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Intermittent Hypoxia and Human Diseases 2012
DOI: 10.1007/978-1-4471-2906-6_16
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Adaptation to Intermittent Hypoxia/Hyperoxia Enhances Efficiency of Exercise Training

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Cited by 14 publications
(23 citation statements)
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“…IHT may provoke beneficial effects by preconditioning subsequently protecting the heart and/or the brain against deleterious consequences of ischemia reperfusion [13] . Although the excessive production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) represents an important mechanism of cell damage during hypoxia and reoxygenation in mitochondria initiating cellular death pathways, IHT may optimize mitochondrial metabolism, thus preventing adverse consequences of excess mitochondrial ROS generation [14] , [15] . In addition, IHT stimulates endothelial nitric oxide (NO) production that leads to vasodilatation, opens reserve capillaries [16] , and induces the production of vascular endothelial and fibroblast growth factors to stimulate endothelial proliferation [17] .…”
Section: Introductionmentioning
confidence: 99%
“…IHT may provoke beneficial effects by preconditioning subsequently protecting the heart and/or the brain against deleterious consequences of ischemia reperfusion [13] . Although the excessive production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) represents an important mechanism of cell damage during hypoxia and reoxygenation in mitochondria initiating cellular death pathways, IHT may optimize mitochondrial metabolism, thus preventing adverse consequences of excess mitochondrial ROS generation [14] , [15] . In addition, IHT stimulates endothelial nitric oxide (NO) production that leads to vasodilatation, opens reserve capillaries [16] , and induces the production of vascular endothelial and fibroblast growth factors to stimulate endothelial proliferation [17] .…”
Section: Introductionmentioning
confidence: 99%
“…Further, we hypothesize that the oxygen tensions and intermittent hyperoxia exposure-associated H3K4me3 alteration in our cell culture system may have been due to the increased production of reactive oxygen species (ROS). It is known that higher O 2 tension and re-oxygenation are both accompanied by increased generation of ROS [37,38]. Unlike the in vivo system, culture conditions in vitro lack naturally effective antioxidant systems [39].…”
Section: Discussionmentioning
confidence: 99%
“…As outlined above, mechanisms responsible for hypoxia effects may be either related or unrelated to hypoxia-induced HIF activation as recently reviewed [69], and include improvements of stress resistance on the cellular and systemic level [27,81], glucose homeostasis [41,61] and blood lipid profile [40,64,110], as well as the evocation of antiarrhythmic effects and improved autonomic cardiovascular and respiratory control [27,59], and neuroprotection by upregulating neuroprotectants like VEGF, EPO, antioxidants and nitric oxide (NO), and/or by suppressing apoptosis [66]. Regarding IHHC, reoxygenation, especially when performed under hyperoxic conditions, generates ROS, which may trigger redox-signaling cascades initiating adaptations that contribute to injury resistance, e.g., by membrane-stabilizing effects in the heart, brain, and liver [3,105,106,113]. Although the multitude of signaling pathways involved in hypoxia adaptations and their interactions are far from being fully elucidated, they may not only be used for the benefit of different patient groups but also contribute to (pre-)acclimatization, improved exercise tolerance and training efficiency (demonstrated by Sazontova and colleagues [105,106].…”
Section: Intermittent Hypoxia and Hypoxia-hyperoxia Conditioning In Therapy And The Prevention Of Various Diseasesmentioning
confidence: 99%