Effects of physical training in a hypobaric chamber on the physical performance of competitive triathletes.
Vallier JM, et al. Eur J Appl Physiol Occup Physiol. 1996.
The effects of training in a hypobaric chamber on aerobic metabolism were studied in five high performance triathletes. During 3 weeks, the subjects modified their usual training schedule (approximately 30 h a week), replacing three sessions of bicycling exercise by three sessions on a cycle ergometer in a hypobaric chamber simulating an altitude of 4,000 m (462 mm Hg). Prior to and after training in the hypobaric chamber the triathletes performed maximal and submaximal exercise in normoxia and hypoxia (462 mm g). Respiratory and cardiac parameters were recorded during exercise. Lactacidaemia was measured during maximal exercise. Blood samples were drawn once a week to monitor blood cell parameters and erythropoetin concentrations. Training in the hypobaric chamber had no effect on erythropoiesis, the concentrations of erythropoetin always remaining unchanged, and no effect on the maximal oxygen uptake (VO2max) and maximal aerobic capacity measured in normoxia or hypoxia. Submaximal performance increased by 34% during a submaximal exhausting exercise performed at a simulated altitude of 2,000 m. During a submaximal nonexhausting test, ventilation values tended to decrease for similar exercise intensities after training in hypoxia. The changes in these parameters and the improved performance found for submaximal exercise may have been the result of changes taking place in muscle tissue or the result of training the respiratory muscles.
Transient Hypoxia Stimulates Mitochondrial Biogenesis in Brain Subcortex by a Neuronal Nitric Oxide Synthase-Dependent Mechanism
Diana R. Gutsaeva, Martha Sue Carraway, Hagir B. Suliman, Ivan T. Demchenko, Hiroshi Shitara, Hiromichi Yonekawa and Claude A. Piantadosi
Journal of Neuroscience 27 February 2008, 28 (9) 2015-2024; DOI: https://doi.org/10.1523/JNEUROSCI.5654-07.2008
The adaptive mechanisms that protect brain metabolism during and after hypoxia, for instance, during hypoxic preconditioning, are coordinated in part by nitric oxide (NO). We tested the hypothesis that acute transient hypoxia stimulates NO synthase (NOS)-activated mechanisms of mitochondrial biogenesis in the hypoxia-sensitive subcortex of wild-type (Wt) and neuronal NOS (nNOS) and endothelial NOS (eNOS)-deficient mice. Mice were exposed to hypobaric hypoxia for 6 h, and changes in immediate hypoxic transcriptional regulation of mitochondrial biogenesis was assessed in relation to mitochondrial DNA (mtDNA) content and mitochondrial density. There were no differences in cerebral blood flow or hippocampal PO2 responses to acute hypoxia among these strains of mice. In Wt mice, hypoxia increased mRNA levels for peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1 α), nuclear respiratory factor-1, and mitochondrial transcription factor A. After 24 h, new mitochondria, localized in reporter mice expressing mitochondrial green fluorescence protein, were seen primarily in hippocampal neurons. eNOS−/− mice displayed lower basal levels but maintained hypoxic induction of these transcripts. In contrast, nuclear transcriptional regulation of mitochondrial biogenesis in nNOS−/− mice was normal at baseline but did not respond to hypoxia. After hypoxia, subcortical mtDNA content increased in Wt and eNOS−/− mice but not in nNOS−/− mice. Hypoxia stimulated PGC-1α protein expression and phosphorylation of protein kinase A and cAMP response element binding (CREB) protein in Wt mice, but CREB only was activated in eNOS−/− mice and not in nNOS−/− mice. These findings demonstrate that hypoxic preconditioning elicits subcortical mitochondrial biogenesis by a novel mechanism that requires nNOS regulation of PGC-1α and CREB.
Effects of training at simulated altitude on performance and muscle metabolic capacity in competitive road cyclists.
Terrados N, et al. Eur J Appl Physiol Occup Physiol. 1988.
Differences between the effects of training at sea level and at simulated altitude on performance and muscle structural and biochemical properties were investigated in 8 competitive cyclists who trained for 3-4 weeks, 4-5 sessions/week, each session consisting of cycling for 60-90 min continuously and 45-60 min intermittently. Four subjects, the altitude group (AG), trained in a hypobaric chamber (574 torr = 2300 m above sea level), and the other four at sea level (SLG). Before and after training work capacity was tested both at simulated altitude (574 torr) and at sea level, by an incremental cycle ergometer test until exhaustion. Work capacity was expressed as total amount of work performed. Venous blood samples were taken during the tests. Leg muscle biopsies were taken at rest before and after the training period. AG exhibited an increase of 33% in both sea level and altitude performance, while SLG increased 22% at sea level and 14% at altitude. Blood lactate concentration at a given submaximal load at altitude was significantly more reduced by training in AG than SLG. Muscle phosphofructokinase (PFK) activity decreased with training in AG but increased in SLG. All AG subjects showed increases in capillary density. In conclusion, work capacity at altitude was increased more by training at altitude than at sea level. Work capacity at sea level was at least as much improved by altitude as by sea level training. The improved work capacity by training at altitude was paralleled by decreased exercise blood lactate concentration, increased capillarization and decreased glycolytic capacity in leg muscle.
Aerobic fitness influences the response of maximal oxygen uptake and lactate threshold in acute hypobaric hypoxia.
Randomized controlled trial
Koistinen P, et al. Int J Sports Med. 1995.
We studied 12 highly trained athletes, 6 male ice-hockey players and 6 cross-country skiers (2 females, 4 males). All of them participated in a maximal electrically braked bicycle ergometer test in a hypobaric chamber at the simulated altitude of 3000m (520 mmHg) and in normobaric conditions two days apart in random order. The maximal oxygen uptake was 57.4 +/- 7.1 (SD) ml/kg/min in normobaria (VO2maxnorm) and 46.6 +/- 4.9 (SD) ml/kg/min in hypobaric hypoxia (VO2maxhyp). The decrease in maximal oxygen uptake (delta VO2max) at the simulated altitude of 3000m correlated significantly (p < 0.05, r = 0.61) to the maximal oxygen uptake in normobaric conditions (VO2maxnorm). The lactate threshold was 43.5 +/- 6.4 (SD) ml/kg/min in normobaria (VO2LTnorm) and 36.5 +/- 4.2 (SD) ml/kg/min in hypobaric hypoxia (VO2LThyp). The decrement (delta VO2LT) of lactate threshold in hypoxia correlated significantly (p < 0.01, r = 0.68) with the lactate threshold in normobaric conditions (VOLTnorm). Thus we observed the largest reduction of both maximal oxygen uptake and lactate threshold during exercise at hypobaric hypoxia in the most fit athletes.
Intermittent hypobaric hypoxia induces altitude acclimation and improves the lactate threshold.
Casas M, et al. Aviat Space Environ Med. 2000.
The physiological responses to short-term intermittent exposure to hypoxia in a hypobaric chamber were evaluated. The exposure to hypoxia was compatible with normal daily activity. The ability of the hypoxia program to induce hematological and ventilatory adaptations leading to altitude acclimation and to improve physical performance capacity was tested. Six members of a high-altitude expedition were exposed to intermittent hypoxia and low-intensity exercise (in cycle-ergometer) in the INEFC-UB hypobaric chamber over 17 d, 3-5 h x d(-1), at simulated altitude of 4,000 m to 5,500 m. Following this hypoxia exposure program, significant increases were found in packed cell volume (41 to 44.6%; p<0.05), red blood cells count (4.607 to 4.968 10(6) cells x microL(-1); p<0.05), and hemoglobin concentration (14.8 to 16.4 g x dL(-1); p<0.05), thus implying an increase in the blood oxygen transport capacity. Significant differences in exercise blood lactate kinetics and heart rate were also observed. The lactate vs. exercise load curve shifted to the right and heart rate decreased, thus indicating an improvement of aerobic endurance. These results were associated with a significant increase in the ventilatory anaerobic threshold (p<0.05). Significant increases (p<0.05) in pulmonary ventilation, tidal volume, respiratory frequency, O2 uptake, CO2 output and ventilatory equivalents to oxygen (VE/Vo2) and carbon dioxide (VE/co2) were observed at the ventilatory threshold and within the transitional zone of the curves. We conclude that short-term intermittent exposure to moderate hypoxia, in combination with low-intensity exercise in a hypobaric chamber, is sufficient to improve aerobic capacity and to induce altitude acclimation.
The effect of intermittent training in hypobaric hypoxia on sea-level exercise: a cross-over study in humans.
Hendriksen IJ, et al. Eur J Appl Physiol. 2003.
The purpose of this study was to examine the effect of intermittent training in a hypobaric chamber on physical exercise at sea level. Over a 10 day period, 16 male triathletes trained for 2 h each day on a cycle ergometer placed in a hypobaric chamber. Training intensity was at 60%-70% of the heart rate reserve. There were 8 subjects who trained at a simulated altitude of 2,500 m, the other 8 trained at sea level. A year later, a cross-over study took place. Baseline measurements were made on a cycle ergometer at sea level, which included an incremental test until exhaustion and a Wingate Anaerobic Test. Altogether, 12 subjects completed the cross-over study. At 9 days after training in hypoxia, significant increases were seen in maximal power output (.W(max))(5.2%), anaerobic mean power (4.1%), and anaerobic peak power (3.8%). A non-significant increase in maximal oxygen uptake (.VO(2max)) of 1.9% was observed. At 9 days after training at sea level, no significant changes were seen in .W(max)(2.1%), .VO(2max) (2.0%), anaerobic mean power (0.2%) and anaerobic peak power (0.2%). When comparing the results of the two training regimes, the anaerobic mean power was the only variable that showed a significantly larger increase as a result of training at altitude. And, although the differences in percentage change between the two training protocols were not significant, they were substantial for as well as for anaerobic peak power. The results of this study indicate that intermittent hypobaric training can improve the anaerobic energy supplying system, and also, to a lesser extent, the aerobic system. It can be concluded that the overall results of the cross-over study showed predominantly improvements in the anaerobic metabolism at variance with the previous study of our own group, where the relative .VO(2max) and .W(max) increased by 7%.
Intermittent hypobaric hypoxia stimulates erythropoiesis and improves aerobic capacity.
Rodríguez FA, et al. Med Sci Sports Exerc. 1999.
PURPOSE: The purpose of the study was to examine the effect of a very short intermittent exposure to moderate hypoxia in a hypobaric chamber on aerobic performance capacity at sea level and the erythropoietic response. The effects of hypobaric hypoxia alone and combined with low-intensity exercise were also compared.
METHODS: Seventeen members of three high-altitude expeditions were exposed to intermittent hypoxia in a hypobaric chamber over 9 d at simulated altitude, which was progressively increased from 4000 to 5500 m in sessions ranging from 3 to 5 h x d(-1). One group (N = 7; HE group) combined passive exposure to hypoxia with low-intensity exercise on a cycle ergometer. Another group (N = 10; H group) was only exposed to passive hypoxia. Before and after the exposure to hypoxia, medical status, performance capacity, and complete hematological and hemorheological profile of subjects were evaluated.
RESULTS: No significant differences were observed between the two groups (HE vs H) in any of the parameters studied, indicating that hypoxia alone was responsible for the changes. After the acclimation period, a significant increase in exercise time (mean difference: +3.9%; P < 0.01), and maximal pulmonary ventilation (+5.5%; P < 0.05) was observed during the maximal incremental test at sea level. Individual lactate-velocity curves significantly shifted to the right (P < 0.05), thus revealing an improvement of aerobic endurance. A significant increase was found in PCV (42.1-45.1%; P < 0.0001), RBC count (5.16 to 5.79 x 10(6) x mm(-3); P < 0.0001), reticulocytes (0.5 to 1.1%; P < 0.0001) and hemoglobin (Hb) concentration (14.2 to 16.7 g x dL(-1); P < 0.002).
CONCLUSIONS: It was concluded that short-term hypobaric hypoxia can activate the erythropoietic response and improve the aerobic performance capacity in healthy subjects.
Intermittent hypoxia improves endurance performance and submaximal exercise efficiency.
Katayama K, et al. High Alt Med Biol. 2003.
The purpose of the present study was to elucidate the influence of intermittent hypobaric hypoxia at rest on endurance performance and cardiorespiratory and hematological adaptations in trained endurance athletes. Twelve trained male endurance runners were assigned to either a hypoxic group (n = 6) or a control group (n = 6). The subjects in the hypoxic group were exposed to a simulated altitude of 4500 m for 90 min, three times a week for 3 weeks. The measurements of 3000 m running time, running time to exhaustion, and cardiorespiratory parameters during maximal exercise test and resting hematological status were performed before (Pre) and after 3 weeks of intermittent hypoxic exposure (Post). These measurements were repeated after the cessation of intermittent hypoxia for 3 weeks (Re). In the control group, the same parameters were determined at Pre, Post, and Re for the subjects not exposed to intermittent hypoxia. The athletes in both groups continued their normal training together at sea level throughout the experiment. In the hypoxic group, the 3000 m running time and running time to exhaustion during maximal exercise test improved. Neither cardiorespiratory parameters to maximal exercise nor resting hematological parameters were changed in either group at Post, whereas oxygen uptake (.V(O2)) during submaximal exercise decreased significantly in the hypoxic group. After cessation of intermittent hypoxia for 3 weeks, the improved 3000 m running time and running time to exhaustion tended to decline, and the decreased .V(O2) during submaximal exercise returned to Pre level. These results suggest that intermittent hypoxia at rest could improve endurance performance and submaximal exercise efficiency at sea level in trained endurance athletes, but these improvements are not maintained after the cessation of intermittent hypoxia for 3 weeks.
Muscle energetics in short-term training during hypoxia in elite combination skiers.
Kuno S, et al. Eur J Appl Physiol Occup Physiol. 1994.
Four well-trained combination skiers were studied through pre- and post-training for the effects of short-term intermittent training during hypoxia on muscle energetics during submaximal exercise as measured by Phosphorus-31 nuclear magnetic resonance and maximal aerobic power (VO2max). The hypoxia and training in the cold was conducted in a hypobaric chamber and comprised 60-min aerobic exercise (at an intensity equivalent to the blood lactate threshold), using a cycle ergometer or a treadmill twice a day for 4, consecutive days at 5 degrees C, in conditions equivalent to an altitude of 2000 m (593 mm Hg). No change in VO2max was observed over the training period, while in the muscle energetics during submaximal exercise, the values of phosphocreatine/(phosphocreatine+inorganic phosphate) and intracellular pH were found to be significantly increased by training during hypoxia. During recovery, the time constant of phosphocreatine was found to have been significantly reduced [pre, 27.9 (SD 6.7) s; post, 22.5 (SD 4.7) s, P < 0.01]. The observed inhibition of phosphocreatine as well as that of intracellular pH changes after training during hypoxia and quicker recovery of phosphocreatine in submaximal exercise tests, may indicate improved oxidative capacity (i.e. a high adenosine 5′-triphosphate formation rate) despite the short-term hypoxia training.
Aerobic capacity during acute exposure to simulated altitude, 914 to 2286 meters.
Randomized controlled trial
Squires RW, et al. Med Sci Sports Exerc. 1982.
In order to systematically assess the effects of acute exposure to moderate hypoxia on aerobic capacity (VO2max), 12 men (regular participants in recreational distance running) performed six treadmill-graded exercise tests (GXTs) in a hypobaric chamber. GXTs 1 and 6 were performed at ambient (control) altitude (362 m, barometric pressure = 730 mmHg). GXTs 2-5 were administered during 1-2 h of exposure to barometric pressures of 681, 656, 632, and 574 mmHg simulating altitudes of 914, 1219, 1524, and 2286 m, respectively, with the order of presentation randomized and blinded for each subject. The mean VO2max for GXTs 1 and 6 (control altitude) were essentially identical with a test-retest correlation of r = 0.92. During peak exercise, HR max was unchanged by hypoxia, while VO2max was significantly lower than the control by 4,8, 6.9, and 11.9% at 1219, 1524, and 2286 m, respectively. SaO2@max percent during maximal exercise was significantly reduced from the control by 3.5, 3.6, 7.0, and 11.6% at 914, 1219, 1524, and 2286 m, respectively. It was concluded that VO2max, in physically well-conditioned persons living at 362 m, is reduced during acute exposure to 1219 m and above.
Respiratory Muscle Training and Exercise Endurance at Altitude.
Helfer S, et al. Aerosp Med Hum Perform. 2016.
BACKGROUND: Climbing and trekking at altitude are common recreational and military activities. Physiological effects of altitude are hypoxia and hyperventilation. The hyperventilatory response to altitude may cause respiratory muscle fatigue and reduce sustained submaximal exercise. Voluntary isocapnic hyperpnea respiratory muscle training (VIHT) improves exercise endurance at sea level and at depth. The purpose of this study was to test the hypothesis that VIHT would improve exercise time at altitude [3600 m (11,811 ft)] compared to control and placebo groups.
METHODS: Subjects pedaled an ergometer until exhaustion at simulated altitude in a hypobaric chamber while noninvasive arterial saturation (Sao2), ventilation (VE), and oxygen consumption (Vo2) were measured.
RESULTS: As expected, Sao2 decreased to 88 ± 4% saturation at rest and to 81 ± 2% during exercise, and was not affected by VIHT. VIHT resulted in a 40% increase in maximal training VE compared to pre-VIHT. Exercise endurance significantly increased 44% after VIHT (P = <0.001). Vo2 (30 ± 3 ml · kg(-1) · min(-1)) and heart rate (177 ± 10 bpm) did not change during exercise and were not affected by VIHT (P = 0.531). Pre-VIHT VE increased 21-27% during the initial 12 min of exercise, after which it decreased 17% at 17.7 ± 6.0 min. VE at altitude post-VIHT increased more (49%) for longer (21 min) and decreased less (11% at 25.4 ± 6.7 min).
DISCUSSION: VIHT improved exercise time at altitude and sustained VE. This suggests that VIHT reduced respiratory muscle fatigue and would be useful to trekkers and military personnel working at altitude. Helfer S, Quackenbush J, Fletcher M, Pendergast DR. Respiratory muscle training and exercise endurance at altitutde. Aerosp Med Hum Perform. 2016; 87(8):704-711.
Performance enhancement through training at medium altitude– from the perspective of sports medicine].
Hofmann P. Wien Med Wochenschr. 2000.
In the last 20 years, maximal oxygen uptake (VO2max) of athletes in different sport disciplines has increased, and the world records in endurance sports have improved markedly. One of the factors that has influenced the increase in endurance performance has been perceived to be altitude training. In this paper we describe the advantages and disadvantages of a “regular” altitude training (live high/train high) aiming to improve sea level performance and compare it with a new method, the so called “live high/train low” method. This method uses the advantages and avoids the side effects of altitude exposure. Several papers have shown that altitude training is able to improve VO2max but the individual response may be substantially different. In most cases it is not possible to prove statistical significance and therefore we have no data about differences between both altitude training methods. However, it is suspected that the risk of overtraining is reduced in the high/low method. Although not statistically significant it is suggested that the “high/low” method can more efficiently improve endurance performance at sea level. A monitoring of submaximal variables of exercise performance is recommended to avoid overtraining and to control the development of performance. From the current knowledge the “live high/train low” method is suggested to be the more effective altitude training method for athletes.
Metabolic adaptations may counteract ventilatory adaptations of intermittent hypoxic exposure during submaximal exercise at altitudes up to 4000 m.
Faulhaber M, et al. PLoS One. 2012.
Intermittent hypoxic exposure (IHE) has been shown to induce aspects of altitude acclimatization which affect ventilatory, cardiovascular and metabolic responses during exercise in normoxia and hypoxia. However, knowledge on altitude-dependent effects and possible interactions remains scarce. Therefore, we determined the effects of IHE on cardiorespiratory and metabolic responses at different simulated altitudes in the same healthy subjects. Eight healthy male volunteers participated in the study and were tested before and 1 to 2 days after IHE (7 × 1 hour at 4500 m). The participants cycled at 2 submaximal workloads (corresponding to 40% and 60% of peak oxygen uptake at low altitude) at simulated altitudes of 2000 m, 3000 m, and 4000 m in a randomized order. Gas analysis was performed and arterial oxygen saturation, blood lactate concentrations, and blood gases were determined during exercise. Additionally baroreflex sensitivity, hypoxic and hypercapnic ventilatory response were determined before and after IHE. Hypoxic ventilatory response was increased after IHE (p<0.05). There were no altitude-dependent changes by IHE in any of the determined parameters. However, blood lactate concentrations and carbon dioxide output were reduced; minute ventilation and arterial oxygen saturation were unchanged, and ventilatory equivalent for carbon dioxide was increased after IHE irrespective of altitude. Changes in hypoxic ventilatory response were associated with changes in blood lactate (r = -0.72, p<0.05). Changes in blood lactate correlated with changes in carbon dioxide output (r = 0.61, p<0.01) and minute ventilation (r = 0.54, p<0.01). Based on the present results it seems that the reductions in blood lactate and carbon dioxide output have counteracted the increased hypoxic ventilatory response. As a result minute ventilation and arterial oxygen saturation did not increase during submaximal exercise at simulated altitudes between 2000 m and 4000 m.
Training in hypoxia and its effects on skeletal muscle tissue.
Hoppeler H, et al. Scand J Med Sci Sports. 2008.
It is well established that local muscle tissue hypoxia is an important consequence and possibly a relevant adaptive signal of endurance exercise training in humans. It has been reasoned that it might be advantageous to increase this exercise stimulus by working in hypoxia. However, as long-term exposure to severe hypoxia has been shown to be detrimental to muscle tissue, experimental protocols were developed that expose subjects to hypoxia only for the duration of the exercise session and allow recovery in normoxia (live low-train high or hypoxic training). This overview reports data from 27 controlled studies using some implementation of hypoxic training paradigms. Hypoxia exposure varied between 2300 and 5700 m and training duration ranged from 10 days to 8 weeks. A similar number of studies was carried out on untrained and on trained subjects. Muscle structural, biochemical and molecular findings point to a specific role of hypoxia in endurance training. However, based on the available data on global estimates of performance capacity such as maximal oxygen uptake (VO2max) and maximal power output (Pmax), hypoxia as a supplement to training is not consistently found to be of advantage for performance at sea level. There is some evidence mainly from studies on untrained subjects for an advantage of hypoxic training for performance at altitude. Live low-train high may be considered when altitude acclimatization is not an option.
Nonhematological mechanisms of improved sea-level performance after hypoxic exposure.
Gore CJ, et al. Med Sci Sports Exerc. 2007.
Altitude training has been used regularly for the past five decades by elite endurance athletes, with the goal of improving performance at sea level. The dominant paradigm is that the improved performance at sea level is due primarily to an accelerated erythropoietic response due to the reduced oxygen available at altitude, leading to an increase in red cell mass, maximal oxygen uptake, and competitive performance. Blood doping and exogenous use of erythropoietin demonstrate the unequivocal performance benefits of more red blood cells to an athlete, but it is perhaps revealing that long-term residence at high altitude does not increase hemoglobin concentration in Tibetans and Ethiopians compared with the polycythemia commonly observed in Andeans. This review also explores evidence of factors other than accelerated erythropoiesis that can contribute to improved athletic performance at sea level after living and/or training in natural or artificial hypoxia. We describe a range of studies that have demonstrated performance improvements after various forms of altitude exposures despite no increase in red cell mass. In addition, the multifactor cascade of responses induced by hypoxia includes angiogenesis, glucose transport, glycolysis, and pH regulation, each of which may partially explain improved endurance performance independent of a larger number of red blood cells. Specific beneficial nonhematological factors include improved muscle efficiency probably at a mitochondrial level, greater muscle buffering, and the ability to tolerate lactic acid production. Future research should examine both hematological and nonhematological mechanisms of adaptation to hypoxia that might enhance the performance of elite athletes at sea level.
Same Performance Changes after Live High-Train Low in Normobaric vs. Hypobaric Hypoxia.
Saugy JJ, et al. Front Physiol. 2016.
PURPOSE: We investigated the changes in physiological and performance parameters after a Live High-Train Low (LHTL) altitude camp in normobaric (NH) or hypobaric hypoxia (HH) to reproduce the actual training practices of endurance athletes using a crossover-designed study.
METHODS: Well-trained triathletes (n = 16) were split into two groups and completed two 18-day LTHL camps during which they trained at 1100-1200 m and lived at 2250 m (P i O2 = 111.9 ± 0.6 vs. 111.6 ± 0.6 mmHg) under NH (hypoxic chamber; FiO2 18.05 ± 0.03%) or HH (real altitude; barometric pressure 580.2 ± 2.9 mmHg) conditions. The subjects completed the NH and HH camps with a 1-year washout period. Measurements and protocol were identical for both phases of the crossover study. Oxygen saturation (S p O2) was constantly recorded nightly. P i O2 and training loads were matched daily. Blood samples and VO2max were measured before (Pre-) and 1 day after (Post-1) LHTL. A 3-km running-test was performed near sea level before and 1, 7, and 21 days after training camps.
RESULTS: Total hypoxic exposure was lower for NH than for HH during LHTL (230 vs. 310 h; P < 0.001). Nocturnal S p O2 was higher in NH than in HH (92.4 ± 1.2 vs. 91.3 ± 1.0%, P < 0.001). VO2max increased to the same extent for NH and HH (4.9 ± 5.6 vs. 3.2 ± 5.1%). No difference was found in hematological parameters. The 3-km run time was significantly faster in both conditions 21 days after LHTL (4.5 ± 5.0 vs. 6.2 ± 6.4% for NH and HH), and no difference between conditions was found at any time.
CONCLUSION: Increases in VO2max and performance enhancement were similar between NH and HH conditions.
Effect of respiratory muscle training on maximum aerobic power in normoxia and hypoxia.
Esposito F, et al. Respir Physiol Neurobiol. 2010.
To assess the effects of respiratory muscle training (RMT) on maximum oxygen uptake (VO2max) in normoxia and hypoxia, 9 healthy males (age 24 +/- 4 years; stature 1.75 +/- 0.08 m; body mass 72 +/- 9 kg; mean +/- SD) performed on different days maximal incremental tests on a cycle ergometer in normoxia and normobaric hypoxia (FIO2=0.11), before and after 8 weeks of RMT (5 days/week). During each test, gas exchange variables were measured breath-by-breath by a metabolimeter. After RMT, no changes in cardiorespiratory and metabolic variables were detected at maximal exercise in normoxia. On the contrary, in hypoxia expired and alveolar ventilation (V(E(and V(A), respectively) at maximal exercise were significantly higher than pre-training condition (+12 and +13%, respectively; P < 0.05). Accordingly, alveolar O2 partial pressure (PAO2) after RMT significantly increased by approximately 10%. Nevertheless, arterial PO2 and VO2max did not change with respect to pre-training condition. In conclusion, RMT improved respiratory function but did not have any effect on VO2max, neither under normoxic nor hypoxic condition. In hypoxia, the significant increase in V(E) and V(A) at maximum exercise after training lead to higher alveolar but not arterial PO2 values, revealing an increased A-a gradient. This result, according to the theoretical models of VO2max limitation, seems to contradict the lack of VO2max increase in hypoxia, suggesting a possible role of increased ventilation-perfusion mismatch.
The effects of intermittent hypoxia training on hematological and aerobic performance in triathletes.
Ramos-Campo DJ, et al. Acta Physiol Hung. 2015.
The aim of the present research was to analyze modifications on hematological and aerobic performance parameters after a 7-week intermittent hypoxia training (IHT) program. Eighteen male trained triathletes were divided in two groups: an intermittent hypoxia training group (IHTG: n: 9; 26.0 ± 6.7 years; 173.3 ± 5.9 cm; 66.4 ± 5.9 kg; VO₂max: 59.5 ± 5.0 ml/kg/min) that conducted a normoxic training plus an IHT and a control group (CG: n: 9; 29.3 ± 6.8 years; 174.9 ± 4.6 cm; 59.7 ± 6.8 kg; VO₂max: 58.9 ± 4.5 ml/kg/min) that performed only a normoxic training. Training process was standardized across the two groups. The IHT program consisted of two 60-min sessions per week at intensities over the anaerobic threshold and atmospheric conditions between 14.5 and 15% FiO₂. Before and after the 7-week training, aerobic performance in an incremental running test and hematological parameters were analyzed. After this training program, the IHTG showed higher hemoglobin and erythrocytes (p < 0.05) values than in the CG. In terms of physiological and performance variables, between the two groups no changes were found. The addition of an IHT program to normoxic training caused an improvement in hematological parameters but aerobic performance and physiological variables compared to similar training under normoxic conditions did not increase.
The impact of moderate altitude on exercise metabolism in recreational sportsmen: a nuclear magnetic resonance metabolomic approach.
Messier FM, et al. Appl Physiol Nutr Metab. 2017.
Although it is known that altitude impairs performance in endurance sports, there is no consensus on the involvement of energy substrates in this process. The objective of the present study was to determine whether the metabolomic pathways used during endurance exercise differ according to whether the effort is performed at sea level or at moderate altitude (at the same exercise intensity, using proton nuclear magnetic resonance, 1H NMR). Twenty subjects performed two 60-min endurance exercise tests at sea level and at 2150 m at identical relative intensity on a cycle ergometer. Blood plasma was obtained from venous blood samples drawn before and after exercise. 1H NMR spectral analysis was then performed on the plasma samples. A multivariate statistical technique was applied to the NMR data. The respective relative intensities of the sea level and altitude endurance tests were essentially the same when expressed as a percentage of the maximal oxygen uptake measured during the corresponding incremental maximal exercise test. Lipid use was similar at sea level and at altitude. In the plasma, levels of glucose, glutamine, alanine, and branched-chain amino acids had decreased after exercise at altitude but not after exercise at sea level. The decrease in plasma glucose and free amino acid levels observed after exercise at altitude indicated that increased involvement of the protein pathway was necessary but not sufficient for the maintenance of glycaemia. Metabolomics is a powerful means of gaining insight into the metabolic changes induced by exercise at altitude.