ArticleBMC cardiovascular disorders2014
Endurance training or beta-blockade can partially block the energy metabolism remodeling taking place in experimental chronic left ventricle volume overload.
Article in BMC cardiovascular disorders, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Multiscale model calibrated with a Bayesian algorithm predicts long-term outcomes of treatments for mitral valve regurgitation in animal models.Biomechanics and modeling in mechanobiology · 2026Article
- Contributions of mechanical loading and hormonal changes to eccentric hypertrophy during volume overload: A Bayesian analysis using logic-based network models.PLoS computational biology · 2025Article
- Effects of early exercise on cardiac function and lipid metabolism pathway in heart failure.Journal of cellular and molecular medicine · 2023Article
- Systemic Bioinformatic Analyses of Nuclear-Encoded Mitochondrial Genes in Hypertrophic Cardiomyopathy.Frontiers in genetics · 2021Article
- Article
- Moderate-intensity exercise allows enhanced protection against oxidative stress-induced cardiac dysfunction in spontaneously hypertensive rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2019Article
- Multiple short-chain dehydrogenases/reductases are regulated in pathological cardiac hypertrophy.FEBS open bio · 2018Article
- An "Exercise" in Cardiac Metabolism.Frontiers in cardiovascular medicine · 2018Review
- Female rats with severe left ventricle volume overload exhibit more cardiac hypertrophy but fewer myocardial transcriptional changes than males.Scientific reports · 2017Article
- Transcriptional Changes Associated with Long-Term Left Ventricle Volume Overload in Rats: Impact on Enzymes Related to Myocardial Energy Metabolism.BioMed research international · 2015Article
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10 authors at 3 institutions in 1 country.
Funding
Abstract
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.
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