There was shown an antiarrhythmic effect of adaptation to intermittent hypobaric hypoxia in ischemia, reperfusion, experimental infarction and postinfarction cardiosclerosis (F.Z. Meerson, 1988). These results was obtained in whole animal experiments. In our study it was demonstrated that the antiarrhythmic effect of adaptation to hypoxia persisted in hearts after isolation, in absence of the effect of neural and humoral factors on the organ. Adaptation of animals to intermittent hypoxia was produced by "stepwise" elevations in an altitude chamber: first day--1000 m; second day--2000 m; third day--3000 m and rest of the days--to 4000 m above sea level. The course of doses adaptation to hypoxia lasted for 40 days; each daily exposure lasted 5 hours. The analysis of arrythmogenic and contractural effects of hypercalcium perfusion and "calcium paradox" phenomenon shows a significant decrease of these effects in hearts of adapted animal. The bioelectrical activity investigation of papillary muscles cardiomyocytes, obtained from hearts of adapted animals, was shown, in hypercalcium perfusion condition, a complex of antiarrhythmogenic changes which was expressed in limitation of rest and action potentials decreasing and in maintenance of the action potential duration. In papillary muscles, obtained from adapted animals, the contracture and the depression of contractility was also smaller. In experiments on resting papillary muscles we found that adaptation to intermittent hypoxia significantly decreased contractural and depolarizing effects of low-sodium perfusion. Thus adaptation to intermittent hypobaric hypoxia resulted, at cardiomyocytes level, in a complex of antiarrhythmic changes which may indicate a protective effect of this kind of adaptation in cardiac arrhythmias.