Endurance training or beta-blockade can partially block the energy metabolism remodeling taking place in experimental chronic left ventricle volume overload

BMC Cardiovascular Disorders

Research Article

Suzanne Gascon¹  Jacques A Rousseau¹  Otman Sarrhini¹  Roger Lecomte¹  Marie Arsenault²  Dominic Lachance²  Wahiba Dhahri²  Marie-Claude Drolet²  Élise Roussel²  Jacques Couet² 

[1] Centre d’imagerie moléculaire de Sherbrooke, Centre de recherché Étienne-LeBel, Centre Hospitalier Universitaire de Sherbrooke, Université de Sherbrooke, Sherbrooke, Canada;Groupe de recherche sur les valvulopathies, Centre de Recherche, Institut Universitaire de cardiologie et de pneumologie de Québec, Université Laval, 2725, Chemin Sainte-Foy, G1V 4G5, Québec City, Québec, Canada;

关键词: Carvedilol;    Endurance Training;    Sham Animal;    Myocardial Metabolism;    Aortic Regurgitation;   

DOI  :  10.1186/1471-2261-14-190

 received in 2014-09-25, accepted in 2014-12-11,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundPatients with chronic aortic valve regurgitation (AR) causing left ventricular (LV) volume overload can remain asymptomatic for many years despite having a severely dilated heart. The sudden development of heart failure is not well understood but alterations of myocardial energy metabolism may be contributive. We studied the evolution of LV energy metabolism in experimental AR.MethodsLV glucose utilization was evaluated in vivo by positron emission tomography (microPET) scanning of 6-month AR rats. Sham-operated or AR rats (n = 10-30 animals/group) were evaluated 3, 6 or 9 months post-surgery. We also tested treatment intervention in order to evaluate their impact on metabolism. AR rats (20 animals) were trained on a treadmill 5 times a week for 9 months and another group of rats received a beta-blockade treatment (carvedilol) for 6 months.ResultsMicroPET revealed an abnormal increase in glucose consumption in the LV free wall of AR rats at 6 months. On the other hand, fatty acid beta-oxidation was significantly reduced compared to sham control rats 6 months post AR induction. A significant decrease in citrate synthase and complex 1 activity suggested that mitochondrial oxidative phosphorylation was also affected maybe as soon as 3 months post-AR.Moderate intensity endurance training starting 2 weeks post-AR was able to partially normalize the activity of various myocardial enzymes implicated in energy metabolism. The same was true for the AR rats treated with carvedilol (30 mg/kg/d). Responses to these interventions were different at the level of gene expression. We measured mRNA levels of a number of genes implicated in the transport of energy substrates and we observed that training did not reverse the general down-regulation of these genes in AR rats whereas carvedilol normalized the expression of most of them.ConclusionThis study shows that myocardial energy metabolism remodeling taking place in the dilated left ventricle submitted to severe volume overload from AR can be partially avoided by exercise or beta-blockade in rats.

【 授权许可】

Unknown   
© Lachance et al.; licensee BioMed Central. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.