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Obesity is a chronic metabolic disorder defined by excessive accumulation of body fat relative to lean tissue. Clinical studies show that obesity is associated with ventricular dysfunction and not consistent impairment of systolic performance. Experimental models that induce obesity by diet have been used as an alternative to study the consequences of cardiac abnormalities resulting from accumulation of fat. Researchs show that cardiac function in obese animals may be preserved, diminished or increased. Alterations in energy substrates, inhibition of the glycolytic pathway by fatty acids and reduced activity of the enzyme pyruvate dehydrogenase (PDH) may contribute to cardiac dysfunction induced by obesity. Due to the lack of research evaluating the relationship between cardiac function and energy metabolism in obesity, the objective of this study was to test the hypothesis that the myocardial energy imbalance between fatty acids and glucose, caused by obesity, leads to cardiac dysfunction. The functional impairment in the obese animals is due to deficit of adenosine triphosphate (ATP), glycolytic pathway for calcium (Ca) pump of sarcoplasmic reticulum (SERCA2). For this purpose, was inhibited the myocardial glycolytic pathway by administration of iodoacetate. Moreover, energy metabolism was also assessed by stimulation of PDH by dichloroacetate. Thirty-day-old male Wistar rats were assigned to one of two groups (n=30 each): control (C) and obese (Ob). The C group was fed a standard diet and Ob group was fed cycles of four highfat diets for 30 weeks. The total body fat was measured from the sum of the individual fat pad weights (epididymal, retroperitoneal and visceral) and the obesity defined by adiposity index. The nutritional and metabolic profiles of these animals were also evaluated. The cardiac remodeling process was assessed by structural and functional analysis. The structure was analyzed post-death for macroscopic study. Myocardial performance of isolated papillary muscle from the left ventricle (LV) was evaluated by under baseline conditions and after inotropic maneuvers. Comparisons between experimental groups (control and obese rats) were performed using Students-t test for independent samples. The cardiac function, after inotropic maneuvers, was analyzed by two-way analysis of variance (ANOVA) for repeated measures and complemented by Student-Newman-Keuls’s posthoc test for specific differences. The level of significance considered was 5 %. Obesity promoted glucose intolerance, hyperinsulinemia, hyperleptinemia and insulin resistance after 30 weeks. However, the behavior of systolic blood pressure was similar between groups. The post-death macroscopic study showed that obesity doesn’t promote to an increase in heart weight and heart chambers at 30 weeks. Obesity did not cause myocardial stiffness and damage on cardiac function under baseline conditions. Several inotropic maneuvers no make evident changes between control and obese, since the behavior of developed tension (DT) was similar between the groups. The return values of DT and resting tension (RT) to baseline levels, after an increase in frequency of stimulation, exhibited that the availability of energy in the two groups was similar. The stimulation of glycolytic pathway by dichloroacetate, did not promote alteration between the control and obese. The inhibition with iodoacetate showed that glycolytic pathway in obesity is not impaired. The linear regression analysis of RT displayed that control rats showed greater contracture than obese. In conclusion, the energy imbalance on obesity does not cause cardiac dysfunction. On the contrary, the prioritization of fatty acids utilization provides protection to cardiac muscle during the inhibition of glycolysis, suggesting that this pathway is fewer used by obese myocytes.

Influência da oxidação de glicose sobre a função miocárdica de ratos obesos