Altitude Training | Hypoxic Training

Authors:

http://www.researchgate.net/publication/8097717_Effects_of_hypoxic_interval_training_on_cycling_performance

Oct 06,2010 - Dubai, UAE – 6 October, 2010: For decades, spending time in high altitude conditions has been the most successful natural method to effectively enhance oxygen absorption, transport and utilisation by the body. With the prevalence of type 2 diabetes mellitus and metabolic syndrome one of the highest in the world, discoveries in molecular medicine showing the enormous potential in targeted usage of high altitude climate conditions allows for new strategies for therapy and prevention of the disease in the UAE.

According the Dr Richard Reyes, founder and medical director of the Reyes Longevity Programme, there is a well defined sequence of molecular events which result in the correction of the components of the metabolic syndrome; high cholesterol and triglycerides, high blood pressure, low HDL, type 2 diabetes and insulin resistance.

“The main difference in high altitudes compared to sea level conditions is the decreasing air pressure with increasing height,” says Dr Reyes. “As the air gets ‘thinner’ and the body absorbs less oxygen, the heart rate and breathing increases. The low oxygen saturation in the blood, also known as hypoxia, causes a chain of positive biological adaptations. An increase in red blood cell production, better utilisation of nutrients in muscles and tissues, increased economy of the cardiovascular system and the optimisation of the heart rate at rest are only a few examples of how high altitude conditions can work towards correcting the components of the metabolic syndrome.”

Dr Reyes will be speaking at the 3rd International Congress in Aesthetic, Anti-Aging Medicine & Medical Spa Middle East (ICAAM), which will be held at the Al Bustan Rotana Hotel, Dubai, UAE from 26 to 27 November 2010. Leading experts in aesthetics and anti-aging medicine will be on site to demonstrate latest techniques and showcase latest anti-aging research such as the use of high-altitude climate to correct the metabolic syndrome.

“Changes in response to high altitude can be seen after just one or two hours of training exposure per week,” says Dr Reyes. “Correcting the disrupted metabolic process can go a long way towards slowing down the aging process. Cellular aging is understood in part to be due to the accumulation of the effects of oxidative stress and free radical formation. Exposure to altitude counteracts both of these – it is well recognised that people who live in the mountains have longer lives than those at sea level.”

http://bignews.biz/?id=925256

Medicine and science in sports and exercise. 01/09/2006;

http://www.researchgate.net/publication/6899290_Leukocyte%27s_Hif-1_expression_and_training-induced_erythropoietic_response_in_swimmers

By: Mona Brown

October 1, 2010

In recent months FAA Administrator Babbitt has promoted specific tailored hypoxia training, along with high-altitude handling, for commercial and private pilots who want to fly at high altitude. Indeed, FAA Title 14 of the Code of Federal Regulations (14CFR) establishes mandatory requirements for high-altitude training using military altitude chambers at 15 U.S. locations, but few chambers are available for candidates in other countries and theoretical presentation is often the limit of studies. However, Biomedtech Australia at Moorabbin, Melbourne, has developed a range of hypoxicators under the trademarks of “go2altitude” and “Altipower” that can provide an acceptable alternative to training in the chamber.

In the last 30 years several accidents have highlighted the importance of hypoxia training. On Sept. 25, 1979, an instructor and student on type conversion were killed in the crash of Beech King Air 200 G-BGHR. Investigators blamed the accident on oxygen system failure. Two decades later, on Oct. 25, 1999, Learjet 35 N47BA crashed, killing the crew and four passengers, including golfer Payne Stewart. The accident was attributed to the airplane’s failure to pressurize. The Sept. 4, 2000, crash of Beech Super King Air 200 VH-SKC killed the pilot and seven passengers. Investigators attributed the accident to a pressurization failure. Finally, a Boeing 737 (5B-DBY) crashed Aug. 14, 2005, killing the crew and 115 passengers. Failure to pressurize was listed as the cause.

The Greek AAIASB report into the 737 accident includes a recommendation that “EASA/JAA should require practical hypoxia training as a mandatory part of flight crew and cabin crew training. This training should include the use of recently developed hypoxia training tools that reduce the amount of oxygen a trainee receives while wearing a mask and performing tasks.” The Biomedtech system was demonstrated to airline personnel at a CAA seminar as an option for hypoxia training.

Researchers were already studying hypoxia before World War I, but it was not until the mid-1930s that the Mayo Clinic investigated the effect of varying the oxygen proportion of air supplied to a pilot’s mask. Unfortunately, it was impossible to measure gas proportions accurately, and the results were inconclusive.

After the 1968 Olympics at Mexico City it became obvious that athletes who trained at high altitude had a significant advantage over those who had trained at lower levels, and Simon Bassovitch of Biomedtech Australia at Moorabbin, Melbourne, started to research the feasibility of providing a portable simulated high-altitude training environment for athletes.

The result was called “hy­­poxicators” and by 1992 Bassovitch specialized in the supply of these systems, which varied the ratio of oxygen to nitrogen to achieve a particular altitude. These hypoxicators–used by athletes worldwide–can help pilots recognize hypoxia without the use of an altitude chamber. Using membrane technology to vary the required oxygen/nitrogen mix, Biomedtech has eliminated the need for cumbersome gas cylinders. The examinee has to hold a breathing mask to his face, experiencing all symptoms of oxygen starvation while being asked to carry out various exercises. All test results are recorded automatically and copies are presented to the candidate in written or DVD form.

Since there is no requirement to have an altitude chamber, trainees need not meet the medical standards required to experience explosive decompression, providing greater flexility of operation.

The effects of concurrent hypoxic/endurance training on mitochondrial respiration in permeabilized fibers in trained athletes were investigated. Eighteen endurance athletes were divided into two training groups: normoxic (Nor, n = and hypoxic (H, n = 10). Three weeks (W1-W3) of endurance training (5 sessions of 1 h to 1 h and 30 min per week) were completed. All training sessions were performed under normoxic [160 Torr inspired Po(2) (Pi(O(2)))] or hypoxic conditions ( approximately 100 Torr Pi(O(2)), approximately 3,000 m) for Nor and H group, respectively, at the same relative intensity. Before and after the training period, an incremental test to exhaustion in normoxia was performed, muscle biopsy samples were taken from the vastus lateralis, and mitochondrial respiration in permeabilized fibers was measured. Peak power output (PPO) increased by 7.2% and 6.6% (P < 0.05) for Nor and H, respectively, whereas maximal O(2) uptake (Vo(2 max)) remained unchanged: 58.1 +/- 0.8 vs. 61.0 +/- 1.2 ml.kg(-1).min(-1) and 58.5 +/- 0.7 vs. 58.3 +/- 0.6 ml.kg(-1).min(-1) for Nor and H, respectively, between pretraining (W0) and posttraining (W4). Maximal ADP-stimulated mitochondrial respiration significantly increased for glutamate + malate (6.27 +/- 0.37 vs. 8.51 +/- 0.33 mumol O(2).min(-1).g dry weight(-1)) and significantly decreased for palmitate + malate (3.88 +/- 0.23 vs. 2.77 +/- 0.08 mumol O(2).min(-1).g dry weight(-1)) in the H group. In contrast, no significant differences were found for the Nor group. The findings demonstrate that 1) a 3-wk training period increased the PPO at sea level without any changes in Vo(2 max), and 2) a 3-wk hypoxic exercise training seems to alter the intrinsic properties of mitochondrial function, i.e., substrate preference.

Journal of applied physiology (Bethesda, Md. : 1985).

http://www.researchgate.net/publication/6803051_Effects_of_intermittent_hypoxic_training_on_amino_and_fatty_acid_oxidative_combustion_in_human_permeabilized_muscle_fibers

European journal of applied physiology. 01/11/2007;

http://www.researchgate.net/publication/6202789_Effects_of_intermittent_hypoxic_training_on_cycling_performance_in_well-trained_athletes

European journal of applied physiology. 01/11/2008;

http://www.researchgate.net/publication/23482667_Effect_of_intermittent_hypoxic_training_on_HIF_gene_expression_in_human_skeletal_muscle_and_leukocytes

European journal of applied physiology. 01/04/2009;

FULL ARTICLE

http://www.researchgate.net/researcher/38177302_Belle_Roels

2010 by Oleg Bassovitch

Recently published Letter to the Editor titled “Intermittent hypoxic training: risks versus benefits” (Hinghofer-Szalkay, 2010) suggested inquiring into the  long-term risks of Intermittent Hypoxic Training” (IHT), that is also called Therapeutic Hypoxia (TH). The letter points at potential risk of Reactive Oxygen Species (ROS) formation. From the biomedical point of view it is important to separate hazards associated with the use of a device / system and physiological risks and benefits of the therapy itself.

Undoubtfully, a device for human or animal treatments must be meeting essential requirements for medical devices e.g. electrical medical safety and electromagnetic compatibility (IEC 60601-1, 2007).

Devices and systems for hypoxia intervention are called “hypoxicators” and were recently suggested by Australian Therapeutic Goods Administration being mandatory regulated for all applications (TGA, 2008). Hypoxicator falls under the common definition of medical device because of it intended use e.g. “modification of physiological process” (Council Directive 93/42/EEC, 1993).

This letter is a brief review of physiological risks associated with the use of hypoxicators and IHT for human performance enhancement, in both athletic and sedentary populations.

ACCESS TO FULL ARTICLE

http://www.springerlink.com/content/4632×38184754513/