Abstract
Objectives
The effects of living and training have not been compared at different altitudes in well trained subjects.
Methods
Nine international swimmers lived and trained for 13 days similarly at 1200 m (T1200) and 1850 m (T1850). The two altitude training periods were separated by six weeks of sea level training. Before and after each training trip, subjects performed, at an altitude of 1200 m, an incremental exercise test to exhaustion of 5 × 200 m swims and a maximal test over 2000 m.
Results
There was no difference in V̇o2max after each training trip: the before values were 58.5 (5.6) and 60.4 (6.7) ml/kg/min and the after values were 56.2 (5.2) and 57.1 (4.7) ml/kg/min for T1200 and T1850 respectively. The 2000 m performance had improved during T1200 (1476 (34) to 1448 (45) seconds) but not during T1850 (1458 (35) v 1450 (33) seconds). Mean cell volume increased during T1850 (86.6 (2.8) to 88.7 (2.9) µm3) but did not change during T1200 (85.6 (2.9) v 85.7 (2.9) µm3). The proportion of reticulocytes decreased during T1200 (15.2 (3.8)% to 10.3 (3.4)%) and increased during T1850 (9.3 (1.6)% to 11.9 (3.5)%).
Conclusions
The short term effects of 13 days of training at 1200 m on swimming performance appear to be greater than the same type of training for the same length of time at 1850 m. As mean cell volume and proportion of reticulocytes only increased during training at 1850 m, the benefits of training at this altitude may be delayed and appear later on.
Keywords: swimming performance, V̇o 2 max , hypoxia, haematological variables, altitude training
Although many endurance athletes invest considerable amounts of time in training at altitude, the practical benefits gained remain to be clearly established.1 The exposure time and height appear to be the most important mediators of sea level performance. Many different strategies have been used. Three strategies are still being investigated. One approach, “living high‐training low”, combines altitude acclimation with low altitude training to ensure high quality training.2,3 The opposite strategy “living low‐training high” has also been proposed.4,5,6 Although these two methods of altitude training have been shown to be effective,3,5,6,7 logistically and financially they are difficult to accomplish. Thirdly, the traditional “living high‐training high” strategy consists of a constant stay at altitude—that is, living and training at altitude.8 The primary goal of these strategies is to enhance training stimulus. Considering the “high‐high” method, few studies have addressed the question whether exposure to low (∼1000–1500 m) or moderate (∼1800–2500 m) altitude would induce differences in performance and physiological/haematological variables in highly trained sea level athletes.9,10,11 Moderate altitude may induce enhancements in haematological variables—for example, an increase in the oxygen carrying transport system—but, less favourably, may also decrease training intensity.7 In contrast, low altitudes are favourable for maintenance of training intensity, but may be too limited to induce any modification of haematological variables. Most studies have reported on performance2,7,10 or haematological4 responses to moderate or high altitude cycling or running training, but only a few have investigated the effects of altitude training on swimming performance.12,13
Therefore the aim of this study was to investigate if living and training at 1850 m would induce different physiological adaptations, leading to greater improvement in swimming performance, than living and training for a similar length of time at 1200 m.
Methods
Subjects
Eight international swimmers gave written informed consent to participate. All were healthy, sea level residents, who were familiar with the tests and equipment used in the experiment. None had recently made a trip to high altitude—that is, for three months before the first stay at altitude. The mean (SD) characteristics of the subjects were: age, 16.3 (0.9) years; height, 180.3 (6.8) cm; weight, 68.0 (6.8) kg; swimming (400 m medley; 400–1500 m freestyle) performance level, 80.2 (4.9)% of world records.
Experimental design
Figure 1 presents an overview of the experimental design. The subjects lived and trained at 1200 m (T1200) and 1850 m (T1850) for 13 days each, separated by six weeks of sea level training. During the training camps, the barometric pressure was recorded daily with an atmospheric barometer (Sensor Medics, Yorba Linda, California, USA) and confirmed with data obtained from the national weather institute (Météo France). Before and during the periods studied, training loads were controlled and quantified as described by Avalos et al.14 Before and after each training period, a medical examination was completed and blood samples were taken at rest. Subjects performed a swim incremental exercise test to exhaustion of 5 × 200 m with gas exchange analysis15 (K4b2; Cosmed, Rome, Italy) and on the next day, a maximal swimming test over 2000 m. All swimming tests were conducted at an altitude of 1200 m in an indoor 25 m swimming pool; the temperature of the water was 26°C. All tests were performed at the same time of day to control for the effects of diurnal variation.
Figure 1 Experimental design.
Incremental test to exhaustion
This test consisted of five consecutive 200 m efforts of increasing velocity, with 15 second rest intervals. The velocity of each swim was determined from each swimmer's personal best competition time in that distance measured in the preceding month. The first 200 m effort was set at 30 seconds less than the personal best competition time, with the time to complete the remaining efforts decreasing by five seconds with each stage. The final 200 m was performed at maximal velocity. The subject adjusted their velocity using auditory signals at 12.5 m intervals, delimited by visual marks along the bottom of the pool. Exhaustion coincided with: (a) heart rate (HR) approaching the maximal theoretical HR (220 – age); (b) V̇o2 levelling off even with an increase in intensity. Maximal speed (Vmax, m/s) was defined as the speed reached during the last 200 m. End exercise lactate concentration (Lactate Pro, Arkray, Japan)16 was recorded after the test from fingertip blood samples.
2000 m test
Subjects were instructed to achieve their fastest time over a 2000 m swimming test, and mean velocity (Vavg, m/s) and stroke rate (SR; cycles/min) were measured for each 25 m using a chronometer (Professional Sports Timer, Silva, Sollentuna, Sweden) with frequency meter base 3. Stroke length (SL; m/cycle) was calculated for each 25 m by dividing velocity by SR. These values were then averaged for each 100 m.
Gas analysis
Before and after each training camp, gas exchange was measured during the incremental test to exhaustion to determine maximal oxygen uptake during the five 200 m swims (V̇o2max; ml/kg/min), Vmax (m/s), maximal ventilation (V̇Emax; litres/min), maximal volume (Vt, ml/min), and maximal heart rate (HRmax; beats/min). The K4b2 was connected to a snorkel (Aquatrainer), validated by Keskinen et al.15 The snorkel was designed so that K4b2 standard procedures were kept as constant as possible. Only the K4b2 setup was changed to calculate the ventilatory variables with an accurate fraction of inspired oxygen—for example, at 1200 m—rather than with the default version (sea level). Further information on the snorkel and K4b2 setup is given by Keskinen et al.15 This snorkel measured expired gas during swimming without significantly increasing forward resistance. However, in pilot experiments, the increase in time to complete an open turn with the snorkel was estimated to be on average 1.6 seconds longer than a standard tumble turn. The above variables were measured, breath by breath, and averaged every 30 seconds. Calibration was performed following the manufacturer's guidelines.15 Energy cost (ml/kg/m) during the last 200 m swim was calculated using the following equation: Energy cost = V̇o2/60/V.17 V̇o2max was determined as the highest 30 second averaged V̇o2 value and was always reached during the last stage.
Haematological variables
Blood samples at rest were obtained by venepuncture on four occasions: before and after T1200 and before and after T1850. Samples were analysed, following standard procedures, within two hours of the blood being drawn, using the Pentra 120 Retic (abx, Montpellier, France) for several variables: red blood cells (106/mm3), haemoglobin (g/l), packed cell volume, mean cell volume (MCV; μm3), averaged globular content of haemoglobin (%), averaged corpuscular concentration of haemoglobin (pg), red blood discs (103/mm3), reticulocytes (%), averaged reticulocyte volume (μm3), and soluble transferrin receptor (nmol/l).
Statistical analysis
All values are reported as mean (SD). All data were grouped. The influence of the two training altitudes on the measured variables was, after analysis of normality and homogeneity of variance of the tested samples, analysed using two way analysis of variance (two altitudes (1200 and 1850 m) × time (before and after)). Significant effects were subsequently analysed using the Student‐Newman‐Keuls post hoc test. All analyses were completed using SigmaStat 2.3 (Jandel Corporation, San Rafael, California, USA). Statistical significance was accepted at p<0.05.
Results
There was a significant difference in blood pressure between T1200 and T1850: 660.8 (7.0) v 628.3 (8.5) mm Hg.
Training load
As the training programme was repeated, the training loads for the two training camps were similar: 188 133 and 219 550 arbitrary units, with 86% and 84% below or at the onset of blood lactate accumulation at 1200 m and 1850 m respectively. The loads increased progressively for three weeks, and, during the week before each training trip, they were kept similar (1% difference): 201 481 (156 043) and 203 717 (143 679) arbitrary units for T1200 and T1850 respectively.
Incremental test to exhaustion
During T1850 a significant decrease in HRmax was noticed (p<0.05; F = 9.18): 188.0 (10.4) to 181.0 (6.8) beats/min, whereas no difference was observed after T1200: 186.9 (5.9) and 183.6 (4.3) beats/min before and after respectively. End exercise lactate concentration decreased significantly (p<0.05; F = 4.65) during T1850 from 7.1 (1.6) to 6.4 (1.9) mmol/l. No difference was found during T1200: 6.9 (1.6) v 6.9 (1.8) mmol/l. None of the other variables changed (table 1).
Table 1 Physiological variables measured during incremental test to exhaustion (n = 8).
| 1200 m | 1850 m | |||
|---|---|---|---|---|
| Before | After | Before | After | |
| Weight (kg) | 68.0 (6.8) | 66.4 (7.1) | 66.6 (5.5) | 66.4 (5.6) |
| V̇o2max (ml/kg/min) | 58.5 (5.6) | 56.2 (5.2) | 60.4 (6.7) | 57.1 (4.7) |
| V̇Emax (litres/min) | 110.9 (18.9) | 119.2 (12.7) | 120.2 (18.3) | 127.6 (16.7) |
| Vtmax (ml/min) | 2.45 (0.3) | 2.59 (0.3) | 2.58 (0.3) | 2.65 (0.4) |
| ECmax (ml/kg/m) | 0.70 (0.09) | 0.73 (0.09) | 0.65 (0.06) | 0.66 (0.05) |
| Perf (s) | 146.3 (5.3) | 144.1 (5.3) | 139.9 (5.7) | 138.9 (4.2) |
| Vmax (m/s) | 1.37 (0.05) | 1.39 (0.05) | 1.43 (0.06) | 1.44 (0.04) |
Values are mean (SD).
V̇o2max, Highest value for oxygen uptake averaged over 30 seconds; V̇Emax, highest value for ventilation averaged over 30 seconds; Vtmax, highest value for volume averaged over 30 seconds; ECmax, highest value for energy cost averaged over 30 seconds for the last 200 m; Perf, time of the last 200 m; Vmax, highest velocity.
2000 m
The 2000 m performance improved during T1200 from 1476 (34) to 1448 (45) seconds (p = 0.01; F = 11.88), whereas no change was observed at T1850: 1458 (35) v 1450 (33) seconds. The SR increased significantly (p = 0.009, F = 10.84) only at T1200 from 32.6 (3.6) to 33.9 (3.2) cycles/min, and the SL decreased significantly (p = 0.03, F = 7.09) from 2.29 (0.25) to 2.15 (0.19) m/cycle. SR and SL at T1850 were 32.4 (3.8) and 33.5 (4.1) and 2.28 (0.27) and 2.19 (0.26) before and after respectively.
Haematological variables
Table 2 shows the haematological variables measured.
Table 2 Haematological variables (n = 8).
| Variable | 1200 m | 1850 m | ||
|---|---|---|---|---|
| Before | After | Before | After | |
| RBC (106/mm3) | 5.14 (0.3) | 5.21 (0.4) | 5.36 (0.3) | 5.33 (0.3) |
| Hb (g/l) | 147 (9) | 149 (11) | 157 (10) | 159 (9) |
| PCV | 43.9 (2.6) | 44.7 (3.1) | 46.4 (2.4) | 47.2 (2.3) |
| AGCH (%) | 33.4 (0.5) | 33.4 (0.5) | 33.9 (0.7) | 33.7 (0.7) |
| ACCH (pg) | 28.6 (0.7) | 29.0 (0.9) | 29.3 (1.0) | 29.8 (0.9) |
| RBD (103/mm3) | 269.1 (28.7) | 304.3 (24.4)* | 237.8 (42.2)† | 268.1 (43.1)*† |
| sTfR (nmol/l) | 19.0 (5.10) | 22.3 (4.1)* | 23.0 (4.1) | 32.6 (7.1)*† |
Values are mean (SD).
RBC, Red blood cells; Hb, haemoglobin; PCV, packed cell volume; AGCH, averaged globular content of haemoglobin; ACCH, averaged corpuscular concentration of haemoglobin; RBD, red blood discs; sTfR, soluble transferrin receptor.
*p<0.05 for the differences between measurements before and after the training period at the same altitude.
†p<0.05 for the differences between measurements at different altitudes at a matched time point.
MCV increased significantly (p<0.001; F = 57.6) during T1850 from 86.6 (2.8) to 88.7 (2.9) µm3 but not during training at T1200: 85.6 (2.9) v 85.7 (2.9) µm3. The proportion of reticulocytes decreased significantly (p = 0.05; F = 5.30) during T1200 from 15.2 (3.8)% to 10.3 (3.4)% but increased (p<0.01; F = 22.14) during T1850 from 9.3 (1.6)% to 11.9 (3.5)%.
Discussion
The main finding of this study is that 13 days of living and training at low altitude (1200 m) in previously non‐acclimatised people was associated with a greater improvement in endurance performance than the same type of training, the same training loads, and the same training period at 1850 m. However, the changes in haematological variables in athletes living and training at 1200 m were minor compared with those at 1850 m.
Endurance performance
There are many altitude training sites around the world: Thredbo, Australia (1365 m); Font‐Romeu, France (1850 m); Colorado Springs, USA (1860 m); Kunming, China (1895 m). However, the different altitude effects have not been compared. Therefore the topic of this study should be of practical interest for coaches.
This study shows that, even at low altitude, endurance performance is improved by training. It is interesting that no improvement in V̇o2max was observed in this study, at either 1200 m or 1850 m. It is well known that endurance performance may be independent of V̇o2max for well trained athletes.18 Apparently there is a limitation in the possibilities of the O2 transport system. According to the model of Knight et al,19 V̇o2max is about 80% controlled by central factors. Cardiac flow may reach a limiting value beyond which it is very difficult for adaptation to occur. The commonly held view that V̇o2max is set essentially by the O2 transport system (maximal cardiac output and O2 carrying capacity) is fundamentally correct for exercises with large muscle groups at sea level. However, at altitude, other factors, such as ventilation and mitochondrial capacity, assume a substantial role in setting V̇o2max.20 However, as Fulco et al21 have mentioned, it should be noted that small, statistically non‐significant training induced improvements can result in a significant increase in endurance performance. Moreover, in well trained athletes in whom it is difficult to induce an increase V̇o2max, a small improvement in performance may make the difference between winning and losing.2 Other investigators have shown that predominantly aerobic training produced no significant effects on aerobic performance markers such as V̇o2max.22,23,24
Maximal performances depend on maximal metabolic power of the athlete and on the economy of locomotion, hence the importance of assessing swimming economy of locomotion.
The decrease in maximal lactate concentration observed after T1850 may be due to an increase in its transport and oxidation as it was shown that altitude acclimation induced changes in lactate metabolism.25 Although the present study was not set up to investigate this—that is, no measurement of monocarboxylate transporters (MCT 1, MCT 4) or enzyme (lactate dehydrogenase)—this change in lactate oxidation may have increased the non‐aerobic energy equipment and therefore influenced the overall performance. The “lactate paradox” is perhaps responsible for this observation. The higher the altitude, the lower the peak, post‐exercise blood lactate concentrations during a given exercise protocol.26 The main functional advantages of the lactate paradox (maintenance of metabolite homoeostasis during fatigue and avoidance of over‐activation of energetically inefficient anaerobic metabolism during hypoxia) have long been recognised,27 but the underlying mechanisms remain obscure.
To our knowledge, this study is the first to report that acclimation at 1200 m or 1850 m induces differences in lactate metabolism in a maximal swimming test. This result has practical interest for swimming, in which prescription of training intensities is commonly related to lactate concentrations.28
Haematological modifications
Several changes were observed in the haematological variables. At 1850 m, MCV and the proportion of reticulocytes increased, suggesting some erythropoietic adaptation at this altitude. A review of many research studies suggests that the appropriate training altitude is 2000–3000 m.29 In contrast, this study shows clearly that, even at 1850 m, haematological variables are significantly modified. So, the minimum altitude necessary for obtaining significant haematological modification is about 1850 m and not >2000 m. It confirms also that polyglobulia is not directly related to short term improvement in endurance performance.
Limitations of this study
The fact that there was no control group is one limitation. However, several epidemiological studies have reported that, if well controlled, longitudinal studies give similar results to those of randomised controlled trials.30 This experimental protocol was a longitudinal design to eliminate as much skewing as possible: the amount and type of training and the duration were kept identical at the two altitudes. A six week period separated the two training periods so that the effects of the first one did not influence the biological and physiological adaptations of the second one.31 Thus, training induced changes may be secondary to those induced by altitude alone, so modifications induced by training were presumably minor in comparison with those induced by altitude. Therefore the observed modifications at T1850 are likely to be altitude induced to a great extent.
What is already known on this topic
Endurance athletes invest considerable amounts of time in altitude training but the practical benefits gained remain unclear
Previous studies have suggested that the appropriate altitude is 2000–3000 m, but there is no information on the differences in the effects of low (1000–1500 m) and moderate (1800–2500 m) altitude training
What this study adds
The short term effects of training for 13 days at 1200 m on swimming performance appear to be greater than the same type of training over the same duration at 1850 m
As mean cell volume and the proportion of reticulocytes had increased only after training at 1850 m, the benefits of training at this altitude may be just delayed
Other potential factors that may explain the observed difference in performance between T1200 and T1850 are diet, temperature, and/or sleep. Although a well balanced diet was provided at both altitudes, individual intake of macronutrients and micronutrients and iron rich foods may have been different and therefore may have affected performance. Temperature could not have played a large role in the differences in performance because the training sessions and tests were performed indoors at a consistent temperature. Altitude can cause apnoeic and hypopnoeic respiratory events during sleep and therefore induce sleep disturbances, which have been shown to decrease physical work capacity.32 However, the effects vary widely between individuals.
Practical applications
Training at altitude in preparation for competition is often used by athletes. This study indicates that training at low altitude (1000–1200 m) can be immediately followed by competition because of its short term effects on performance, whereas training at higher altitude (1800–2000 m) may require a longer period before the benefits to be accrued in competition.
Conclusion
The short term effects of 13 days living and training at 1200 m on swimming performance appear to be greater than the same type of training for the same duration at 1850 m. Specific submaximal adaptations may explain the improvement in aerobic performance. In addition, the decrease in maximal lactate concentration and heart rate may partly explain why performance evaluated immediately after 1850 m exposure did not improve. However, as MCV and the proportion of reticulocytes increased only during T1850, the benefits of training at 1850 m on endurance performance may appear later. Further investigations are required to understand the effects of different altitudes and hypoxic methods on endurance.
Acknowledgements
This study was supported by the International Olympic Committee and the French Ministry of Sport.
Abbreviations
HR - heart rate
MCV - mean cell volume
SL - stroke length
SR - stroke rate
V̇o2max - maximal oxygen uptake
Vmax - maximal speed
Footnotes
Competing interests: none declared
References
- 1.Bailey D M, Davies B, Budgett R.et al Recovery from infectious mononucleosis after altitude training in an elite middle distance runner. Br J Sports Med 199731153–154. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Levine B D, Stray‐Gundersen J. A practical approach to altitude training: where to live and train for optimal performance enhancement. Int J Sports Med 199213(suppl 1)S209–S212. [DOI] [PubMed] [Google Scholar]
- 3.Levine B D. Intermittent hypoxic training: fact and fancy. High Alt Med Biol 20023177–193. [DOI] [PubMed] [Google Scholar]
- 4.Dehnert C, Hutler M, Liu Y.et al Erythropoiesis and performance after two weeks of living high and training low in well trained triathletes. Int J Sports Med 200223561–566. [DOI] [PubMed] [Google Scholar]
- 5.Geiser J, Vogt M, Billeter R.et al Training high‐living low: changes of aerobic performance and muscle structure with training at simulated altitude. Int J Sports Med 200122579–585. [DOI] [PubMed] [Google Scholar]
- 6.Stray‐Gundersen J, Chapman R F, Levine B D. “Living high‐training low” altitude training improves sea level performance in male and female elite runners. J Appl Physiol 2001911113–1120. [DOI] [PubMed] [Google Scholar]
- 7.Levine B D, Stray‐Gundersen J. “Living high‐training low”: effect of moderate‐altitude acclimatization with low‐altitude training on performance. J Appl Physiol 199783102–112. [DOI] [PubMed] [Google Scholar]
- 8.Mathieu‐Costello O. Muscle adaptation to altitude: tissue capillarity and capacity for aerobic metabolism. High Alt Med Biol 20012413–425. [DOI] [PubMed] [Google Scholar]
- 9.Niess A M, Fehrenbach E, Strobel G.et al Evaluation of stress responses to interval training at low and moderate altitudes. Med Sci Sports Exerc 200335263–269. [DOI] [PubMed] [Google Scholar]
- 10.Saunders P U, Telford R D, Pyne D B.et al Improved running economy in elite runners after 20 days of simulated moderate‐altitude exposure. J Appl Physiol 200496931–937. [DOI] [PubMed] [Google Scholar]
- 11.Wilber R L, Holm P L, Morris D M.et al Effect of F(I)O(2) on physiological responses and cycling performance at moderate altitude. Med Sci Sports Exerc 2003351153–1159. [DOI] [PubMed] [Google Scholar]
- 12.Roberts D, Smith D J. Training at moderate altitude: iron status of elite male swimmers. J Lab Clin Med 1992120387–391. [PubMed] [Google Scholar]
- 13.Truijens M J, Toussaint H M, Dow J.et al Effect of high‐intensity hypoxic training on sea‐level swimming performances. J Appl Physiol 200394733–743. [DOI] [PubMed] [Google Scholar]
- 14.Avalos M, Hellard P, Chatard J C. Modeling the training‐performance relationship using a mixed model in elite swimmers. Med Sci Sports Exerc 200335838–846. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Keskinen K L, Rodriguez F A, Keskinen O P. Respiratory snorkel and valve system for breath‐by‐breath gas analysis in swimming. Scand J Med Sci Sports 200313322–329. [DOI] [PubMed] [Google Scholar]
- 16.Pyne D B, Boston T, Martin D T.et al Evaluation of the Lactate Pro blood lactate analyser. Eur J Appl Physiol 200082112–116. [DOI] [PubMed] [Google Scholar]
- 17.Di Prampero P E. The energy cost of human locomotion on land and in water. Int J Sports Med 1986755–72. [DOI] [PubMed] [Google Scholar]
- 18.Acevedo E O, Goldfarb A H. Increased training intensity effects on plasma lactate, ventilatory threshold, and endurance. Med Sci Sports Exerc 198921563–568. [PubMed] [Google Scholar]
- 19.Knight D R, Schaffartzik W, Poole D C.et al Effects of hyperoxia on maximal leg O2 supply and utilization in men. J Appl Physiol 1993752586–2594. [DOI] [PubMed] [Google Scholar]
- 20.Di Prampero P E. Factors limiting maximal performance in humans. Eur J Appl Physiol 200390420–429. [DOI] [PubMed] [Google Scholar]
- 21.Fulco C S, Rock P B, Cymerman A. Improving athletic performance: is altitude residence or altitude training helpful? Aviat Space Environ Med 200071162–171. [PubMed] [Google Scholar]
- 22.Meeuwsen T, Hendriksen I J, Holewijn M. Training‐induced increases in sea‐level performance are enhanced by acute intermittent hypobaric hypoxia. Eur J Appl Physiol 200184283–290. [DOI] [PubMed] [Google Scholar]
- 23.Terrados N, Melichna J, Sylven C.et al Effects of training at simulated altitude on performance and muscle metabolic capacity in competitive road cyclists. Eur J Appl Physiol Occup Physiol 198857203–209. [DOI] [PubMed] [Google Scholar]
- 24.Vallier J M, Chateau P, Guezennec C Y. Effects of physical training in a hypobaric chamber on the physical performance of competitive triathletes. Eur J Appl Physiol Occup Physiol 199673471–478. [DOI] [PubMed] [Google Scholar]
- 25.McClelland G B, Brooks G A. Changes in MCT 1, MCT 4, and LDH expression are tissue specific in rats after long‐term hypobaric hypoxia. J Appl Physiol 2002921573–1584. [DOI] [PubMed] [Google Scholar]
- 26.Hochachka P W, Rupert J L, Monge C. Adaptation and conservation of physiological systems in the evolution of human hypoxia tolerance. Comp Biochem Physiol A Mol Integr Physiol 19991241–17. [DOI] [PubMed] [Google Scholar]
- 27.Hochachka P W, Bianconcini M S, Parkhouse W S.et al On the role of actomyosin ATPases in regulation of ATP turnover rates during intense exercise. Proc Natl Acad Sci USA 1991885764–5768. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 28.Pyne D B, Lee H, Swanwick K M. Monitoring the lactate threshold in world‐ranked swimmers. Med Sci Sports Exerc 200133291–297. [DOI] [PubMed] [Google Scholar]
- 29.Burtscher M, Nachbauer W, Baumgartl P.et al Benefits of training at moderate altitude versus sea level training in amateur runners. Eur J Appl Physiol Occup Physiol 199674558–563. [DOI] [PubMed] [Google Scholar]
- 30.Kunz R, Khan K S, Neumayer H H. Observational studies and randomized trials. N Engl J Med. 2000;343: 1194–5; author reply 1196–7, [DOI] [PubMed]
- 31.Miyashita M. Key factors in success of altitude training for swimming. Res Q Exerc Sport 199667(suppl 3)S76–S78. [DOI] [PubMed] [Google Scholar]
- 32.Aguillard R N, Reidel B W, Lichstein K L.et al Daytime functioning in obstructive sleep apnea patients, exercise tolerance, subjective fatigue, and sleepiness. Appl Psychophysiol Biofeedback 199823207–217. [DOI] [PubMed] [Google Scholar]