Supplemental data to Labbé et al. AJP 2025 (figures and tables)

We recently observed in a “two-hit” murine HFpEF model (Angiotensin II (AngII) + High-Fat Diet (HFD) or MHS) that stopping AngII, normalizing the diet, and introducing voluntary exercise (VE) helped reverse cardiac damage and improved exercise capacity. It was unclear if correcting the diet or introducing VE contributed to the left ventricle (LV) reverse remodelling (RR) in addition to removing the hypertensive stressor, AngII.To study the extent of reverse remodelling and myocardial recovery in our murine model, we investigated cardiac resiliency to a second MHS after an extended period of remission of 12 weeks instead of the four we already studied. We also investigated the relative contribution of physical activity and diet correction to RR.