Source: Annual Congress 2010 - Exercise training: new groups, new methods and outcomes
Disease area: Airway diseases

Abstract

It is known that IHT is effective stimulus for evoking the respiratory, cardiovascular, and metabolic adaptations. It augments exercise tolerance by enhancing stress resistance and improving oxygen delivery. In patients with COPD IHT increases FCV, ERV, improves mucociliary clearance of sputum. But changes in non-specific immune resistance of organism during IHT treatment is vague. To elucidate this point we investigated immunological responses to IHT in 10 healthy subjects 25-35 years old. IHT was administered for 5 min of hypoxia (12% O₂), 4 times per day with 5-min periods of room air inspiration during two weeks. Phagocyting function and bactericide activity of neutrophils, IgM, IgG, IgA, circulating immune complexes (CIC) were determined by routine methods before and after IHT. It was shown that IHT doesn‘t affect number of various types of leucocytes in healthy subjects, CD4⁺, CD8⁺ T-lymphocytes, basic classes of immunoglobulins and CIC. As a result of IHT, the enhancement of natural resistance system occurs, including complement activation (by 82%), the increase in phagocytic capacity of neutrophils (by 15%) with a decrease in their spontaneous (by 40%) and increase in reserve (by 69%) bactericidity. Most parameters sensitive to intermittent hypoxia manifest their major modifications in one week after the course of training. Thus, humoral and cellular factors of non-specific resistance are sensitive to such regime of IHT. Their activity increases significantly. It leads to enhancement of natural protection of organism.Conclusion: Taking into account the known bronchodilatory action of IHT and detected now immunomodulatory effects of IHT, this therapy can be advisable for treatment of COPD.

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Citations should be made in the following way:
T. Serebrovska, V. Ishchuk, I. Nikolsky (Kyiv, Ukraine). Prospects of intermittant hypoxia training (IHT) implementation in treatment of COPD. Eur Respir J 2010; 36: Suppl. 54, 4871

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