A 5000 m untrained individuals, natives at sea level, maintain about 70% of VO2 max measured in control conditions, native individuals at sea level, but not well-trained athletes develop only 55% of their VO2 max measured at sea level. In contrast, athletes who specialize in long term courses in high altitude natives usually at altitudes between 1500 and 3000 m, retain a higher percentage (76%). Surprisingly, Second-generation Tibetan born and brought up to 1300 m, 5000 m inclined to retain the highest percentage (85-90%), among all groups studied so far, their VO2 max. The latter subject, brought for the first time at 5000 m, shows other interesting features, some also found in Tibetans born and living permanently at about 4000 m. In general they are characterized by lower hemoglobin concentrations (g ~ 12%) than in Caucasians (~ 15 g%). At the peak of a comprehensive exercise, then they are characterized by high values \u200b\u200bof maximum heart rate (~ 180 beats per minute) (in Caucasians, the maximum heart rate is drastically reduced to 5000 m, up to 150-160 beats per minute) e di saturazione arteriosa in O2 (%SaO2 ~80%) (i Caucasici desaturano considerevolmente, da ~95% a 70-75%). Tutte queste osservazioni inducono a ritenere che Tibetani nati a bassa quota abbiano mantenuto alcune delle caratteristiche salienti dei loro antenati, favorevoli alla vita in condizioni di ipossia cronica. 
I muscoli scheletrici di alpinisti Caucasici nativi a livello del mare acclimatati all’alta quota o esposti ripetutamente a gradi estremi di ipossia, nativi e residenti in alta quota, e giovani tibetani nati e vissuti a Kathmandu (1300 m) ma appartenenti a una popolazione esposta per migliaia anni a quote comprese tra 3000 e 4000 m sono tutti caratterizzati da una densità volumetrica mitocondriale significativamente lower than normally found in people native and resident at sea level. Since the mitochondrion is the organelle where intracellular redox reactions take place in the cellular respiratory chain, and where the O2 is "consumed" by acting as a terminal acceptor of electrons transported along the chain, we can assume a role of O2 same as a regulator of mitochondrial biogenesis.
The chronic shortage of O2, ie, could lead to a reduction of gene expression for enzymes and proteins responsible for oxidative phosphorylation. The Tibetan population has become such a reduction could be an acquired trait.
Hypoxia induces a chronic remodeling phenotype of the organism, which is the source of long-term adaptive responses. The molecular mechanisms underlying the adaptations to chronic hypoxia are poorly known. In each case the activation of specific genes is considered a mechanism by which hypoxia triggers long-term adaptive responses. In general, the genes activated by hypoxia fall into two categories: genes that are "induced" within minutes of exposure to hypoxia ("immediate early genes, IEGs) and genes activated more slowly, including the best known are the genes for erythropoietin (EPO), the endothelial growth factor vascolare (VEGF) ed il trasportatore 1 del glucosio (GLUT 1).
Studiando il sistema respiratorio, un gruppo di ricercatori dell'Università del Wisconsin di Madison ha identificato una proteina chiave, chiamata BDNF (fattore neurotrofico di derivazione cerebrale), e coinvolta nell'apprendimento, responsabile della capacità del corpo di mantenere una respirazione appropriata anche in condizioni difficili. La scoperta, pubblicata il 14 dicembre sulla rivista online "Nature Neuroscience", potrebbe fornire spunti per l'ideazione di nuovi farmaci, cure o metodi per prevenire disturbi potenzialmente letali come l'apnea del sonno, la sindrome della morte improvvisa del neonato e alcune lesioni legate al midollo spinale. Ogni pochi secondi, inhale and then release a breath of fresh air. If for any reason this procedure was prevented, for example, if oxygen levels are too low or if the airways were blocked, our bodies respond accordingly. In the case of oxygen deprivation, neurons in the brain cells send messages to the motor, ordering the muscles involved in breathing to work harder.
As a result, the person would be deeper breaths. If the fault is experienced on a regular breathing, the respiratory system remembers this and will respond more vigorously in the future. This change of behavior is called by scientists "plasticity Neural. In some cases, however, the respiratory system seems unable to remember past experiences. Gordon Mitchell, principal author of the study, says that patients who suffer from sleep apnea - a disorder in which breathing stops while you sleep - may have "memory" of inadequate breathing. To study the mechanism, the researchers exposed mice at intervals of three to five minutes of hypoxia, or a decrease of oxygen. By measuring the activity later in the phrenic nerve associated breathing, have found that the nerve had developed a memory of the lack of oxygen. To find out what caused this memory, the scientists analyzed segments of the spinal cord, the ricerca specifica di cambiamenti della proteina BDNF (fattore neurotrofico di derivazione cerebrale), che sostiene e addirittura stimola alcune funzioni neurali nel cervello. I risultati dimostrano che i periodi intermittenti di calo di ossigeno aumentano del 56% le concentrazioni di proteina BDNF nel nervo frenico. 
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