Methylglyoxal (MG) is a highly reactive small carbonyl that generates Advanced Glycation End-products (AGEs) and both compounds are increased during diabetes, myocardial infarction (MI), and in inflammatory diseases. MI can trigger autophagy, a mechanism of cellular recycling that generates energy in situations of nutrient deprivation. However, the benefit of autophagy when stimulated in the presence of AGEs is still not clear. Therefore, the objective of this study was to evaluate the role of methylglyoxal in the activation of autophagy and on cardiac remodeling. To this, 90 male Wistar rats were randomized into Sham, MI, and MI pretreated with MG (7 days, 75 mg/kg/day, twice a day) or rapamycin (24 and 4 hours, 8 mg/kg). Echocardiography was performed by a blinded researcher 24 hours after the surgery and soon after the animals were killed and samples were prepared for western blot. MG treatment did not increase AGEs in the heart tissue or impair ejection fraction, fractional shortening, and chamber remodeling assessed 24 hours after the MI. However, it caused a 9-fold increase in mTOR activation (p=0.02) without changing the content of autophagy related proteins (LC3II/I ratio and p62). Curiously, Rapamycin, a known activator of autophagy, did not prevent heart remodeling. In conclusion, the glycating agent MG given before MI increases mTOR signaling without affecting autophagy and does not alter cardiac remodeling. Financial support: Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), Fundação de Incentivo à Pesquisa do Hospital de Clínicas de Porto Alegre (FIPE-HCPA), and Fundo de Amparo à Pesquisa do RS (Fapergs).