Beta-Adrenergic receptors desensitization is not involved in exercise-induced cardiac fatigue: NADPH oxidase-induced oxidative stress as a new trigger

Journal article


Vitiello, Damien, Boissiere, Julien, Doucende, Gregory, Gayrard, Sandrine, Polge, Anne, Faure, Patrice, Goux, Aurelie, Tanguy, Stephane, Obert, Phillippe, Reboul, Cyril and Nottin, Stephane. (2011). Beta-Adrenergic receptors desensitization is not involved in exercise-induced cardiac fatigue: NADPH oxidase-induced oxidative stress as a new trigger. Journal of Applied Physiology. 111(5), pp. 1242 - 1248. https://doi.org/10.1152/japplphysiol.00449.2011
AuthorsVitiello, Damien, Boissiere, Julien, Doucende, Gregory, Gayrard, Sandrine, Polge, Anne, Faure, Patrice, Goux, Aurelie, Tanguy, Stephane, Obert, Phillippe, Reboul, Cyril and Nottin, Stephane
Abstract

Prolonged strenuous exercise (PSE) induces transient left ventricular (LV) dysfunction. Previous studies suggest that β-adrenergic pathway desensitization could be involved in this phenomenon, but it remains to be confirmed. Moreover, other underlying mechanisms involving oxidative stress have been recently proposed. The present study aimed to evaluate the involvement of both the β-adrenergic pathway and NADPH oxidase (Nox) enzyme-induced oxidative stress in myocardial dysfunction in rats following PSE. Rats were divided into 4 groups: controls (Ctrl), 4-h exercised on treadmill (PSE), and 2 groups in which Nox enzyme was inhibited with apocynin treatment (Ctrl APO and PSE APO, respectively). We evaluated cardiac function in vivo and ex vivo during basal conditions and isoproterenol stress. GSH/GSSG ratio, cardiac troponin I (cTnI) release, and lipid peroxidation (MDA) were evaluated. PSE induced a decrease in LV developed pressure, intrinsic myocardial contractility, and relaxation associated with an increase in plasma cTnI release. Our in vivo and ex vivo results demonstrated no differences in myocardial response to isoproterenol and of effective dose 50 between control and PSE rats. Interestingly, the LV dysfunction was reversed by apocynin treatment. Moreover, apocynin prevented cellular oxidation [GSH/GSSG ratio: PSE APO rats vs. PSE rats in arbitrary units (au): 1.98 ± 0.07 vs. 1.35 ± 0.10; P < 0.001]. However, no differences in MDA were observed between groups. These data suggest that myocardial dysfunction observed after PSE was not due to β-adrenergic receptor desensitization but could be due to a signaling oxidative stress from the Nox enzyme.

Keywordsmyocardial dysfunction; β-adrenergic pathway; oxidative stress
Year2011
JournalJournal of Applied Physiology
Journal citation111 (5), pp. 1242 - 1248
PublisherAmerican Physiological Society
ISSN8750-7587
Digital Object Identifier (DOI)https://doi.org/10.1152/japplphysiol.00449.2011
Scopus EID2-s2.0-81355132776
Page range1242 - 1248
Research GroupSports Performance, Recovery, Injury and New Technologies (SPRINT) Research Centre
Publisher's version
File Access Level
Controlled
Place of publicationUnited States of America
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