[Individual characteristics of human adaptation to intermittent hypoxia: possible role of genetic mechanisms]

Fiziol Zh (1994). 2007;53(2):16-24.
[Article in Ukrainian]

Abstract

The majority of the adaptation processes to hypoxia is based on transcriptional regulation by hypoxia-inducible factors--HIFs. Recently the allele polymorphism of oxygen-dependent degradation domain of HIF-lalpha has been described. It consists in the replacement of cytosine for thymine in 1772 location (C1772-->T). The physiological significance of such replacement is obscure. In the investigation of 26 healthy elderly subjects (58.5 +/- 0.7 yr) we tried to verify whether HIF-lalpha polymorphism in exon 12 may identify individual features of adaptation to intermittent hypoxia training (IHT) (isocapnic hypoxic rebreathing technique, 5-min sessions with 5 min rest intervals, 3 times daily during 10 days). The distribution of HIF-l alpha genotypes for C1772-->T were studied by using the polymerase chain reaction and restriction analysis. We detected that all subjects from the group had C/C genotype. Meanwhile, the broad spectrum of adaptive reactions to IHT was observed, from the best adaptation up to disadaptation. IHT enhanced HVRs in the range of 167% - 5%, blood malon dialdehyde content varied from a decrease by 46% up to an increase by 88%, the changes of superoxide dismutase activity varied from +64% to -56% etc. These results suggest that the C1772-->T polymorphism in HIF- 1alpha does not contribute to individual peculiarities of adaptation to IHT. Because the activity of HIF-lalpha is regulated by multiple steps including the transcriptional level, the effect of the polymorphism in enother exons on the adaptive reactions remains to be elucidated.

MeSH terms

  • Adaptation, Physiological / genetics*
  • DNA / genetics
  • Female
  • Genotype
  • Humans
  • Hypoxia / genetics
  • Hypoxia / physiopathology*
  • Hypoxia-Inducible Factor 1, alpha Subunit / genetics*
  • Male
  • Middle Aged
  • Polymerase Chain Reaction
  • Polymorphism, Genetic*

Substances

  • HIF1A protein, human
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • DNA