The effect of intermittent hypoxic training on lung and heart tissues of healthy rats.
BACKGROUND
Recently, particular attention has been focused on the problem of the beneficial influence of intermittent hypoxia (IH) on the human organism. However, knowledge regarding the negative effects of intermittent hypoxic training (IHT) on cellular adaptive mechanisms remains limited. The aim of the present study was to investigate: 1) lung and heart ultrastructural changes under IHT; and 2) the adequateness of morphological and morphometric methods to determine the constructive and destructive displays of hypoxia.


METHODS
Adult male Wistar rats underwent IHT every day for 7-28 days. Lung and heart tissues were assessed by morphological and cellular morphometric methods.


RESULTS
We observed evident ultra structural changes of the lung air-blood barrier (LABB) by the 7-10(th) day of training. Structural damage of LABB was most considerable after 2 weeks of IHT exposure, its ultrastructure partially normalized by the end of the IHT 4-weeks course: there was diminishing of LABB hydration and disappearance of areas of its destruction. The structural changes in the heart blood-tissue barrier (HBTB) were considerably less marked compared with those in LABB during the 1(st) and 2(nd) weeks of training. Heart tissue structural changes increased by the end of the fourth week of IHT. Both tissue cells revealed no significant necrotic damage of mitochondria after IHT, while changes relating to the energy-directed restructuring of mitochondria were observed. We hypothesized that acute moderate hypoxia promotes a specific type of mitosis in lung and heart tissues.


CONCLUSIONS
Ultrastructural changes in the rat lung and heart tissues depend on IHT duration. The phenomenon of "micromitochondria within mitochondria" is an additional adaptive mechanism for IH exposure.
Department of Hypoxia, O.O. Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kiev, Ukraine.
Katerina
K
Rozova
Iryna
I
Mankovska
D000222:Adaptation, Physiological; D000818:Animals; D006321:Heart / Q000187:drug effects; D000860:Hypoxia / Q000378:metabolism*; D008168:Lung / Q000378:metabolism / Q000648:ultrastructure*; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism / Q000648:ultrastructure*; D009206:Myocardium / Q000378:metabolism / Q000648:ultrastructure*; D010100:Oxygen / Q000008:administration & dosage*; D010101:Oxygen Consumption; D010805:Physical Conditioning, Animal / Q000379:methods*; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values
D010100:Oxygen