Myocardial ischemic tolerance in rats subjected to endurance exercise training during adaptation to chronic hypoxia

Kód výsledku v 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>

Nalezeny alternativní kódy

RIV/00216208:11310/17:10368556

Výsledek na webu

<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>

Jazyk výsledku

angličtina

Název v původním jazyce

Myocardial ischemic tolerance in rats subjected to endurance exercise training during adaptation to chronic hypoxia

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

Myocardial ischemic tolerance in rats subjected to endurance exercise training during adaptation to chronic hypoxia

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30105 - Physiology (including cytology)

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2017

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Applied Physiology

ISSN

8750-7587

e-ISSN

—

Svazek periodika

122

Číslo periodika v rámci svazku

6

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

1452-1461

Kód UT WoS článku

000404377000010

EID výsledku v databázi Scopus

2-s2.0-85021058492