Myocardial ischemic tolerance in rats subjected to endurance exercise training during adaptation to chronic hypoxia
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F17%3A00475735" target="_blank" >RIV/67985823:_____/17:00475735 - isvavai.cz</a>
Alternative codes found
RIV/00216208:11310/17:10368556
Result on the web
<a href="http://dx.doi.org/10.1152/japplphysiol.00671.2016" target="_blank" >http://dx.doi.org/10.1152/japplphysiol.00671.2016</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1152/japplphysiol.00671.2016" target="_blank" >10.1152/japplphysiol.00671.2016</a>
Alternative languages
Result language
angličtina
Original language name
Myocardial ischemic tolerance in rats subjected to endurance exercise training during adaptation to chronic hypoxia
Original language description
Chronic hypoxia and exercise are natural stimuli that confer sustainable cardioprotection against ischemia-reperfusion (I/R) injury, but it is unknown whether they can act in synergy to enhance ischemic resistance. Inflammatory response mediated by tumor necrosis factor-alpha (TNF-alpha) plays a role in the infarct size limitation by continuous normobaric hypoxia (CNH), whereas exercise is associated with anti-inflammatory effects. This study was conducted to determine if exercise training performed under conditions of CNH (12% O2) affects myocardial ischemic resistance with respect to inflammatory and redox status. Adult male Wistar rats were assigned to one of the following groups: normoxic sedentary, normoxic trained, hypoxic sedentary, and hypoxic trained. CNH increased TNF-alpha and interleukin-6 levels and the expression of TNF-alpha type 2 receptor, nuclear factor-kappaB (NF-kappaB), inducible nitric oxide synthase (iNOS), cytosolic phospholipase A2, cyclooxygenase-2, manganese superoxide dismutase (MnSOD), and catalase. None of these effects occurred in the normoxic trained group, whereas exercise in hypoxia abolished or significantly attenuated CNH-induced responses, except for NF-kappaB, iNOS, and MnSOD. Both CNH and exercise reduced infarct size, but their combination provided the same degree of protection as CNH alone. In conclusion, exercise training does not amplify the cardioprotection conferred by CNH. High ischemic tolerance of the CNH hearts persists after exercise, possibly by maintaining the increased antioxidant capacity despite attenuating TNF-alpha-dependent protective signaling.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30105 - Physiology (including cytology)
Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2017
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Journal of Applied Physiology
ISSN
8750-7587
e-ISSN
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Volume of the periodical
122
Issue of the periodical within the volume
6
Country of publishing house
US - UNITED STATES
Number of pages
10
Pages from-to
1452-1461
UT code for WoS article
000404377000010
EID of the result in the Scopus database
2-s2.0-85021058492