Description:Glutamine is a critical amino acid that serves as an energy source, building block, and signaling molecule for both the heart tissue and the immune system. However, the role of glutamine metabolism in regulating cardiac remodeling following myocardial infarction (MI) is unknown. In this study, we show that glutamine metabolism is altered both in the remote (contractile) area and in infiltrating macrophages in the infarct area after MI in adult male mice by permanent left anterior descending artery occlusion. Using untargeted metabolomics in extracted LV macrophages, we found that metabolites related to glutamine metabolism were differentially altered at days 1, 3, and 7 after MI. Glutamine metabolism in live cells was found to be increased after MI relative to no MI controls. Gene expression in the remote area of the heart indicated a loss of glutamine metabolism. Glutamine administration improved LV function at days 1, 3, and 7, which was associated with improved contractile and metabolic gene expression.