnaire were not different between groups. The mean GSQS value for sleep quality during the intervention period was comparable for all groups (2.0 ± 0.9, 2.0 ± 1.1, and 2.1 ± 1.0 for LHTLH, LHTL, and LLTL, respectively; P = 0.93), indicating no disturbed sleep. Similarly, no difference in GSQS waking state (1.2 ± 0.6, 1.2 ± 0.6, and 1.1 ± 0.5 for LHTLH, LHTL, and LLTL, respectively; P = 0.90) was observable.
Overall training load was closely matched among the three groups during the study (3534 ± 412, 3702 ± 570, and 3179 ± 309 a.u. for LHTLH, LHTL, and LLTL, respectively; P = 0.35). No difference in mean field hockey training load occurred during the lead-in period (981 ± 142, 1054 ± 196, and 1070 ± 55 a.u.; P = 0.57), 2-wk intervention period (976 ± 112, 985 ± 143, and 1016 ± 99 a.u.; P = 0.86), and 3-wk postintervention period (987 ± 142, 981 ± 142, and 1094 ± 254 a.u.; P = 0.59) among the LHTLH, LHTL, and LLTL groups. Note that no significant difference (P = 0.90) in mean training load monitored during both specific RSH (590 ± 76 a.u.) and RSN (594 ± 35 a.u.) sessions was observable.
Compared with Pre, both hypoxic groups similarly increased their Hbmass at Post-1, with no further change at Post-2 [LHTLH: 888 ± 107, 924 ± 114 (P < 0.001), and 912 ± 127 g (P < 0.01); LHTL: 931 ± 131, 957 ± 140 (P < 0.001), and 956 ± 137 g (P < 0.001)] (Fig. 2). Note that the increase in Hbmass at Post-1 and Post-2, which exceeded the typical error of 1.6% for the CO rebreathing procedure, occurred in 18 and 15 of the 23 subjects composing the two intervention groups, respectively. Hbmass remained unchanged for LLTL at Pre, Post-1, and Post-2 (929 ± 171, 934 ± 170, and 930 ± 163 g, respectively). Finally, no significant correlation among Pre, Post-1, and/or Post-2 changes in Hbmass and any physical performance data could be evidenced.
With the exception of CMJ height (time effect, P < 0.05), none of the vertical jump test data displayed a main effect of condition or any significant interaction between time and condition (Table 2).
From Pre to Post-1, the intervention resulted in similar increases in YYIR2 performance in LHTLH [from 520 ± 165 to 615 ± 162 m; +21% (95% CI, 7% to 36%); P < 0.01] and LHTL [from 540 ± 126 to 647 ± 147 m; +22% (95% CI, 10% to 34%); P < 0.001], whereas no significant change occurred in LLTL [from 413 ± 89 to 427 ± 96 m; +4% (95% CI, −19% to 26%)] (Fig. 3). At Post-2, both hypoxic groups further increased their YYIR2 performance by a mean of +45% (95% CI, 21% to 74%) (764 ± 227 m) and +19% (95% CI, 21% to 75%) (789 ± 187 m) in reference to Pre and Post-1 (both P < 0.001), respectively.
During the RSA test (Fig. 4), cumulated sprint time decreased from Pre to Post-1 in both LHTLH [from 27.23 ± 1.15 to 23.23 ± 1.02 s; −3.6% (95% CI, −5% to −2%); P < 0.001] and LHTL [from 27.05 ± 0.81 to 26.54 ± 0.77 s; −1.9% (95% CI, −3% to −1%); P < 0.01], with no significant change in LLTL [from 26.98 ± 1.03 to 26.81 ± 1.47 s; −0.7% (95% CI, −3% to 1%)]. Compared with Pre, cumulated sprint time at Post-2 remained significantly shorter (P < 0.001) for LHTLH [26.21 ± 1.09 s; −3.5% (95% CI, −5% to −2%)], whereas no difference was observed for LHTL [26.63 ± 0.90 s; −1.5% (95% CI, −3% to 0%)] and LLTL [26.86 ± 1.31 s; −0.8% (95% CI, −3% to 1%)]. Sprint decrement score [averaged for all conditions, 4.0% (95% CI, −1% to 9%)] did not change throughout the protocol (P = 0.14).
To the best of our knowledge, the present study is the first randomized, double-blind, controlled investigation verifying the usefulness of combining hypoxic training methods when attempting to improve sea-level performance in elite team-sport athletes. We have administered “traditional” LHTL with RSH (namely, “LHTLH” hypoxic training) and compared its immediate (few days) and prolonged (few weeks) effects with a combination of LHTL and RSN. Our results are clear and compelling: first, similar increases in Hbmass and specific aerobic fitness (YYIR2 performance) in the two intervention groups despite a low altitude (≥200 h); second, YYIR2 performance was further enlarged at Post-2 in reference to Post-1 in the two intervention groups, whereas Hbmass was maintained; and third, RSA was improved in the two intervention groups yet with twice-larger gains measured at Post-1 in LHTLH compared with LHTL. Three weeks after the intervention, RSA performance improvements were only maintained in the LHTLH group. Overall, this short-term LHTLH method (i.e., 14 d of LHTL exposure + 6 RSH sessions, as performed “in season”) demonstrated greater effects on Hbmass and sport-specific physical performance (YYIR2 and RSA) than did LHTL and LLTL training in elite field hockey players, with the benefits lasting for at least 3 wk postintervention.
LHTL(H) as stimulus for increasing Hbmass
In the present study, we have demonstrated that 14 d of LHTL in normobaric hypoxia at ∼2800–3000 m were sufficient to immediately increase Hbmass by ∼3%–4%. This increase is greater than the magnitude observed in previous studies with similar hypoxic doses in normobaric hypoxia or is in line with longer exposure (i.e., 1% for every 100 h) to hypobaric hypoxia (18). More specifically, our results are very similar to those involving team-sport populations. Reportedly, Hbmass increased by ∼3%–4% after (i) 18–19 d of preseason moderate-altitude (∼2100 m) training camp in elite AFL players (28); (ii) 10 d of simulated LHTL in international-level water-polo players (12); and (iii) 13 d spent at 3600 m altitude in U17 soccer players (41). Direct comparisons of Hbmass gains between the aforementioned studies are difficult because the magnitude of hypoxia-induced hematological changes would differ according to various “dose–response” relationships (25), training content (31), and individual responsiveness (6). Of importance, with no significant difference in training load between our three groups, the lack of change in Hbmass in the LLTL group would indicate that any specific hockey practice/training-induced increase in Hbmass is unlikely for this short period. Despite ongoing debate surrounding the importance of hematological factors in driving adaptations induced by chronic exposure to hypoxia (18), it has been acknowledged that, in elite endurance (16) and team-sport (28) athletes, hypoxia-induced Hbmass response is inversely related to its initial level (27). In our study, preintervention Hbmass values (mean of the three groups, 916 ± 133 g) were in agreement with those measured in other team-sport athletes (926 ± 118 g, ranging from 721 to 1023 g in AFL, soccer, field hockey, and water-polo players) (12,19,28,41).
With similar room confinement time for our two intervention groups, the addition of six RSH sessions (∼5 h at a simulated altitude of 3000 m) for LHTLH had no measurable impact on Hbmass increase. This demonstrates that hypoxic dose is the main factor for Hbmass increase and that RSH per se has no “erythropoietic” effect. It is also known that, at moderate altitude, the occurrence of negative side effects (e.g., AMS symptoms) is very low (35). This was confirmed with the present athletes who displayed low perceptual scores to questionnaires. Taken as a whole, this fully supports the notion that a relatively short period of normobaric hypoxic LHTL or LHTLH exposure (∼2 wk and low hypoxic dose of ∼200 h at simulated altitudes of ∼2800–3000 m) may be sufficient to increase Hbmass in team-sport athletes.
Immediate effect on sea-level physical performance
The aforementioned increase in Hbmass at Post-1 was also transposed into an immediate improved specific aerobic performance, as evidenced by the large (∼21%) and similar increase in YYIR2 distance in the two intervention groups. Note that the absence of an increase in jumping performance after LHTL, combined with repeated sprinting (under hypoxic or normoxic conditions), would suggest that leg power was not modified in response to such training and was therefore probably not directly involved in marked aerobic performance gains. Our substantial in-season increments in YYIR2 performance are in line with the findings of Galvin et al. (11), who reported that a 4-wk RSH treadmill sprint intervention induced +33% improvements in well-trained academy rugby players’ intermittent running performance (i.e., Yo-Yo Intermittent Recovery level 1). Therefore, the present data confirm that within no more than 14 d of residing in simulated altitude (irrespective of additional RSH training) there were substantial ergogenic benefits of LHTL for elite team-sport athletes when tested at sea level.
Along with YYIR2 performance, improvement in RSA also occurred in our two experimental groups, with a twofold superior benefit seen in LHTLH compared with LHTL (cumulated sprint time, −3.6% vs −1.9%, respectively). In addition to this shorter cumulated sprint time, the unchanged percentage of sprint decrement observed at Post-1 strengthens this result. By using sport-specific ecological training and testing setting (i.e., repeated sprinting on synthetic grass with players wearing their field hockey shoes inside a mobile inflatable hypoxic marquee under normobaric hypoxic conditions), the present results therefore strengthen the validity of previous studies (5,9,11,33). In particular, it appears of practical relevance to solve some of the problems related to the congested calendars of the majority of professional team-sport athletes, which do not allow players to afford time for the usually recommended 3- to 4-wk blocks of altitude training. Furthermore, it suggests that the proposed mechanisms (see later) were not blunted by the Hbmass increase. The rationale for this study was based on the assumption that, if the LHTL paradigm works to improve sea-level “endurance” performance and if additional RSH works to improve sea-level-specific performance (i.e., higher tolerance for repeated-sprint exercises) (5,9,30), then the physiological benefits of the LHTLH method must derive from the combination of these two hypoxic methods. Whereas the mechanisms behind coupling different hypoxic methods are currently unknown, our findings provide evidence that both “aerobic” and “anaerobic” benefits acutely improve sea-level team-sport physical performance.
Although the main mechanism for improved sea-level performance after “traditional” LHTL exposure relies on an increase in red cell mass (23), other hypoxia-induced physiological adaptations are possible and may include improved muscle buffer capacity (17). Similarly, exercise capacity during high-intensity intermittent tasks depends not only on Hbmass but also on molecular adaptations at the skeletal muscle level and on the efficiency of the neuromuscular system (8,9,11). When used in isolation (8), RSH was superior to RSN in enhancing peripheral adaptations (i.e., oxidative capacity, capillary density, and muscle glycolytic potential, as well as increased expression of hypoxia inducible factor 1α and downstream genes for oxygen and transport) (9,38). Pending confirmatory research, this would suggest a hypoxia-induced increase in anaerobic glycolytic activity in muscle and a more efficient use of fast-twitch muscle fibers (8,9). With comparable Post-1 Hbmass gain between LHTLH and LHTL, the twice-larger improvement in RSA in the former group, compared with the latter group, is likely linked to the aforementioned RSH-specific adaptations. Nevertheless, one limitation relates to our inability to examine the independent effects of repeated-sprint training and residing in hypoxia. Although the addition of a group of players living near sea level with additional RSN would have improved our test design, increasing our sample number was unrealistic in our cohort of elite players.
Delayed effects on sea-level performance
When players were retested 3 wk after completion of the hypoxic intervention, the LHTLH and LHTL groups displayed maintenance of Hbmass but enhancement of YYIR2 performance at Post-2 in reference to Post-1, whereas only LHTLH players were able to preserve their hypoxia-induced RSA gains. Within competitive field hockey matches, research has reported a reduction in total distances achieved by players at high intensity (26). Bearing in mind that decisive events during competitive games are often reliant on transient RSA (10,32), the larger improvement in RSA performance in LHTLH players compared with LHTL players is likely to give them further competitive edge in the most intense periods of a game or toward match end. Three main components have been suggested to primarily influence rate of deacclimatization or change in performance (i.e., training responsiveness and exercise capacity) after an altitude training stimulus (7): timing in decay in Hbmass, consequences of ventilatory acclimatization, and alterations in biomechanical and neuromuscular factors associated with force production. In the present study, the increase (∼3%) in Hbmass at Post-2 appears consistent with the model estimated by Gore et al. (18), which was susceptible to be maintained for up to 20 d after LHTL. Considering the paucity of data describing the decay and/or normalization of hematological response after return to sea level, it is unclear whether a period of reacclimatization to sea level is necessary to obtain the full effects of additional high-intensity altitude training, whereas this effect may well relate to ventilatory factors (i.e., time course of the decay of ventilatory acclimatization with return to sea level ). In our study, however, there was no difference in YYIR2 improvement during the postaltitude periods between LHTLH and LHTL, making it unlikely that the postintervention improvement represents a generic “delayed” response to altitude. Conversely, it could be hypothesized that, due to the positive acclimatization response to hypoxia, the ability to train at a higher level after return to sea level may allow achievement of higher fitness levels (i.e., improved training responsiveness). Although postintervention training load was strictly controlled and monitored for 3 wk (i.e., similar between groups), it cannot be completely ruled out that easier subjective ratings to produce the same “external physical output” may have resulted from the LHTLH intervention, which deserves further research attention. Finally, although speculative, hypoxia-induced improvement in the active musculature neural drive (4) may have up-regulated musculoskeletal stiffness, leading to faster stride frequencies and thereby better sea-level RSA (3). Reportedly, after 28 d of LHTL—where, out of as many as 40 total training sessions, seven training sessions classified as higher intensity were performed at lower altitudes (365–1150 m), no alteration in stride length, stride frequency, ground contact, or aerial time was observed in a group of six elite distance runners tested at common racing speeds (18–25 km·h−1) (21). However, as this later study neither recruited team-sport participants nor employed sprinting speeds, with measurements restricted to the period immediately after intervention, more research is required.
This study is the first to combine traditional LHTL with RSH, compared with similar training in normoxia, in team-sport players and to determine its short-term (few days) and long-term (3 wk) effects on hematological parameters and sport-specific physical performance. With only a low hypoxic dose (≥200 h), “LHTLH” conducted for 2 wk during the in-season period of elite field hockey players is an attractive intervention to elicit “aerobic” and “anaerobic” benefits for improving sea-level performance. Our results displayed similar immediate up-regulated Hbmass and increase in specific aerobic performance in the two experimental groups. However, the superiority of LHTLH to LHTL was demonstrated in the RSA test with twice-larger acute performance gains, with those being well maintained at least for 3 wk after the LHTLH intervention only. This advocates that nonhematological factors outside the role played by oxygen-carrying capacity are probably more robust to explain performance enhancement and/or maintenance after LHTLH. Determination of optimal characteristics for combining hypoxic methods and identification of the hematological, ventilatory, and biomechanical mechanisms of adaptation and individual rates of decay in deacclimatization of the newly proposed LHTLH method also require future research.
The authors would like to thank the ASPETAR staff for administrative and technical support, and use of their facilities. The authors are indebted to Mr. Paolo Gugelmann for his outstanding laboratory assistance with the optimized CO rebreathing method. Last but not the least, the authors acknowledge the dedicated participants, as well as their technical staff, for their excellent compliance and cooperation during training and testing.
This research was funded by a grant awarded by ASPETAR (Qatar Orthopedic and Sports Medicine Hospital) to the Aspire Zone Foundation, Qatar (AF/C/ASP1905/11).
The authors have no conflicts of interest, source of funding, or financial ties to disclose, and no current or past relationship with companies or manufacturers that could benefit from the results of the present study.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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