Altitude Training | Hypoxic Training

To find the path to long life and health, Dan Buettner and team study the world’s “Blue Zones,” communities whose elders live with vim and vigor to record-setting age. Common diet and lifestyle habits that keep them spry past age 100.

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About 30 years ago, a neurodevelopmental model of mental disorders was proposed. It has now been widely accepted and developed. This model suggests that abnormalities in brain development during pre- and perinatal life lead to psychotic manifestation in adolescence or young adulthood. Evidence points to the negative role of hypoxia in early life, but the role of hypoxia in some risk factors is not clear. The use of hypoxia for the treatment and prevention is also still poorly covered in the literature. The aim of this review is to integrate current knowledge about the role of hypoxia in the mental disorders neurodevelopment, in their treatment and prevention, and in increasing mental capacity. Data are cited about the important role of hypoxia in almost any risk factor: pre-eclampsia, infection/inflammation, hypoxia/ischemia, preterm birth, asphyxia at birth, and in stimulation of neurogenesis. The changes in the brain stimulated by excessive, pathologic neurogenesis may lead to abnormal communications in the neural network, causing abnormal associations, ideas, and acts, i.e. mental disorder. Data are provided about the use of hypoxic hypoxia for mental disorder therapy: high mountains, hypobaric chamber, and normobaric Interrupted Hypoxic Training. Using hypoxia showed positive results both in animal experiments and in the clinic. The surprising coincidence of the effects of some psychotropic medications and hypoxia suggests that the active principle of psychotropic medications may be hypoxia. Data are cited that corroborate the possible connection between genius and mental malfunctions. Animal model data show that the influence of a moderate, but not excessive, hypoxia results in a moderate increase in neurogenesis, leading to increased mental capacity.

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Despite the great progress of psychiatry, many of its fundamental problems remain unresolved. Obviously, new ideas that expand the present understanding of such problems are useful. In this paper, the following hypothesis is proposed: mental disorders are caused by hypoxic phenomena, stimulating hypertrophied growth of a neural network; treatment should be directed towards the damaging of abnormal elements of this network; successful treatment is inevitably accompanied by moderate retrograde amnesia. Based on this hypothesis, the connection between etiology, pathogenesis, and therapy of mental disorders is described, the role of retrograde amnesia is shown, and potential new methods of treatment (shaking, vibration, and ultrasound) are predicted. To test the hypothesis, some means are discussed. The first means is based on the analysis of the reasons of unsuccessful clinical trials of the method of mental disorders treatment by acute hypoxic hypoxia (USA, 1938 - 1940). Such a method, according to the hypothesis, should damage the abnormal elements of a neural network as a result of acute hypoxia. Analysis of the equipment and procedure shows that the trials were unsuccessful as a result of insufficiently powerful hypoxic influence. Improvements to this method are proposed. When using this method, it is advisable to measure the cerebral blood oxygenation index and reduce it by regulating the oxygen concentration in the hypoxic gas mixture given to the patient. This reduction should continue until the patient reaches a state of moderate retrograde amnesia. It is also advisable to note the blood oxygenation index value at the moment when the patient lapses into unconsciousness, and then, on the basis of this value, estimate a necessary power (i.e., acuteness and duration) of hypoxic hypoxia. Other means for testing the hypothesis are also discussed: retrospective analysis of the results of electroconvulsive therapy, and testing the predicted methods of treatment.

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Looking for a new weight loss plan? Try living on top of a mountain. Twenty obese men spent a week near the top of Germany’s highest peak and saw their metabolism speed up, their appetite diminish, and more pounds melt off than they likely would have had they stayed at home, a new study reports. However, the study lacked a control group, so firm conclusions are tough to draw, other researchers say.

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In a comprehensive review on training, Midgley and McNaughton’s first sentence state’s “The maximal oxygen uptake (VO2max) has been suggested to be the single most important physiological capacity in determining endurance running performance” (2006). Based on this notion, training for distance runners has become fixated on the concept of VO2max. Training to enhance VO2max is the subject of numerous review articles and popular coaching material. A whole theory of training has evolved based on the idea of training at the speed that corresponds with VO2max, and at certain percentages of VO2max (Daniels, 2005). Given the emphasis on this particular parameter one would assume that it must be very closely tied with performance and fatigue. It’s not.
In the following paper the limitations of VO2max will be discussed. Including the legitimacy of the variable itself, why it arose to such prominence, the efficacy of basing training paces off of it, should we even train to improve it, and how closely it ties to performance.

How the VO2max concept developed:
The ability to measure oxygen consumption first arose in the early 1920’s. It was in 1923, when A.V. Hill and his partner H. Lupton came up with the idea there being an upper limit on oxygen consumption. In an experiment which consisted of Hill running at various speeds around a grass track while measuring VO2, it was found that Hill reached a VO2max of 4.080 L/min at a speed 243m/min (Bassett, 2000). Despite increases in speed, his VO2 did not increase, leading Hill to conclude that there is a maximum limit to oxygen consumption, or in his words:
“In running the oxygen requirement increases continuously as the speed increases attaining enormous values at the highest speeds: the actual oxygen intake, however, reaches a maximum beyond which no effort can drive it… The oxygen intake may attain its maximum and remain constant merely because it cannot go any higher owing to the limitations of the circulatory and respiratory system” (Noakes, 2008, pg. 575).

These findings led to two lasting conclusions. First, that VO2max is limited by the circulatory and respiratory system. The second conclusion was the result of trying to device a laboratory test for determining VO2max, in which thirty years later, Taylor et al. decided that during a graded exercise test, a VO2max was obtained when a plateau occurred in VO2 (Noakes, 2008). However, in Taylor’s original definition, a plateau was not a true plateau but it rather consisted of a VO2 increase of less than 150ml/min from one workload to the next. These findings led to the idea that in order for a true VO2max to be reached, a plateau of the VO2 should occur.

FULL ARTICLE:
http://stevemagness.blogspot.com/2009/12/fallacy-of-vo2max-and-vo2max.html