To conclude, we claim that robust compensatory mechanisms in the hearts of female ApoE/LDLR−/− mice including increased vascular responsiveness to NO and increased generation of PGI2 could, at least partly, explain preserved whole body V’O2max as well as full cardiac adaptation to exercise of female ApoE/LDLR−/− mice despite peripheral and coronary atherosclerosis progression. This evidence concerns the gene LDLR and coronary atherosclerosis.