title: Protective effects of intermittent hypoxic adaptation on myocardium and its mechanisms.
abstract: Intermittent hypoxic adaptation offers as many beneficial effects in protecting against myocardial injuries as chronic continuous hypoxic adaptation. However, chronic continuous hypoxic adaptation readily causes some adverse effects on the organism, which may be prevented by intermittent hypoxic adaptation. As an approach to potentiate the protective effects, intermittent hypoxic adaptation is also much easier to apply to subjects who are not living at high altitude. The mechanisms underlying the cardioprotective effects of intermittent hypoxic adaptation are less understood, although great similarities exist between chronic continuous and intermittent hypoxic adaptation. The participation of several factors, such as myocardial vascularity, coronary blood flow, and cardiomyoglobin, which comprise the oxygen uptake system is not apparent, while the more efficient energetic metabolism after intermittent hypoxic adaptation may be a mechanism for cardioprotection. The possible roles of several signaling transduction pathways, including adrenoceptors, prostaglandins, and the adenosinergic system, in the beneficial effects of intermittent hypoxia are compared to those of chronic continuous hypoxic adaptation. Antioxidant enzymes and stress proteins may also be part of the mechanisms contributing to the cardioprotection of the intermittent hypoxic adaptation. As the cardioprotective effects of intermittent hypoxic adaptation employ multifold mechanisms, their clear elucidation needs more efforts.
authors.affiliation: Shanghai Institute of Physiology, Chinese Academy of Sciences, Shanghai, China.
authors.forename: J
authors.initials: J
authors.lastname: Zhuang
authors.forename: Z
authors.initials: Z
authors.lastname: Zhou
mesh_terms: D000222:Adaptation, Physiological; D000241:Adenosine / Q000502:physiology; D000818:Animals; D004734:Energy Metabolism; D006360:Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D010088:Oxidoreductases / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D011453:Prostaglandins / Q000502:physiology; D011941:Receptors, Adrenergic / Q000378:metabolism
chemical_list: D006360:Heat-Shock Proteins; D011453:Prostaglandins; D011941:Receptors, Adrenergic; D010088:Oxidoreductases; D000241:Adenosine; D010100:Oxygen