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
Authors | Vitiello, Damien, Boissiere, Julien, Doucende, Gregory, Gayrard, Sandrine, Polge, Anne, Faure, Patrice, Goux, Aurelie, Tanguy, Stephane, Obert, Phillippe, Reboul, Cyril and Nottin, Stephane |
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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. |
Keywords | myocardial dysfunction; β-adrenergic pathway; oxidative stress |
Year | 2011 |
Journal | Journal of Applied Physiology |
Journal citation | 111 (5), pp. 1242 - 1248 |
Publisher | American Physiological Society |
ISSN | 8750-7587 |
Digital Object Identifier (DOI) | https://doi.org/10.1152/japplphysiol.00449.2011 |
Scopus EID | 2-s2.0-81355132776 |
Page range | 1242 - 1248 |
Research Group | Sports Performance, Recovery, Injury and New Technologies (SPRINT) Research Centre |
Publisher's version | File Access Level Controlled |
Place of publication | United States of America |
https://acuresearchbank.acu.edu.au/item/8v4xv/beta-adrenergic-receptors-desensitization-is-not-involved-in-exercise-induced-cardiac-fatigue-nadph-oxidase-induced-oxidative-stress-as-a-new-trigger
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