INTERMITTENT HYPOXIC TRAINING
DR JOHN HELLEMANS FRNZCGP, Sports Medicine Practitioner/Coach
Dr MIKE HAMLIN, Sports Scientist
Introduction
Altitude training was first introduced into the western world on a larger scale following the Mexico Olympics (1964). At the time it was noticed that endurance athletes suffered when competing in the Games and they were unable to get close to their best times. Athletes who had acclimatized prior to the games fared much better. More significantly when returning to sea-level to compete following the games, many personal best times and world records were set. For a long time however scientist found little evidence of benefits from altitude training despite significant perceived benefits experienced by athletes and coaches.
There are different expectations around altitude training, between the coach/athlete and the scientist. For the coach and athlete the proof in the experience is enough, while scientists are not satisfied until benefits are proven, double blind and without doubt. Scientists are still arguing the benefits of conventional altitude training (live high/train high). The high/low model has been given the thumbs up by athletes, coaches and scientists, while the benefits of altitude simulation are still hotly debated. Coaches and athletes all over the world continue to experiment with the different methods of altitude exposure.
In the mid 1990’s altitude training became an official part of the New Zealand Triathlon High Performance Programme. Initial live high/train high camps in Northern America and Europe were followed by live high/train low camps, mainly in Northern America. In recent years an altitude training facility has been discovered in the South Island of New Zealand, which is now used regularly by triathletes. The facility (www.snowfarm.nz.com) lends itself to the live high/train low model as well as to the live high/train high and train low model. Altitude simulators can be used in addition to artificially increase hypoxic intensity.
Conventional Altitude Training (Live High/Train High)
It is the authors experience that 1500m-2000m is the optimum altitude for conventional altitude training. More experienced athletes can live (and train) higher. Less side effects are experienced at the recommended level of 1500m-2000m and the quality of training can generally be maintained. There is extensive evidence in the literature regarding the structural and haematological adaptations of conventional high altitude training (live high-train low) as illustrated in fig. 1.
(fig. 1)Adaptations to Hypoxia
|
Structural |
Haematological |
|
â Muscle fibre size |
á EPO |
|
á Capillary density |
á Haemoglobin |
|
á Mitochondrial density |
á Haematocrit |
|
á Myoglobin stores |
á 2,3-DPG |
|
á Oxidative enzymes |
It is also well documented that training velocity, in particular at the higher intensity scale, generally decreases at altitude. This applies particularly to running and swimming. In view of the diminished air resistance the velocity of biking on flat terrain actually increases. For the disciplines of swimming and running athletes are generally able to maintain their sea level high intensity (anaerobic) pace up to 2-3 minutes. Shortening high intensity intervals to within 2-3 minutes is therefore one way of maintaining some race-pace intensity when training at altitude. In the first few days in particular many athletes experience one or more side effects from high altitude exposure (fig. 2.)
(fig. 2)Side Effects of Altitude
Most athletes need to decrease their training frequency and duration somewhat and their training intensity significantly, especially in the first week of altitude exposure.
Living High/Training Low
Benjamin Levine and James Stray-Gunderson presented evidence in the late 1990’s regarding the benefits of living high (optimal physiological adaptation) and training low (optimal training adaptations). They compared 3 groups of athletes. One group lived low and train low, another lived high and train high and the third lived high and trained low. Their observations are summarised in Fig 3.
(fig. 3)High/Low Study
Levine, Stray, Gunderson
|
High - High |
High - Low |
Low-Low |
|
|
VO2 max |
á |
á |
ß à |
|
Red cells |
á |
á |
ß à |
|
Velocity at VO2max |
â |
á |
ß à |
|
Velocity at Maximal Steady State |
â |
á |
ß à |
|
5 km time trial |
â á |
á |
ß à |
Responders versus Non-Responders
The same authors made the following observations regarding Non Responders (fig4)
(fig. 4)Observations Non-Responders
Chapman, Stray-Gunderson, Levine 1998
Individual variations in response to different forms of altitude training have resulted in a recommendation where altitude training might need to be based on an individual prescription basis as indicated in Fig 5.
(fig. 5)Individual Prescriptions
1. Live High - Train High
2. Live High - Train Low
3. Live Low - Train Low
4. Live Very High - Train High
5. Live Semi-High - Train Sea Level
6. Live Low - Train High
Altitude Simulation
The different forms of altitude simulation are summarised in Fig 6.
(fig. 6)Altitude Simulation
Intermittent Hypoxic Training
Intermittent Hypoxic Training is intermittent exposure to hypoxic (9-15%) and normoxic air for 1-2 hours per day for 2-3 weeks, while being sedentary. Because of the intermittent nature of the exposure, high levels of altitude, resulting in a significant drop of oxygen saturation in the blood, can be achieved. Machines that provide intermittent hypoxic training are called Hypoxicators. Generally they provide air containing 9-15% of oxygen which is comparable to an altitude of 6,600m-2,700m. Recently a hand-held device call an Alti-power has been launched. This "rebreathing" model is suitable for home use and can be carried around easily when travelling. Individual protocols are based on a 10-minute hypoxic test that is usually done with a 10-minute exposure to 11-13% of oxygen. Oxygen saturation is measured by pulse oxymetry during the test and based on the result an individual protocol is prescribed for the user. Fig. 7 summarises the protocols for the 3 main groups of users of intermittent hypoxic training; athletes, patients and mountaineers.
(fig. 7)
|
PaSO2 |
Week 1 |
Week 2 |
Week 3 |
|
Athletes |
88-92% |
84-88% |
80-84% |
|
Patients |
92-96% |
88-92% |
84-88% |
|
Mountaineers |
84-88% |
80-84% |
76-80% |
PaSO2 is arterial oxygen saturation as measured by pulse oximetry
Adaptations to intermittent hypoxia relate to:
The oxygen carrying and processing mechanisms of the body are improved by an increase in EPO, reticulocytes, haemoglobin, haematocrit, 2, 3/DPG, microcirculation, myoglobin, mitochondria and oxidative enzymes. Few studies have shown an increase in EPO, except when measured during the time of hypoxic exposure;(Lyopov, Hypoxic Medical Journal 1993) and due to the short half-life of erythropoetin (5-7 hours) no significant increases might be detected outside the time of hypoxic exposure.
As far as the respiratory response is concerned, animal studies show an increase in alveolar surface, diffusion capacity of the alveolar capillaries, and an increase in the capillary bed, the vital capacity and ventilation.
The neuro-endocrine response shows an increased tolerance to stress. This is due to an increase in beta-endorphins and serotonin centrally, as well as a decrease in norepinephrine, centrally. Peripherally there is an increase in beta-endorphins, prostaglandins and prostacyclin and a decrease in catecholamines. The metabolic adaptation shows an increase in cytochrome p 450, 7 alpha cholesterol hydroxylase, an increase in the metabolic rate and buffering capacity. An increase in insulin sensitivity has also been well documented. The immune system generally shows a positive response by an increase in beta lymphocyte activation, antibody formation, interferon tumor necrosis factor and antioxidant enzymes. There is a decrease in T lymphocyte activation and stress induced depression of killer cells.
Of special note is the cardio protective effect of intermittent hypoxic training including a decrease in LDL cholesterol, total cholesterol, body weight, dependence on cigarette smoking (central effect), blood pressure, a diminished risk of arrhythmia and also a reduction in cardiac oxygen consumption. The changes in the immune system results in the lowering of immune complexes and therefore a significant reduction in allergic reactions.
In view of the general physiological and metabolic adaptations, intermittent hypoxic training can be used as an adjunct therapy in the medical field, for chronic conditions including chronic fatigue, stress, depression, cardio-vascular disease, hypertension, elevated cholesterol levels, allergies, dermatitis, asthma, gastro-intestinal disorders, gynaecological disorders and hormonal disorders. The main differences between chronic hypoxic exposure and intermittent hypoxic exposure are summarised in Fig 8.
(fig. 8)Hypoxic Exposure
|
Continuous |
Intermittent |
|
Stress |
Minimal stress |
|
Fixed dose |
Dose control |
|
Disadaption syndrome |
No disadaption syndrome |
|
Reduced anti-oxidant activity |
Increased anti-oxidant activity |
|
Stronger response genetic transcription factor (HIF-1) |
Contra-indications to intermittent hypoxic training include acute illness, grade 2 and 3, chronic obstructive airways disease, multiple sclerosis and terminal illness.
Results of a study on 3 weeks of intermittent hypoxic training by the first author completed in 1998 on 10 elite athletes showed the following results in haematology and performance as measured by time trials (fig 9)
(fig. 9) results IHT study 1998
Haemoglobin Increase by 4.4% ± 2.1% (PC 0.05)
Hematocrit Increase by 4.8% ± 1.3% (PC 0.05)
Reticulocytes Increase by 28.7% ± 19.2% (PC 0.05)
Performance Improvement 3.1% ± 1.7% (PC 0.05)
No control group was included in the 1998 study
A recently held double blind study on 22 multi-sport endurance athletes by the authors again investigated effects of intermittent hypoxic training (IHT) on 3km time trial performance and haematological factors. Both groups breathed through hand held facemasks for a total of 90 minutes per day, on an average of
5 days per week, for 3 weeks. Subjects received either normobaric hypoxic gas or normo-ambient air via a Go2 Altitude hypoxicator device. The protocol consisted of 13% oxygen in Day 1 and 2, 12% in Day 3-5, 11% Week 2 and 10% Week 3. In the placebo group hypoxic air was substituted with ambient air. Individual 3km time trials were completed on a 400m synthetic outdoor running track under controlled conditions.
The IHT group showed an improvement of 2.3% in their 3km time following IHT exposures, while the placebo group did not improve. The chances that the true difference is substantial, is very likely. The results are summarised in Fig 10.
|
Fig 10. Mean changes in 3-km performance at 2 and 17 days post IHT and placebo exposures, and the chances that the true difference in the changes is substantial. |
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|
Change in performance (%) |
Chance that the true difference is substantiala |
|||||||||||||
|
IHT |
Placebo |
Difference ± 95% CL |
P |
% |
Qualitative |
|||||||||
|
2-d post |
-2.3 |
-0.6 |
-1.7 ± 2.3 |
.14 |
85 |
Likely |
||||||||
|
17-d post |
-2.2 |
0.1 |
-2.3 ± 2.1 |
.03 |
96 |
Very likely |
||||||||
|
aSubstantial is an improvement in performance of > 0.5%. P: p value. ± 95% CL: add and subtract this number to the mean effect to obtain the 95% confidence limits for the true difference. |
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|
The results of haematology testing were as follows (fig 11) |
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Fig 11. Mean changes in blood parameters 2 and 12 days post IHT and placebo exposures, and the chances that the true difference in the changes is substantial. |
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|
Days post-exposure |
Change in measure (%) |
Chance that the true difference is substantiala |
||||||||||||
|
IHT |
Placebo |
Difference ± 95% CL |
P |
% |
Qualitative |
|||||||||
|
Hemoglobin (%) |
2 |
-0.9 |
-1.1 |
0.2 ± 3.2 |
.90 |
23 |
Unlikely |
|||||||
|
12 |
-0.7 |
-3.2 |
2.5 ± 4.2 |
.23 |
70 |
Possible |
||||||||
|
Hematocrit (%) |
2 |
-0.8 |
-2.3 |
1.5 ± 3.1 |
.44 |
78 |
Likely |
|||||||
|
12 |
-0.6 |
-4.2 |
3.6 ± 4.1 |
.08 |
96 |
Very likely |
||||||||
|
Mean Cell Volume |
2 |
-0.3 |
0.1 |
-0.4 ± 0.8 |
.31 |
1 |
Almost certainly not |
|||||||
|
(%) |
12 |
-0.5 |
-0.4 |
-0.1 ± 0.9 |
.83 |
6 |
Unlikely |
|||||||
|
Mean Cell |
2 |
0.1 |
0.6 |
-0.5 ± 1.1 |
.37 |
2 |
Very unlikely |
|||||||
|
Hemoglobin (%) |
12 |
-0.8 |
0.7 |
-1.5 ± 1.4 |
.04 |
1 |
Almost certainly not |
|||||||
|
Reticulocytes (%) |
2 |
4.2 |
-19.3 |
23.5 ± 21.1 |
.03 |
97 |
Very likely |
|||||||
|
12 |
10.7 |
-3.9 |
14.6 ± 21.7 |
.18 |
87 |
Likely |
||||||||
|
White Cells (%) |
2 |
-6.5 |
-9.5 |
3.0 ± 15.9 |
.70 |
64 |
Possible |
|||||||
|
12 |
-1.6 |
-19.2 |
17.6 ± 16.8 |
.04 |
98 |
Very likely |
||||||||
|
Serum Iron (%) |
2 |
-23.5 |
22.3 |
-45.8 ± 38.2 |
.02 |
98 |
Very likely |
|||||||
|
12 |
-61.9 |
18.5 |
-80.4 ± 41.8 |
.01 |
99 |
Almost certain |
||||||||
|
Ferritin (%) |
2 |
-6.7 |
10.2 |
-16.9 ± 19.7 |
.09 |
67 |
Possible |
|||||||
|
12 |
-14.4 |
-4.5 |
-9.9 ± 21.2 |
.35 |
40 |
Possible |
||||||||
|
aChances for a substantial change in blood parameters, where substantial is 0.2 of the baseline between-subject standard deviation for each measure. ± 95% CL: add and subtract this number to the mean effect to obtain the 95% confidence limits for the true difference. |
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