Although exercise training (ExT) is an important therapeutic strategy for improving quality of life in patients with chronic heart failure (CHF), the central mechanisms by which ExT is beneficial are not well understood. The angiotensin II type 1 receptor (AT1R) plays a pivotal role in the development of CHF, and is upregulated in a number of tissues due in part to transcription factor nuclear factor kappa B (NF-κB). In addition, AT1R is marked for internalization and recycling via G protein coupled receptor kinase (GRK) phosphorylation. Because previous studies have shown that the beneficial effects of ExT in CHF rely on a reduction in Ang II, we hypothesized ExT would decrease AT1R, GRK5 and NF-κB protein expression in the paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) of CHF rats. Following infarction by coronary artery ligation, animals were exercised four weeks post-surgery on a treadmill at a final speed of 25 m/min for 60 minutes, 5 days/week for 6 weeks. Western blot analysis of PVN and RVLM micropunches revealed an upregulation of AT1R, GRK5 and NF-κB in the infarcted group that was reversed by ExT. Furthermore, the relative expression of phosphorylated AT1R and AT1R/GRK5 physical association was increased in the CHF sedentary group, and reversed by ExT. Overexpression of GRK5 in cultured CATH.a neurons blunted angiotensin II-mediated upregulation of AT1R and NF-κB; conversely, silencing of GRK5 exacerbated angiotensin II-mediated AT1R and NF-κB upregulation. Taken together, increased GRK5 may regulate AT1R expression in CHF, and ExT mitigates AT1R and its pathway components.