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The Benefits of Altitude Training on Human Performance

The Benefits of Altitude Training on Human Performance                          Adam Khan


Altitude training is a method many athletes have used and are continuing to use as a means of maximising their sporting potential. The reason for training at altitude is that the environmental hypoxia encountered by the body causes numerous physiological changes. These changes can be split into both haematological and metabolic ones, which is how this review will discuss them. Haematological effects involve stimulation of erythropoiesis, leading to an increased red blood cell

(RBC) mass and haemoglobin concentration in the blood. There is also the involvement of changes in Myoglobin concentration. On the metabolic side, altitude training has been shown to have an effect on the buffering capacity of muscles, as well as their mechanical efficiency and levels of oxidative and glycolytic enzymes. The benefits of these physiological changes in humans (in the context of athletic performance) will be explored using original research papers, and the strengths and weaknesses of this evidence will be analysed.


Physiological Effects of Altitude Training:

One of the most well-known effects of altitude training is the hypoxia-induced increase in erythropoietin (EPO) levels which in turn causes an increase in RBC mass. This increase in RBC mass results in a higher concentration of the oxygen-carrying molecule Haemoglobin in the blood. It has been shown that an individual’s absolute maximal oxygen uptake or VO2Max is increased by approximately 200 ml/min per g/dl increase in Hb (Bailey, Davies 1997). VO2Max is a measure of the maximum amount of oxygen the body can utilise during a set period of strenuous exercise, and is linked to aerobic endurance. Hence an increase in VO2Max due to exposure to altitude can theoretically lead to an increase in aerobic endurance (VO2Max), making it clear why many athletes choose to implement altitude training into their regimes.

Since lowering PO2 leads to an increase in Hb concentration, it would appear that the higher an athlete can train the greater the benefits of altitude on their performance. The issue with this approach is that with a reduction in PO2 comes an increase in certain factors which are detrimental to athletic performance. Acute mountain sickness for example usually presents above altitudes of 2,000-3,000 m, with symptoms potentially occurring at even lower altitudes in elite-level athletes. Sustained exposure to altitudes beyond 4,500 m have also been shown to lead to a reduction in muscle mass. Perhaps just as important is the fact that athletes may be unable to train at their normal work rate under conditions of decreased PO2 at altitude, and this detraining effect or reduction in work rate may outweigh the beneficial aspects of acclimatising to altitude (Bailey, Davies 1997).

There are generally three different types of altitude training in terms of the altitude procedure.

These are the Live-High Train-High Model (LH + TH), Live-High Train-Low Model (LH + TL), and Live-Low Train-High Model (LL + TH). The introduction of the LH + TL model is significant since in theory it should allow athletes to benefit from the physiological changes of living at altitude (such as increased erythropoiesis, higher Hb concentration and raised VO2Max), whilst continuing to train at their normal intensity at sea level. Thus this appears to solve the undesirable detraining effect observed when athletes train at altitude (Bailey, Davies 1997).


Relevance to Athletes in Individual Sports:

Evidently there are several physiological changes that altitude training can allow athletes to benefit from. It is easy to appreciate how an increased Hb concentration and VO2Max can improve the athletic performance of a 5,000 m runner or a swimmer, due to their increased ability to transport oxygen around their body and increased aerobic capacity.

Relevance to Athletes in Team Sports:

It is not just individual athletes who are utilising altitude training but also sporting teams, at a somewhat expensive cost. This section is going to discuss the evidence for altitude training being beneficial to human performance in the context of team sports.

Team sports generally require frequent short bursts of high-intensity work, which break up the longer periods of submaximal effort. Physiological changes which have relevance to this type of performance are those that impact upon either sprint performance, or an individual’s ability to recover from maximal/near-maximal exercise. The schematic in Figure 1 (Bishop, Girard 2013) neatly summarises some of the factors affecting these two variables.


Figure 1: This summarises the primary physiological factors impacting upon physical performance in team sport; these can be split into factors which affect either sprint performance or the ability to recover from maximal or near maximal effort (Bishop, Girard 2013).


Sprint Performance:

The importance of sprint performance is illustrated by the fact that in football straight sprinting is the action most frequently preceding a goal. The main determinants of sprint performance are stride length and stride frequency, with an increase in one or both of these factors leading to an increased sprint speed. Improvements in the stride length aspect are associated with improvements in power – which itself is linked to strength, elastic strength, dynamic flexibility and rate of ATP supply. Improvements in stride frequency are associated with intramuscular coordination (Bishop, Girard 2013).

Maximal effort sprints depend on rapid and frequent ATP turnover, stimulated by breakdown of phosphocreatine and anaerobic glycolysis. Athletes in team sports may be able to increase sprint performance via improvements in their ability to “deplete large amounts of high-energy phosphates at a fast rate” (Bishop, Girard 2013) which is essentially anaerobic capacity. Anaerobic performance on equipment such as ergometers is normally not affected negatively by altitude, due to increased anaerobic energy release which makes up for reduced aerobic ATP production. The reduced levels of oxygen available to the muscles at altitude causes increased anaerobic energy release which is thought to stimulate improved anaerobic capacity, aiding sprinting performance.

In terms of muscle strength, a component of stride length, hypoxia alone is not believed to be able to increase maximal muscle strength or sprint-speed. However there is a hypothesis that systemic hypoxia coupled with resistance training can significantly improve muscle strength. Resistance training in conditions of systemic hypoxia means a decreased oxygen concentration in blood and tissues leading to a higher build-up of metabolites and anabolic hormones such as growth hormone. Additionally resistance training under conditions of hypoxia stimulates increased recruitment of type II motor units, which could be pushed into adaptation in terms of hypertrophy due to the greater stress being exerted on them (Bishop, Girard 2013).

More research needs to be done on the impacts of altitude training on stride frequency. It is however hypothesised that improved central motor drive due to hypoxia in altitude training may lead to better regulation of musculoskeletal stiffness, thereby producing faster stride frequency and improved sprint performance (Bishop, Girard 2013).



Recovery Between Efforts:

Performance in team sport can also be affected by the ability to recover from maximal or near maximal effort. This recovery ability is determined by aerobic fitness, the most common measure of which is VO2Max. The relevance of VO2Max to performance is indicated by the fact that there is correlation between VO2Max and the distance covered in team sports (Bishop, Girard 2013). Some studies have shown altitude training to improve VO2Max, which itself can clearly lead to better performance in team sports, so the value of altitude training to sporting teams is evident.


Haematological Effects of Altitude Training:

A large portion of the findings relating to altitude training centre on its haematological effects. One particular study (Levine, Stray-Gundersen 1997) is a comprehensive body of work which looks at the effects of Live-High Train-Low altitude training. The study design was influenced by the belief that athletes living at moderate altitude (>2,500 m) whilst training at low altitude would benefit from the physiological changes triggered by altitude acclimatization, whilst avoiding detraining effects associated with high altitude training. After a 2 week lead-in phase of supervised training athletes took part in a 4 week training cycle at sea-level. Laboratory testing and a 5,000 m time trail were conducted in both the first and last weeks of this period. Athletes were then placed into one of three groups:

  • High-Low- live at moderate altitude (2,500 m), train at low altitude (1,200-1,400 m)
  • High-High– live at moderate altitude (2,500 m), train at moderate altitude (2,500-2,700 m)
  • Low-Low– live at sea level (150 m), train at sea level (150 m)

These groups took part in an altitude training camp (at the altitude specified by the group they were placed in) which consisted of the same 4 week training cycle used in the sea level training. Finally the study ended with a return to sea level where the laboratory tests were repeated and athletes attempted a 5,000 m time trail at the end of each week for the next three weeks.

In terms of laboratory testing plasma volume, blood volume, submaximal exercise performance, VO2Max and an anaerobic capacity test were measured both before and after the altitude training camp. Plasma volume was calculated via Evans Blue dye dilution procedure and haematocrit was calculated by micro capillary centrifuge. An estimate for blood volume was obtained by calculating (plasma volume)/(1-haematocrit). RBC mass was calculated by blood volume – plasma volume.

The study was designed very well to focus solely on the effects of altitude on performance, and a lot of care was taken to control any other variables. For instance the 2 week lead-in period allowed them to bring all the athletes up to similar levels of conditioning. Additionally the laboratory tests obtained after the altitude training camp were taken in the same order as those done before the altitude training camp. There was also great attention to detail regarding the logging of athlete diet, as well as fluid intake, bodyweight, general wellbeing and sleep among other factors. Serum ferritin was also measured during the supervised lead-in phase, with all participants being placed on iron maintenance/replacement therapy (Levine, Stray-Gundersen 1997).

When looking at the results of this study there are some important observations made about the effects on blood volumes. In the High-Low and High-High group plasma volume was increased by sea level training, then decreased back to normal after training at altitude. In the sea-level training (control) group plasma volume remained at normal levels. Living at altitude led to a substantial 9% increase in RBC mass, a rise which did not occur in the sea-level group. The decreased plasma volume observed after subjects lived at altitude was counter-acted by the rise in RBC mass, resulting in there being no change in blood volume – there was however an increased ability to carry oxygen due to a higher haemoglobin concentration. This clearly illustrates the haematological impacts of altitude.

Notable effects on VO2Max were also recorded. After undergoing the 2 week lead-in phase, a further 4 week training cycle at sea-level did not cause a significant increase in VO2Max in any group which suggests participants had peaked in terms of their aerobic power. However following the 4 week training period at altitude in the High-Low and High-High groups there was an additional 5% rise in VO2Max. Conversely the same supervised training camp in the sea-level (control) group produced no increase in VO2Max. The rise in VO2Max was “loosely but significantly correlated” (Levine, Stray-Gundersen 1997) with the change in RBC mass and change in haemoglobin concentration during the training camp. These changes in VO2Max can be seen in Figure 2 (Levine, Stray-Gundersen 1997) below. The findings discussed in this paragraph are significant because they show that physiological changes have taken place. This means that any differences in time trial performance between subject groups is unlikely to be due to external factors such as discrepancies in effort, a topic which will be further discussed later.

Figure 2: Maximal oxygen uptake at baseline after lead-in training period (sea level), and after altitude training camp (altitude) which consisted of High-High, High-Low or Low-Low training. P<0.05 compared with previous time point (Levine, Stray-Gundersen 1997).


Maximal steady state VO2 also did not change significantly in any of the groups during the 4 week period of sea-level training. However, what was different about this data to the results for VO2Max was that maximal steady state VO2 increased significantly only in the high-low group whereas VO2Max increased in both the High-Low and High-High group. The data for maximal steady state VO2 is illustrated in Figure 3 (Levine, Stray-Gundersen 1997) below.




Figure 3: Oxygen uptake (VO2) at maximal steady state, derived from ventilatory threshold at baseline after lead-in training period (sea level), and after altitude training camp (altitude) which consisted of High-High, High-Low or Low-Low training. P<0.05 compared with previous time point (Levine, Stray-Gundersen 1997).


The paper then investigates whether these changes caused by altitude training have an impact on 5,000 m trial times. Participants in all three groups displayed similar improvements to 5,000 m trial times after the initial 4 week training cycle at sea-level. The High-Low group showed a further improvement by an average of 13.4 +/- 10 seconds after their altitude training camp. For the High-High group 5,000 m times were on average 3.3 +/- 9 seconds longer or slower. The sea-level (control) group times were also 26.7 +/- 13 seconds longer (Levine, Stray-Gundersen 1997).

The data above illustrates how improvements were made in the 5,000 m running times of well-trained runners in the High-Low group – through a combination of altitude acclimatization and sea-level training. This level of improvement was not seen in the High-High group or sea-level (control) group. The optimal results achieved by the High-Low group are thought to be due two factors: the first is the effects of acclimatization to living at altitude which involves increased capacity of oxygen carrying in the blood and increased VO2Max, and the second is the maintenance of training intensity and oxygen flux via sea-level training.

This paper highlights that the most important adaptation for improved sea level performance is probably the increase in RBC mass which equates to better oxygen-carrying capacity and ultimately increased aerobic power. Results from treadmill trials which mimicked velocities experienced in 5,000 m races indicated that the increased oxygen-carrying capacity of the blood allowed a lower cardiac output and hence more peripheral diffusion time and oxygen extraction (Levine, Stray-Gundersen 1997).

Participants in the High-High group, who not only lived but also trained at high altitude, experienced a detraining effect. Essentially athletes training at altitude were not able to maintain their sea-level work rates. In the High-High participants any increases in RBC mass and VO2Max were “offset by a reduction in training velocity and oxygen flux, leading to no change in running performance” (Levine, Stray-Gundersen 1997).

The study by Levine and Stray-Gundersen mentions a significant limitation, that participants placed in the Low-Low sea-level training group would not be as motivated as the High-Low or High-High participants due to previously held expectations of a benefit from altitude training. However, the authors state that the sea-level athletes’ excitement at being afforded the use of the world-leading facilities at the San Diego Olympic training centre was sufficient to eliminate disappointment at being placed in the control group. In fact athletes from the control group were said to be “more motivated to perform better on return from the camp to prove that their training experience was every bit as good as their altitude counterparts” (Levine, Stray-Gundersen 1997), therefore it appears unlikely that discrepancies in effort contributed to the differences in performance between groups.

This research (Levine, Stray-Gundersen 1997) recorded the positive impact of altitude training in the performance of well-trained runners. More recent studies (Stray-Gundersen, Chapman et al. 2001) involving several of the same authors aimed to determine whether similar benefits could be seen in elite athletes who are closer to the maximal structural and functional adaptive capacity of the respiratory system. The results are significant as they once again found that High-Low altitude training improved sea-level running performance (this time in 3,000 m trials). Figure 4 (Stray-Gundersen, Chapman et al. 2001) below shows the improvements in 3,000 m performance in elite male and female runners after altitude training.



Figure 4: Changes in 3,000 m performance in elite male (A) and elite female (B) runners in response to a 4 week Live-High Train-Low method of altitude training. *P<0.05, &P<0.10 compared with pre-altitude (Stray-Gundersen, Chapman et al. 2001).


The mechanism of improvement is said to be similar to that previously described in trials with non-elite athletes (Levine, Stray-Gundersen 1997). There is stimulation of erythropoiesis which leads to an apparent increase in delivery of oxygen to peripheral tissues, illustrated by plasma concentrations of EPO almost doubling upon altitude exposure. Further evidence for the stimulation of erythropoiesis is provided by increases in haemoglobin concentration and haematocrit on return to sea level (Stray-Gundersen, Chapman et al. 2001). The fact that evidence for this mechanism was found in both elite and non-elite athletes strongly supports the theory that the benefits of altitude training on performance are mediated via increased erythropoiesis and RBC mass.

Stray-Gundersen, Chapman et al. highlight several limitations in their work. The biggest potential limitation is the lack of a sea-level control group performing the same training as the altitude group, like the control group used in other studies (Levine, Stray-Gundersen 1997). Such a control group is necessary to prove that the improvements in performance are not simply due to the result of a training camp but due to the altitude training itself. Despite this flaw, the authors do attempt to justify the absence of a control group. They determined previously that “at least 2 weeks of controlled training were necessary to overcome the training camp effect” (Stray-Gundersen, Chapman et al. 2001). The study makes the convincing argument the elite athletes used in this research spent months prior to these experiments training in preparation for their national championships, and this amount of training was at least equivalent to the 2 weeks training required to negate the training camp phenomenon. This particular defence of such a limitation is difficult to disagree with.

Investigations have been conducted on the impact of endurance training under simulated hypoxia on molecular adaptation in skeletal muscle. One of the substances measured was HIF-1A, which is the regulatory alpha subunit of the Hypoxia-Inducible Factor 1. It was reported that HIF-1A m-RNA increased after training in hypoxic conditions, irrespective of training intensity (Vogt, Puntschart et al. 2001). In contrast there was no statistically significant change in HIF-1a m-RNA after training in normoxic conditions. The authors suggest that HIF-1 is a crucial factor in the specific response to hypoxia. HIF-1 is a nuclear factor whose DNA-binding activity is induced by hypoxia (Wang, Semenza 1993). It binds at a site in the EPO gene enhancer, thus stimulating transcriptional activation of EPO. This is significant because HIF-1 mediates improved oxygen transport capacity in the blood as a result of increasing haematocrit via EPO (Vogt, Puntschart et al. 2001).

HIF-1 also causes the transcription of genes which produce other proteins such as vascular endothelial growth factor (VEGF). The fact that VEGF is produced via HIF-1 is also significant, since VEGF stimulates induction of neovascularization. Experimental results showed increased levels of the m-RNAs for VEGF and HIF-1a m-RNA after training at high intensity in hypoxic conditions. There was no change in the concentrations of VEGF m-RNA after training in normoxic conditions or low-intensity training in hypoxic conditions, despite the latter conditions producing an increase in the concentrations of HIF-1A mRNA. This set of results seems counter-intuitive since it goes against the concept of HIF- 1 dependent regulation of VEGF. The authors explain that these results are a consequence of the additive effect of mechanical training and hypoxia on production of VEGF. They conclude that intensity of training and the level of hypoxia combine to produce increased steady-state levels of VEGF m-RNA in the group training at high intensity under hypoxic conditions (Vogt, Puntschart et al. 2001).

When examining the haematological effects of altitude training it is pertinent to discuss Myoglobin. Studies examining molecular adaptations in response to hypoxia explored the impact of altitude training on Myoglobin (Mb). There were increased levels of Mb m-RNA, but only after training at high intensity in hypoxic condition. There was no change in Mb m-RNA levels after training at low intensity, or training under normoxic conditions. The authors assume that the increased level of Mb m-RNA seen in subjects who trained at high intensity under hypoxia equates to increased Mb content within their muscle (Vogt, Puntschart et al. 2001). This is a fair assumption to make because other studies have shown that doing work under hypobaric conditions simulating altitude of 2,300 m above sea level produces increased Myoglobin levels in muscle. In one such study subjects trained one leg in normobaric conditions and the other in hypobaric conditions. It was found that concentration of myoglobin increased in the leg trained under hypobaric conditions and decreased in the leg trained under normobaric conditions (Terrados, Jansson et al. 1990).

These data clearly establish that altitude training has the ability to increase myoglobin levels in skeletal muscle, but how does this benefit human performance? Arguably the most well-known function of myoglobin is its ability to act as an O2-storage protein in muscle. The role of Myoglobin in storage of O2 is evidenced by research which observed adaptations in mammals and birds for maximal diving durations. This research was conducted with odontocete species and cetaceans which are both types of marine mammals. They found a close correlation between myoglobin content and maximum dive duration, which is illustrated by the data in Figure 5 (Noren, Williams 2000) below. The odontocete species with longest maximum dive durations (25 to 73 minutes) had 4.32g to 7.87g of myoglobin per 100g wet muscle, whilst the odontocetes with short duration dives (5 to 18.3 minutes) had relatively lower myoglobin contents of 1.81g to 4.03g per 100g of wet muscle (Noren, Williams 2000).

Figure 5: Maximum dive duration relative to skeletal muscle myoglobin content for odontocetes (solid line) and mysticetes (dashed line). Relationships are least squares linear regressions as described in the research. Dotted lines are the 95% confidence intervals around the regression for odontocetes. Genus initials indicate data points, species initial is included if the genus initial is redundant (Noren, Williams 2000).


Another proposed role of Myoglobin is in facilitating O2 diffusion. A study which found that “Mb content is proportional to the shortfall in O2 diffusion and the need for additional O2 supply to meet O2 demands” (Conley, Jones 1996) could be seen as supporting a role for Myoglobin in mediating diffusion of O2.

Hence training under hypoxic conditions can induce increases in myoglobin within skeletal muscle, and this increased myoglobin has several roles, particularly in oxygen storage and facilitated diffusion which will lead to better O2 utility and athletic performance.


Metabolic Effects of Altitude Training:

There is clearly a significant amount of evidence supporting the theory that performance benefits of altitude training are mediated through haematological changes such as increased RBC mass and increased Haemoglobin concentration. However there is also evidence to suggest that the benefits of altitude occur via metabolic changes. Studies have shown that certain forms of altitude training can invoke improvements in buffer capacity in skeletal muscle, and also improve exercise efficiency. One of these studies split participants into a LHTL (Live High Train Low) group and a control group. LHTL participants slept in hypoxic conditions which simulated altitude of 3,000 m for 23 consecutive nights whilst control subjects slept in their own home in normobaric normoxia. Participants of both groups trained and spent their days at 600 m altitude (Gore, Hahn et al. 2001).

Various data was obtained from subject performance in 5 submaximal cycle ergometer tests. The PRE ergometer tests were conducted 4 and 5 days before the LHTL cohort slept at simulated hypoxic altitude, and the POST tests were conducted 2 and 3 days after they slept at simulated altitude. Finally the MID test took place after 11 days of sleeping at simulated altitude. VO2, VCO2, minute ventilation (VE) and respiratory exchange ratio (RER) were measured from each ergometer test, with blood also being analysed for plasma pH, PCO2, and concentrations of bicarbonate and lactate.

The novel finding of this study was that just sleeping in hypoxia induced increased buffer capacity of muscle in vitro, a rise which was attributed to chronic hypoxic exposure alone rather than to the effects of training under hypoxia. Figure 6 (Gore, Hahn et al. 2001) below shows how resting muscle buffering capacity significantly increased in LHTL subjects, while there was no change in control subjects.



Figure 6: Change in resting in-vitro muscle buffering capacity (Bm) PRE and POST 23 nights of simulated altitude. Left graph displays individual data points of LHTL group (n=6) which lived high and trained low with mean +/- SD data indicated by the large symbols. Right graph displays data for the CON group (n=7) of control subjects (Gore, Hahn et al. 2001).


Additionally the LHTL regime “did not coincide with enhanced muscle [H+] regulation” (Gore, Hahn et al. 2001) since there was no change in muscle [H+] post-exercise, and no anaerobic metabolism upregulation. The study points out that there was no increase in lactate accumulation during intense exercise after LHTL which supports the conclusion that anaerobic metabolism is not enhanced after LHTL. Moreover during submaximal cycle ergometry whole body VO2 was significantly lower after 23 nights of sleeping at 3,000 m simulated altitude. The reduced VO2 at the same workload in the absence of increased anaerobic metabolism indicates that sleeping under hypoxic conditions potentially improves mechanical efficiency during exercise (Gore, Hahn et al. 2001).

This reduced VO2 and increased efficiency exhibited by LHTL participants is consistent with other studies which reported greater efficiency of exercise in people native to high altitude compared to low-land dwelling individuals (Hochachka, Stanley et al. 1991). The fall in whole body VO2 in exercise after the LHTL regime is supposedly due to a shift from fat to carbohydrate oxidation (Gore, Hahn et al. 2001). The study also states that submaximal RER was slightly higher after LHTL, which is said to be supportive of the theory that altitude is associated with “an overall shift towards carbohydrate utilization” (Gore, Hahn et al. 2001). Several previously published papers also reported a decreased dependence on fat as a fuel source after acclimatization to altitude (Roberts, Butterfield et al. 1996).

In conclusion, after LHTL training there was a reduction of 7% in VO2Peak and a reduction in whole body oxygen utilization during exercise in normoxia. There is also a 0.8% increase in submaximal cycling efficiency, which is explained by a rise in carbohydrate utilization. There was no change in haemoglobin mass and no sign of accelerated erythropoiesis, which is in contrast to the numerous papers which propose that haematological changes produce the beneficial effects of altitude training. Instead this research supports the view that the benefits of training under hypoxic conditions are potentiated via increased buffering capacity of muscle and increased mechanical efficiency (Gore, Hahn et al. 2001).

A study looked at the impact of altitude training on metabolic capacity of muscle in competitive road cyclists. They studied eight athletes, splitting them into two groups of four. The AG group (altitude group) trained in a hypobaric chamber under pressures of 574 torr which simulated altitude of 2,300 m above sea level, while the control SLG group (sea-level group) trained at sea level. Subjects from both the AG and the SLG group lived at sea-level. Work capacity for participants was measured before and after the training via an incremental cycle ergometer test to exhaustion. Muscle samples were also taken and levels of enzymes including lactate dehydrogenase and citrate synthase were measured (Terrados, Melichna et al. 1988).

The authors state a 33% increase in both sea-level and altitude performance in the AG group after the training period. The effect of the training period in the SLG group caused work capacity to increase 22% at sea level and 14% at altitude. The study also found that blood lactate concentration at a given submaximal load at altitude was significantly more reduced in response to training in the AG group, whilst it increased with training in the SLG group. The authors reason that since there was no change in maximal oxygen uptake, this reduction in blood lactate in the AG group may be due to “more rapid increase in oxygen uptake at each workload” (Terrados, Melichna et al. 1988) after the training period. It is suggested that such an increased rate of oxygen uptake is caused by a faster increase in heart rate and cardiac output (Hagberg, Hickson et al. 1980), plus the denser muscle capillarization observed in the experimental results (Terrados, Melichna et al. 1988).

There was no clear effect of training in the AG or SLG group on muscle oxidative capacity, since there was no change in CS activity – CS referring to citrate synthase. Perhaps this was due to the fact that the subjects of the study were endurance trained athletes who already had high skeletal muscle oxidative capacities pre-study (Terrados, Melichna et al. 1988).

This study gives an alternative viewpoint as to why altitude training stimulates performance benefits in athletes, proposing that there are non-haematological changes occurring. The use of a control sea-level training group adds to the appeal of the study, as does their findings surrounding blood lactate and glycolytic enzymes. However, I am slightly concerned that the study used only 8 subjects, as I feel this a very small sample size from which to come to conclusions about the nonhaematological impacts of altitude training.

A previously described study (Vogt, Puntschart et al. 2001) explored the impact of altitude training on molecular changes in muscle. It was found that training under hypoxia stimulated increases in HIF-1, which led to haematological changes via its effects on EPO. HIF-1 also causes the transcription of genes which produce other proteins such as glycolytic enzymes, which along with EPO and VEGF mediate adaptive responses to hypoxia (Yu, Shimoda et al. 1999) The activation of glycolytic enzymes is important as it allows an increase in glucose oxidation which in turn produces more efficient oxygen utilization (Vogt, Puntschart et al. 2001).

Another variable observed in the study of molecular changes induced by altitude training was oxidative enzymes. There was an increase in levels of m-RNAs encoding oxidative enzymes after training at high intensity in both hypoxia and normoxia, but only minor changes in these m-RNAs after low-intensity training (Vogt, Puntschart et al. 2001). This suggests altitude training increases oxidative capacity, which is in contrast with the earlier mentioned findings (Terrados, Melichna et al. 1988). In the work by Terrados, Melichna et al. the analysis of citrate synthase activity led to the observation that there was no change in oxidative capacity between altitude and sea-level training groups. The authors of that study did note that this could have been due to the fact their study subjects were trained endurance athletes who may have been at the limit of their oxidative capacity. The data from the work by Vogt, Puntschart et al. is from a subject group of thirty untrained male volunteers so perhaps this contradiction simply illustrates how altitude training only significantly impacts oxidative capacity in the untrained individual.

Changes in “combined levels for nuclear- and mitochondrial coded m-RNAs” (Vogt, Puntschart et al. 2001) were in parallel with changes in mitochondrial density. By looking at changes in the nuclear-coded mRNA and mitochondrial-coded m-RNA the authors were able to suggest the concept of “coordinated regulation of nuclear and mitochondrial gene expression” (Vogt, Puntschart et al. 2001).

Since nuclear and mitochondrial gene expression is synchronized via Nuclear Respiratory Factor 1 and 2 (NRF 1, and NRF 2) – and since the study data suggests that hypoxia has an impact on the adaptation of oxidative enzymes and mitochondria – the authors propose the hypothesis that hypoxia and exercise combine to influence NRF-1 and NRF-2. There is potential evidence for cross-communication between NRF-1/NRF-2 and hypoxia signal transduction pathways in the form of data showing that increases in mitochondrial subsarcolemmal fractions corresponded to increases in HIF-1A m-RNA. This trend was only seen when subjects trained under hypoxic conditions. An increase in subsarcolemmal fractions in mitochondria decreases the distance for intracellular oxygen transport. This can be interpreted as the reduction of a limiting factor for oxygen diffusion in tissue, thus training under hypoxic conditions can improve muscular oxygen consumption and performance (Vogt, Puntschart et al. 2001).

These HIF-1-mediated adaptations are beneficial in the context of training and athletic performance, and HIF-1 itself is increased in the study after training under hypoxic conditions over 6 weeks due to persistent adaptations. Hence this is evidence for the benefits of altitude (hypoxic conditions) on athletic performance.




Evidence against Altitude Training Being Beneficial to Human Performance:


The majority of this review has looked at both the haematological and non-haematological effects of altitude training, to determine how this form of training can benefit performance in athletes. This next section is going to look at the evidence against altitude training being beneficial to human performance.

There are many studies mentioned in this review which utilise altitude or simulated altitude to show the benefits of training under hypoxic conditions upon parameters of human performance such as increased VO2Max and aerobic power. These studies also show how performance itself, in the context of athlete time trials, can be increased in subjects who participated in altitude training compared to subjects who trained at sea-level. One of the types of simulated altitude training involves intermittent hypoxic exposure (IHE) which consists of exposing subjects to severe hypobaric hypoxia (~4,500-5,500 m) at rest for 1.5-5 hours a day for 2 to 3 weeks (Rodriguez, Truijens et al. 2007). Essentially IHE is based on short-term hypoxia coupled with training at sea level to induce a response beneficial to performance. Several studies have shown that IHE produces improved aerobic performance capacity and a significant increase in maximal exercise time (Rodriguez, Casas et al. 1999).

The issue with the vast majority of these studies is their inability to include a true placebo/control group to compare with the altitude group. This issue is raised in a study (Rodriguez, Truijens et al. 2007) which was the first randomized, double-blind placebo-controlled research placing athletes under prolonged periods of IHE. The study involved 28 athletes with 13 runners and 15 swimmers. These 28 athletes consisted of 17 men and 11 women, and people who had lived at altitude of above 1,000 m in the previous 6 months were excluded from participating in the study. A randomized, double-blind, placebo-controlled trial was carried out with subjects being exposed to either IHE or a placebo in a hypobaric chamber for 3 hours a day, 5 days a week for a period of 4 weeks. Subjects were matched by sport, sex, time-trial performance, and training history and allocated randomly into a treatment group (hypobaric hypoxia) or placebo group (normoxia). Within each matched pair there was a 50% chance of being placed in either the treatment or control group. Subjects were matched carefully, with matched pairs mostly being members of the same team to minimize training program differences between the groups.

The hypoxia group was exposed to barometric pressures which represented simulated altitude of 4,000-5,500 m, with the level of simulated altitude increasing over the 4 week period to reach 5,500 m towards the end. The normoxia (control group) were subjected to ten minutes of several pressure changes followed by exposure to 500 m altitude. The initial pressure changes in the control group were designed to “provide sufficient pressure changes in the sinuses and tympanic membranes” (Rodriguez, Truijens et al. 2007) so that subjects would not be aware of the final resting pressure. This meant that only the chamber technicians knew which treatment each group was assigned to, with every subject and investigator being blinded until the end of the experiment. This double-blinding was implemented to prevent results being skewed by subjects in the control group not trying as hard in their performance tests due to a pre-conceived idea of altitude training being more beneficial than sea-level training.

The results showed no improvement in performance as well as a lack of a “robust altitude acclimatization effect” (Rodriguez, Truijens et al. 2007). Results from time trials showed no significant change in performance in the hypoxia group compared to the normoxia group. There was not any change in absolute VO2Max resulting directly from the intervention, and the authors did not find any direct effect of IHE on submaximal economy or markers of accelerated erythropoiesis. This is evidence against altitude training being beneficial to human performance.

I wanted to find out why this data contradicts some of the other research that has already been discussed. When looking specifically at the effects of the IHE form of altitude training there are many studies which show that it can be beneficial to performance. One of these pieces of research reported that compared to baseline, subjects exposed to intermittent hypoxic training for 3 weeks exhibited a 2.3% improvement in 3 km time trial performance. Performance of subjects in the control or placebo group improved by only 0.6% (Hamlin, Hellemans 2007). However the results from the study by Rodriguez, Truijens et al. clearly go against these findings, and the authors suggest that this was due to the dose of hypoxia used being “insufficient to have a synergistic effect on performance over sea level training” (Rodriguez, Truijens et al. 2007).

The authors go on to mention several potential factors behind this failure to induce benefits in performance. The first is the fact that the daily duration of hypoxia was limited and the 2 days without hypoxic exposure each week may have negated or diminished the acclimatization effects of hypoxia. Evidence supporting the relevance of duration of hypoxic exposure includes research surrounding HIF-1A. A study showed that upon re-oxygenation after a hypoxic exposure HIF-1 DNA binding is lost rapidly and there is degradation of HIF-1A proteins (Jewell, Kvietikova et al. 2001). This shows how perhaps the design of the study allowed degradation of HIF-1A to the point where it was unable to mediate improvements in performance in response to hypoxic exposure.

The second limitation of the study proposed as a reason for the lack of performance benefit from

IHE is that the performance measurements were not sensitive enough to measure a significant change in performance levels. According to a study, the smallest worthwhile improvement in performance of an athlete at an international event is “0.7-0.4% of the typical within-athlete random variation” (Hopkins, Hawley et al. 1999). The authors concede that the investigation was not sufficiently developed to detect such a small difference.

Another issue with this study is that at the time publication it was the longest study to date to deliver that level of severe and sustained hypobaric hypoxia, with the study lasting 4 weeks. Therefore it is possible that the level of altitude intensity delivered may have had some detrimental side effects on subjects such as reduced recovery, impaired sleep and poor appetite. This may have contributed to the lack of improvement in performance seen in response to IHE. However it has been proposed that the minimum time needed to achieve acclimatization effects is 12 hours exposure per day to an altitude of at least 2,000 m, for at least 3 weeks (Rusko, Tikkanen et al. 2004). This means that a study with a shorter time frame may well have had a reduced number of negative side effects, but it would also have “limited the overall acclimatization response” (Rodriguez, Truijens et al. 2007).

The authors also point out the fact that the study may not have achieved complete blinding of subjects. At the end of the study 91% of subjects were able to guess correctly whether they were in the hypoxia or normoxia group, which may have reduced motivation of subjects in the control normoxia group during performance tests. However, this negative impact on the normoxia participants should only have enhanced any gap with the hypoxia group, making it even more striking that there was in fact no significant difference in performance between the two groups.

To conclude, these factors and limitations I have mentioned may have been the reason behind a lack of improved performance in response to intermittent hypoxic exposure. I propose that a better designed double-blind placebo led randomized trail needs to be conducted to see whether there really is no benefit of IHE when subjects are double-blinded. Personally I believe that altitude training is beneficial to athletic performance, it appears this study was just flawed in some of its design.



This review has discussed the benefits of altitude training in the context of athletic performance. It began by introducing the topic of altitude training and some of the physiological changes it evokes, as well as exploring how these changes can be beneficial in sport. The review then goes on to split the benefits of altitude training into haematological and metabolic changes.

The haematological changes centre on increased RBC mass and increased levels of Haemoglobin. These changes increase the oxygen carrying capacity of the individual, leading to better athletic performance. Training under hypoxia also has the ability to upregulate levels of Hypoxia Inducible Factor 1, which has several effects including the stimulation of an increase in haematocrit and increases in Myoglobin and VEGF. Once again these changes are beneficial to athletic performance.

Metabolic changes induced by training at altitude include improvements in muscle buffering capacity and exercise efficiency. There is also the concept of a reduction in dependence on fat as a fuel, as well as HIF-1-mediated increases in oxidative enzymes and hence increases in oxidative capacity.

It is clear that there is evidence for the benefits of altitude training being mediated by both haematological and metabolic changes. However seeing as there is greater evidence surrounding haematological changes, it appears that this is the primary mechanism by which altitude training can improve human performance.

For completeness there is an evaluation of the evidence against the benefits of altitude training, with the conclusion being made that such studies may contain flaws in their design which prevented subjects from benefits from the effects of training at altitude. In summary altitude training is a useful tool which can be used by athletes, with its clear benefits to performance being mediated primarily by haematological but also metabolic effects.



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