The hypoxic dose required to induce any adaptations and improve performance is still under debate (23,36). Although most recommendations endorse a large exposure, such as 22 h·day−1 over 4 weeks at an altitude of 2,000-2,500 m (36), and question the benefit of a short exposure (23), a current practice by athletes is to use hypoxic facilities for short periods immediately before competition. However, the immediate effects of a short-term sojourn in such rooms or tents are still unclear. Although 90 minutes of hypoxic exposure was sufficient to increase mean plasma concentration of erythropoietin (EPO) (31), such increases in EPO after a brief exposure are insufficient to stimulate reticulocyte production (1). This suggests that if performance is improved after a short-duration exposure, there could be linked factors other than oxygen-carrying capacity.
In line with this, improvement in middle-duration performances were observed on return to sea level after an altitude sojourn (7,32,34), without modification in maximal oxygen consumption. Thus, the improvement in performance may come from other mechanisms; hemodynamic (5,18), ventilatory (16,17,19), or muscular adaptations (15,29) that might induce improvements in economy (11,12,24,33), buffering capacity (11,12), or delayed positive effects of hypoxic ventilatory response (HVR) (16,18,19). To our knowledge, there is a paucity of data regarding the underlying mechanisms that could benefit middle-distance running performance immediately after a short-duration exposure despite the limited hematological adaptations.
Short-duration (2hours) hypoxic exposure has been shown to increase serum erythropoietin observable with a delay (4-6 hours after the onset of exposure), suggesting a potential short-term positive response to hypoxia (20). Contradictorily, change in the distribution of body water, in its hormonal regulation (e.g., aldosterone and arginine vasopressin), and in electrolytes (e.g., sodium and potassium blood and urine concentrations) have been reported (25,26) and might have a negative effect on performance.
Whatever the mechanism, some athletes use normobaric hypoxic rooms or tents to simulate altitude before competition to improve performance. Consequently, since the Sydney 2000 Games, altitude-simulating devices have been banned from the Olympic Village. However, the benefits or the negative side effects of using these altitude rooms or tents on the days preceding the event are not known. Therefore, the objective of this study was to test the effects of a short-duration normobaric altitude exposure on middle-distance running performance to provide some precompetition recommendations to athletes and coaches.
Experimental Approach to the Problem
Sleeping in hypoxic rooms or tents became a general practice in athletes over the last decade. The protocol developed in this study, aimed to test the immediate effects of these devices on performance (1,500-m run). A group of 13 athletes used to running on a treadmill was tested on 2 occasions: after using these devices or in a control condition (random order). In each condition, the performance (i.e., running time) was recorded as the dependent variable in addition to the physiological responses (i.e., blood, ventilatory, and neuromuscular parameters). Furthermore, because these devices can be used both night and day or during the nights only, some of our subjects only slept in a hypoxic environment (n = 6), whereas the second part of the group stayed both night and day in their rooms (n = 7). The dependent variables were analyzed for the global effect of hypoxic exposure (n = 13) and for the interaction with the modality of exposure.
A total of 13 healthy subjects (11 men and 2 women, 29 ± 4 years, 180 ± 8 cm, and 75 ± 6 kg) gave informed written consent to participate in this study. The subjects were recreational athletes (4.8 ± 0.7 h·wk−1 of training). Subjects were used to training on a treadmill and trained regularly across the year without following any specific training plan. Subjects did not use hypoxic devices in their regular training and did not come back from an altitude trip. The procedures complied with the Declaration of Helsinki regarding human experimentation and were approved by the Ethics Committee of the Hospital.
Subjects were randomly divided in 2 groups (with 1 woman in each group). The first group (n = 7, 29 ± 5 years) entered a normobaric altitude room at 0800 hours and remained there for 48 consecutive hours. The second (n = 6, 29 ± 3 years) stayed overnight for 12 hours in the normobaric altitude room (from 2000 to 0800 hours) for 2 consecutive nights. The room simulated an altitude of 1,800 m by oxygen filtration (CAT, Boulder, CO, USA). Both groups performed a running test 6 hours after the final exit of the altitude rooms (i.e., at 1400 hours). The same running test was randomly performed either 1 week before or 1 week after the altitude exposure for control.
Activity and diet were controlled during the 48 hours preceding each testing session. Personalized meals were provided to meet the individual energy requirements calculated using the Harris Benedict Equation (14). The standard menu provided approximately 55% of energy from carbohydrates, 15% energy from protein, and 30% energy from fat.
Each subject performed a familiarization session in which they performed the complete procedure of the test to accustom themselves to the running test.
The running test was a self-paced simulated 1,500 m on a treadmill (Cosmed T170, Rome, Italy) that was previously demonstrated for being reliable (9,22). A double-blind protocol was employed, where both subjects and experimenters only had feedback on the distance covered without any information on time. Time was automatically recorded every 100 m for subsequent analysis of the self-pacing strategy. The exercise was preceded by a standardized warm-up (i.e., 2 minutes of rest, 6 minutes of run at a constant intensity, and 5 minutes of rest). The warm-up intensity and the starting velocity for the 1,500 m were determined during the familiarization session.
Expired gases were collected by a mask enclosing both the mouth and the nose and recorded by a breath by breath analyzer (Cosmed Quark b2, Rome, Italy) for calculation of ventilation (E), O2 consumption (O2), and CO2 production (CO2), and end-tidal partial pressure of CO2 (PETCO2). Heart rate (HR) was recorded by a chest strap (Polar, Electro OY, Kempele, Finland). Running economy (RE) was calculated as the O2/speed ratio at the 600-m mark of the run (Table 1).
The rate of perceived exertion (RPE) was self-assessed by each subject after 200; 500; 800; 1,100; and 1,400 m with a Borg Scale ranging from 6 to 20.
Electromyographic activity (EMG) of the gastrocnemius medialis (GM) and vastus lateralis (VL) were recorded by means of integral dry reusable electrodes with an interelectrode distance of 20 mm (Biometrics SX230, Gwent, United Kingdom) and a reference electrode on the wrist. Skin was shaved, abraded, and washed for low impedance. Electromyographic activity signals were preamplified and filtered (bandwidth 20-450 Hz, gain = 1,000) and recorded at a sampling frequency of 1,000 Hz using Biometrics hardware (Biometrics DataLOG) and dedicated software. Muscle electrical activity was determined for each stride by measuring the mean value of the root mean square (RMS) between the onset and offset of the burst.
A capillary blood sample was taken from the fingertip 3 minutes after the end of the run and analyzed for [La] (Lactate Pro LT-1710, Arkray, Kyoto, Japan).
Arterial Blood Samples
Arterial blood samples were collected from the wrist using a 220-μL capillary syringe (Roche Microsampler, Mannheim, Germany) before the entry in the hypoxic rooms, upon exiting the room (+0 hours), and just before the test (i.e., +6 hours after the exit of the room). Samples were immediately analyzed (CCX CO-Oximeter, Nova Biomedical, Flintshire, United Kingdom) for pH, Hb, PO2, and PCO2.
All variables continuously recorded during the run (time, expired gases, and EMG data) were averaged over each 100 m (i.e., 15 periods). The effect of the simulated altitude sojourns was analyzed for these variables by a 3-way analysis of variance (ANOVA): 2 conditions (Altitude vs. Control − repeated measures) × 15 periods (repeated measures) × 2 groups (continuous sojourn and night sojourns). The same analysis was performed on RPE data but with 5 repeated measures. Lactate values were analyzed by a 2-way ANOVA: 2 conditions (Altitude vs. Control − repeated measures) × 2 groups (continuous sojourn and night sojourns). Arterial blood parameters were analyzed by a 2-way ANOVA: 3 times (repeated measures) × 2 groups (continuous sojourn and night sojourns). Paired comparisons were used as post hoc to further investigate the main effect of time on these parameters. Statistical analyses were performed with Systat software (Systat, Evanston, IL, USA) and the level of statistical significance was set at p ≤ 0.05. Data are reported as mean ± SEMs.
Neither type of normobaric altitude exposure (F(1,11) = 0.17, p = 0.67) modified the time needed to complete the self-paced 1,500 m (360 ± 42 seconds in control vs. 360 ± 45 seconds after altitude exposure, F(1,11) = 0.02, p = 0.89, Figure 1). The evolution of the run velocities recorded per 100 m was also similar between the 2 conditions (F(14,154) = 0.92, p = 0.54) suggesting identical self-pacing strategies (Figure 2).
The VE was higher during the 1,500 m performed after the normobaric altitude exposure than in control condition (F(1,11) = 6.54, p = 0.03) irrespective of the exposure type (F(1,11) = 0.04, p = 0.85). However, neither O2 nor CO2 were modified by the normobaric altitude exposure (F(1,11) < 1.0, p > 0.35 for both). Consequently, the altitude exposure significantly increased the ratios E/O2(F(1,11) = 14.98, p = 0.003) and E/CO2(F(1,11) = 12.63, p = 0.005) irrespective of the type of exposure (F(1,11) < 0.50, p > 0.49 for both). All these parameters significantly fluctuated throughout the 1,500 m (F(14,154) > 16, p < 0.001 for all), but their evolution failed to be significantly affected by the normobaric altitude exposures (F(14,154) < 1.64, p > 0.07 for all parameters cited). The PETCO2 was lower during the 1,500 m performed after the hypoxic exposure than in control condition (F(1,10) = 22.78, p = 0.001) irrespective of the type of exposure (F(1,10) = 1.29, p = 0.28). The data are presented in Table 1.
HR, RE, [La], and RPE
Although HR was elevated during the first 100 m after altitude exposure than in the control condition (F(2,11) = 6.35, p < 0.02), the mean value in HR was not affected by the normobaric altitude exposure (F(1,11) = 0.06, p = 0.82, Table 1). Both RE and RPE (F(1,11) < 0.58, p > 0.46 for both) or their evolution during the run (F < 0.90, p > 0.52 for the both) failed to display any effect of the normobaric altitude exposure (Table 1). Postexercise [La] was not statistically different (F(1,11) = 1.72, p = 0.22) after the altitude sojourn (10.5 ± 2.8 mmol·L−1) compared with control (10.9 ± 2.7 mmol·L−1).
Muscle Electrical Activity
Muscle electrical activity of both the VL (F(1,11) = 2.38, p = 0.15) and the GM (F(1,10) = 0.49, p = 0.50) were not modified by either normobaric altitude exposure protocol (F(1,11) < 2.59, p > 0.13 for both, Table 1).
Arterial Blood Parameters
PO2 failed to display significant variations, but significant changes were observed in Hb, pH, and PCO2 (F(2,18) > 4.37, p < 0.03 for all, Figure 3). Post hoc analysis revealed that the values at the exit of the altitude dormitories were significantly different than those before entry (p < 0.05). However, all investigated parameters returned to their baseline value before the start of the run (p < 0.05).
Similar to a 4 night hypoxia exposure (35), this study observed VE to increase after only 2 nights or days + nights of moderate altitude exposure. However, this did not translate to a change in 1,500-m running performance or a modification in neural drive during the run. Of interest is that some hematological changes potentially beneficial for middle-distance performance were observed immediately after returning to sea level but disappeared within a few hours.
The effect of 2 consecutive nights a week at a simulated altitude of 3,636 m over 3 consecutive weeks was recently tested by Basset et al (2). Their results showed an increase in oxygen-carrying capacity of the blood without a change in performance. However, Roels et al (32) observed that using a relatively low altitude can improve the performance immediately after the exposure, better than a high-altitude exposure that may have a delayed effect on performance. These data lead us to investigate the effect of a moderate altitude exposure (1,800 m), which corresponds to the altitude of several international training sites (e.g., Boulder and Colorado Springs, USA; Nairobi, Kenya; Font Romeu, France; and Kunming, China). One potential detrimental factor for immediate performance when resting or sleeping in hypoxia can be a deteriorated recovery or sleep deprivation. However, it is unlikely that this impacted performance at the moderate simulated altitude as sleep disturbances have only been previously reported when using hypoxic tents (28), not in hypoxic rooms used in the present study (6).
In this study, we tested whether 2 days of hypoxic exposure could improve running performance, despite the expected limited hematological adaptations. Our results failed to observe any beneficial effect of these hypoxic rooms on performance but, interestingly, our data showed that the low-hypoxic dose used in this experiment was sufficient to induce a significant increase in E during the run (Table 1), and transient hematological modifications that disappeared within a few hours of returning to sea level (Figure 3).
The beneficial nonhematological factors of altitude exposure that could improve performance include enhanced muscle efficiency, greater muscle buffering, and the ability to tolerate lactic acid accumulation (for a review see [11,12]). Our data failed to show any change in RE after the normobaric altitude exposure, which contradicts with previous observations of improved RE in the absence of modifications to O2max (27,34). This could be explained by the low-altitude dose (i.e., 2 days at 1,800 m), compared with 29 nights at 3,000 m used by Neya et al (27). Moreover, the possibility of improving RE by hypoxic exposure is still controversial, and some researchers suggest that exercise economy remains unchanged after high-altitude acclimatization (24). Concerning lactic acid buffering, our data showed that the hypoxia exposure decreased PCO2 (p < 0.001), which could reduce H+ level and consequently explain the observed increase (p < 0.05) in pH (13). It was suggested that these adaptations lead to an increased renal bicarbonate excretion, which is the primary buffer of lactic acid (3). However, our results showed a significant recovery in PCO2 and pH in the 6 hours after the return to sea level. The fact that all the blood parameters returned to their basal values at the time of the run probably explains why using hypoxic rooms the nights (+ days) before the run failed to influence the lactate value at the end of the 1,500-m trial.
Furthermore, both the decrement in PCO2 and the increase in pH suggest hyperventilation. Interestingly, even though these 2 blood parameters returned to their basal values at the time of the 1,500-m trial, our data showed a significant increase in VE during the run (Table 1). Previous studies have observed a delayed HVR effect (10,16,17) as either increases in E (17,18) or decreases in PETCO2 (10,16). However, after a short-duration hypoxic exposure, Ricart et al. (30) observed an increase in E during exercise performed in hypoxia but not in normoxia. Our data suggests that a short-term effect of 2 days of hypoxic exposure can increase E during exercise performed in normoxia. The persistence in ventilatory adaptations is confirmed by our data showing that PETCO2 was decreased during exercise at sea level after only 2 days of hypoxic exposure. This increase in E might be beneficial in hypoxemic athletes running at sea level (4,10); however, the decreased PETCO2 observed may be detrimental to performance and be associated with mild hypoxemia (21). The Coast et al. equation (8) suggests that the increase in O2 of the respiratory muscles induced by the increased E would have a negligible impact on RE. Therefore, this explains why our observed increase in E had neither a detrimental nor positive effect in our nonhypoxemic athletes or their 1,500-m performance.
Given that artificially induced hypoxic conditions can significantly enhance performance and possibly violate the spirit of sport (23), the World Anti Doping Agency (WADA) considered including these methods on their prohibited list before ultimately deciding not to in 2007. However, since 2000, the International Olympic Committee has banned these rooms or tents within the Olympic Village considering the use of these rooms in the days preceding the event as doping. In response to this decision, the purpose of this study was to investigate the short-term effect on performance of these devices in the 2 days preceding an event.
Firstly, our data suggest subsistent effects of the HVR after sleeping in these devices elevating E during the subsequent run. However, that failed to alter performance.
Secondly, the use of these normobaric simulating altitude rooms induced some hematological adaptations, but these adaptations disappeared within a few hours and failed to provide any benefit during a 1500-m run performed in the early afternoon.
In summary, the use of these devices was not beneficial the days preceding an event at sea level. Therefore, the decision to ban such rooms or tents within the Olympic Village should not have any adverse effect on performance.
1. Ashenden, MJ, Gore, CJ, Dobson, GP, Boston, TT, Parisotto, R, Emslie, KR, Trout, GJ, and Hahn, AG. Simulated moderate altitude elevates serum erythropoietin but does not increase reticulocyte production in well-trained runners. Eur J Appl Physiol
81: 428-435, 2000.
2. Basset, FA, Joanisse, DR, Boivin, F, St-Onge, J, Billaut, F, Dore, J, Chouinard, R, Falgairette, G, Richard, D, and Boulay, MR. Effects of short-term normobaric hypoxia on haematology, muscle phenotypes and physical performance in highly trained athletes. Exp Physiol
91: 391-402, 2006.
3. Beaver, WL, Wasserman, K, and Whipp, BJ. Bicarbonate buffering of lactic acid generated during exercise. J Appl Physiol
60: 472-478, 1986.
4. Benoit, H, Busso, T, Castells, J, Denis, C, and Geyssant, A. Influence of hypoxic ventilatory response on arterial O2
saturation during maximal exercise in acute hypoxia. Eur J Appl Physiol Occup Physiol
72: 101-105, 1995.
5. Boning, D. Altitude and hypoxia training-a short review. Int J Sports Med
18: 565-570, 1997.
6. Brugniaux, JV, Schmitt, L, Robach, P, Jeanvoine, H, Zimmermann, H, Nicolet, G, Duvallet, A, Fouillot, JP, and Richalet, JP. Living high-training low: tolerance and acclimatization in elite endurance athletes. Eur J Appl Physiol
96: 66-77, 2006.
7. Burtscher, M, Nachbauer, W, Baumgartl, P, and Philadelphy, M. Benefits of training at moderate altitude versus sea level training in amateur runners. Eur J Appl Physiol Occup Physiol
74: 558-563, 1996.
8. Coast, JR, Rasmussen, SA, Krause, KM, O'kroy, JA, Loy, RA, and Rhodes, J. Ventilatory work and oxygen consumption during exercise and hyperventilation. J Appl Physiol
74: 2318-2324, 1993.
9. Currell, K and Jeukendrup, AE. Validity, reliability and sensitivity of measures of sporting performance. Sports Med
38: 297-316, 2008.
10. Dempsey, JA and Forster, HV. Mediation of Ventilatory Adaptations. Physiol Rev
62: 262-346, 1982.
11. Gore, CJ, Clark, SA, and Saunders, PU. Nonhematological mechanisms of improved sea-level performance after hypoxic exposure. Med Sci Sports Exerc
39: 1600-1609, 2007.
12. Gore, CJ and Hopkins, WG. Counterpoint: positive effects of intermittent hypoxia (live high:train low) on exercise performance are not mediated primarily by augmented red cell volume. J Appl Physiol
99: 2055-2057; discussion 2057-2058, 2005.
13. Hansen, JE, Stelter, GP, and Vogel, JA. Arterial pyruvate, lactate, pH, and PCO2
during work at sea level and high altitude. J Appl Physiol
23: 523-530, 1967.
14. Harris, JA and Benedict, FG. A Biometric study of basal metabolism in Man
. Philadelphia, PA: FB Lippincott, 1919.
15. Hoppeler, H and Vogt, M. Muscle tissue adaptations to hypoxia. J Exp Biol
204: 3133-3139, 2001.
16. Katayama, K, Fujita, H, Sato, K, Ishida, K, Iwasaki, K, and Miyamura, M. Effect of a repeated series of intermittent hypoxic exposures on ventilatory response in humans. High Alt Med Biol
6: 50-59, 2005.
17. Katayama, K, Sato, Y, Ishida, K, Mori, S, and Miyamura, M. The effects of intermittent exposure to hypoxia during endurance exercise training on the ventilatory responses to hypoxia and hypercapnia in humans. Eur J Appl Physiol Occup Physiol
78: 189-194, 1998.
18. Katayama, K, Sato, Y, Morotome, Y, Shima, N, Ishida, K, Mori, S, and Miyamura, M. Cardiovascular response to hypoxia after endurance training at altitude and sea level and after detraining. J Appl Physiol
88: 1221-1227, 2000.
19. Katayama, K, Sato, Y, Morotome, Y, Shima, N, Ishida, K, Mori, S, and Miyamura, M. Intermittent hypoxia increases ventilation and Sa(O2
) during hypoxic exercise and hypoxic chemosensitivity. J Appl Physiol
90: 1431-1440, 2001.
20. Knaupp, W, Khilnani, S, Sherwood, J, Scharf, S, and Steinberg, H. Erythropoietin response to acute normobaric hypoxia in humans. J Appl Physiol
73: 837-840, 1992.
21. Koskolou, MD and Mckenzie, DC. Arterial hypoxemia and performance during intense exercise. Eur J Appl Physiol Occup Physiol
68: 80-86, 1994.
22. Laursen, PB, Francis, GT, Abbiss, CR, Newton, MJ, and Nosaka, K. Reliability of time-to-exhaustion versus time-trial running tests in runners. Med Sci Sports Exerc
39: 1374-1379, 2007.
23. Levine, BD. Should ‘artificial’ high altitude environments be considered doping? Scand J Med Sci Sports
16: 297-301, 2006.
24. Lundby, C, Calbet, JA, Sander, M, Van Hall, G, Mazzeo, RS, Stray-Gundersen, J, Stager, JM, Chapman, RF, Saltin, B, and Levine, BD. Exercise economy does not change after acclimatization to moderate to very high altitude. Scand J Med Sci Sports
17: 281-291, 2007.
25. Maresh, CM, Kraemer, WJ, Judelson, DA, Vanheest, JL, Trad, L, Kulikowich, JM, Goetz, KL, Cymerman, A, and Hamilton, AJ. Effects of high altitude and water deprivation on arginine vasopressin release in men. Am J Physiol Endocrinol Metab
286: E20-E24, 2004.
26. Maresh, CM, Noble, BJ, Robertson, KL, and Harvey, JS Jr. Aldosterone, cortisol, and electrolyte responses to hypobaric hypoxia in moderate-altitude natives. Aviat Space Environ Med
56: 1078-1084, 1985.
27. Neya, M, Enoki, T, Kumai, Y, Sugoh, T, and Kawahara, T. The effects of nightly normobaric hypoxia and high intensity training under intermittent normobaric hypoxia on running economy and haemoglobin mass. J Appl Physiol
103: 828-834, 2007.
28. Pedlar, C, Whyte, G, Emegbo, S, Stanley, N, Hindmarch, I, and Godfrey, R. Acute sleep responses in a normobaric hypoxic tent. Med Sci Sports Exerc
37: 1075-1079, 2005.
29. Ponsot, E, Dufour, SP, Zoll, J, Doutrelau, S, N'guessan, B, Geny, B, Hoppeler, H, Lampert, E, Mettauer, B, Ventura-Clapier, R, and Richard, R. Exercise training in normobaric hypoxia in endurance runners. II. Improvement of mitochondrial properties in skeletal muscle. J Appl Physiol
100: 1249-1257, 2006.
30. Ricart, A, Casas, H, Casas, M, Pages, T, Palacios, L, Rama, R, Rodriguez, FA, Viscor, G, and Ventura, JL. Acclimatization near home? Early respiratory changes after short-term intermittent exposure to simulated altitude. Wilderness Environ Med
11: 84-88, 2000.
31. Rodriguez, FA, Ventura, JL, Casas, M, Casas, H, Pages, T, Rama, R, Ricart, A, Palacios, L, and Viscor, G. Erythropoietin acute reaction and haematological adaptations to short, intermittent hypobaric hypoxia. Eur J Appl Physiol
82: 170-177, 2000.
32. Roels, B, Hellard, P, Schmitt, L, Robach, P, Richalet, JP, and Millet, GP. Is it more effective for highly trained swimmers to live and train at 1200 m than at 1850 m in terms of performance and haematological benefits? Br J Sports Med
40: e4, 2006.
33. Saunders, PU, Telford, RD, Pyne, DB, Cunningham, RB, Gore, CJ, Hahn, AG, and Hawley, JA. Improved running economy in elite runners after 20 days of simulated moderate-altitude exposure. J Appl Physiol
96: 931-937, 2004.
34. Schmitt, L, Millet, G, Robach, P, Nicolet, G, Brugniaux, JV, Fouillot, JP, and Richalet, JP. Influence of ‘living hightraining low’ on aerobic performance and economy of work in elite athletes. Eur J Appl Physiol
97: 627-636, 2006.
35. Townsend, NE, Gore, CJ, Hahn, AG, Aughey, RJ, Clark, SA, Kinsmant, A, Mckenna, MJ, Hawley, JA, and Chow, CM. Hypoxic ventilatory response is correlated with increased sumaximal exercise ventilation after live high, train low. Eur J Appl Physiol
94: 207-215, 2005.
36. Wilber, RL, Stray-Gundersen, J, and Levine, BD. Effect of hypoxic “dose” on physiological responses and sea-level performance. Med Sci Sports Exerc
39: 1590-1599, 2007.