Being essentially cut off from the global scientific community, Ukrainian and Russian scientists have developed a new concept for the beneficial use of adaptation to artificial intermittent hypoxia in treating of many diseases. The basic mechanisms underlying intermittent hypoxic training were elaborated mainly in three areas: regulation of respiration, free radical production and mitochondrial respiration. Twenty-year experience of the application of intermittent hypoxic therapy for the treatment of chronic obstructive bronchitis and bronchial asthma allows affirming that the adaptation to this kind of hypoxia causes a significant improvement of the clinical picture or even a complete recovery. The absence of negative side effects, typically observed during drug therapy, and the stimulation of organism’s general, nonspecific resistance, makes the hypoxic therapy a treatment with a future. A special note is devoted to the use of intermittent hypoxic training in industrial health care for the purpose of prophylaxis and treatment of professional diseases.
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Aging is associated with changes in breathing regulation, particularly, in respiratory sensitivity to hypoxic stimuli. One theory of aging holds that reactive oxygen species play a key role in this process. These species have also been implicated in the carotid body O2 sensing. In the present study we investigated hypoxic ventilatory responses (HVR) and antioxidant enzymes activity in healthy young and elderly people under a 14-day adaptation to intermittent hypoxic training (IHT). The elderly demonstrated decreased HVR and blood catalase (CAT) activity on a background of strong negative correlation between the levels of end-tidal CO2 tension and superoxide dismutase (SOD) activity. The adaptation to IHT resulted in increased HVR and SOD activity in both groups, and decreased CAT activity in young persons compared with its augmentation in the elderly. Increased SOD activity testifies to an overproduction of reactive oxygen species during IHT. We hypothesize that reactive oxygen species might potentiate a periodical augmentation of cytosolic Ca2+ in the carotid body. This, in turn, might determine an increase in tyrosine hydroxylase gene expression and promote neurotransmitter synthesis/release, resulting in enhanced HVR.
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