Introduction: Exercise training (ExT) improves functional capacity in older adults with heart failure (HF). However, the molecular mechanisms by which ExT exerts these benefits are unclear. We previously showed that cardiac activin type II receptor (ActRII) signaling increases in aging and HF, and that ActRII inhibition can improve cardiac exercise capacity in aged C57BL/6 mice, a model of age-related HFpEF. Whether cardiac ActRII signaling is modulated by ExT is unknown. Hypothesis: We hypothesized that ExT would attenuate cardiac ActRII signaling in aged mice. Methods: A moderate intensity ExT protocol (treadmill running, 10m/min, 10° incline, 45min/day, 8 weeks) was performed in 25month-old (mo) female C57BL/6 mice (OE). Functional (exercise capacity), molecular, and gravimetric assessments of HF were compared to young (YS, 4mo) and old (OS, 27mo) sedentary controls, along with indicators of downstream ActRII signaling (FSTL3 expression, SMAD3 phosphorylation, senescence, apoptosis markers). Results: After 8 weeks of ExT, exercise capacity increased in OE mice by 2.5±9.9% versus -24.1±4.6% in OS mice (p=0.05). ExT did not induce significant changes in cardiac hypertrophy or natriuretic peptide expression in aged mice, but decreased lung weight to body weight ratios (3.8±0.2(YS) vs 7.4±0.7(OS) vs 5.3±0.4(OE) mg/g, p=0.001). Cardiac ActRII signaling increased with aging and was attenuated with ExT (FSTL3/GAPDH: 1.0±0.01(YS) vs. 2.9±0.1(OS) vs. 1.0±0.2(OE) p=0.01; pSMAD3/SMAD3: 0.8±0.2(YS) vs. 1.5±0.04(OS) vs. 1.1±0.1(OE), p=0.1). Moreover, parallel changes occurred in markers of cardiac senescence (p16: 1.0±0.02(YS) vs. 1.6±0.1(OS) vs. .3±0.02(OE), p=0.02) and apoptosis (BAX: 0.8±0.2(YS) vs. 1.8±0.05(OS) vs. 1.1±0.1(OE), p=0.0007; cleaved caspase 3: 0.8±0.01(YS) vs. 2.2±0.01(OS) vs. 1.0±0.02(OE), p=0.0001), which have been shown to be regulated by ActRII signaling. Conclusions: These findings suggest aerobic ExT attenuates the cardiac ActRII signaling observed in aged mice and slows the age related decline in exercise capacity. Age-associated pathologies linked to ActRII signaling, including cellular senescence and apoptosis, were similarly modulated by ExT.