Heart failure is a syndrome of poor prognosis and high prevalence characterized by low cardiac output. Its development involves a continuous interaction between cardiac dysfunction and compensatory changes such as metabolic and functional alterations and activation of neurohumoral systems. At first, these responses are beneficial, but sustained changes are toxic and determine the progression of disease. One of the major alterations observed in heart failure is related to changes in body composition. These changes are usually weight loss, skeletal muscle atrophy, and in severe cases, cachexia. Cachexia is a predictor of increased mortality and characterized by skeletal muscle atrophy, loss of fat mass and bone. It is caused by dynamic imbalance of anabolic and catabolic systems, which is associated to dyspnea, exercise intolerance and reduction of strength. These factors further worsen the quality of life of patients with heart failure. Therefore, this undergraduate research project, we aim to determine the morphofunctional predictors of cachexia and moments in which these changes occur. Reduced muscle strength, presence of early fatigue, anemia, anorexia and decreased fat mass will be analyzed in an experimental model of chronic myocardial infarction. This animal model will allow the elaboration of a protocol for the determination of the cachexia in rats. It will also allow studies of mechanisms and possible interventions.
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