Chronic exercise training prevents coronary artery stiffening. - GreenMedInfo Summary
Chronic exercise training prevents coronary artery stiffening in aortic-banded miniswine: Role of perivascular adipose-derived advanced glycation end products.
J Appl Physiol (1985). 2019 Jul 11. Epub 2019 Jul 11. PMID: 31295062
Aims Heart failure (HF) is associated with increased large conduit artery stiffness and afterload resulting in stiffening of the coronary arteries. Perivascular adipose tissue (PVAT) and advanced glycation end products (AGE) both promote arterial stiffness, yet the mechanisms by which coronary PVAT promotes arterial stiffness and the efficacy of exercise to prevent coronary stiffness are unknown. We hypothesized both chronic continuous and interval exercise training would prevent coronary PVAT-mediated AGE secretion and arterial stiffness. Methods and Results Yucatan mininature swine were divided into four groups: control-sedentary (CON), aortic-banded sedentary heart failure (HF), aortic-banded HF continuous exercise trained (HF+CONT), and aortic-banded HF interval exercise trained (HF+IT). The left circumflex (LCX) and right coronary artery (RCA) underwent ex vivo mechanical testing, and arterial AGE, elastin and collagen were assessed. Coronary elastin elastic modulus (EEM) and elastin protein were lower, and AGE was increased with HF compared to CON that was prevented by both HF+CONT and HF+IT. Mouse aortic segments treated with swine coronary PVAT-conditioned media had lower EEM, elastin content, greater AGE secretion and arterial AGE accumulation in HF compared with CON, which was prevented by both HF+CONT and HF+IT. Aminoguanidine (AMG), an AGE inhibitor, prevented the reduction in the EEM, arterial elastin content and AGE accumulation in mouse aortic segments treated with PVAT conditioned media in the HF group. Conclusions Our data demonstrate efficacy for chronic continuous and interval exercise to prevent coronary artery stiffness via inhibition of PVAT-derived AGE secretion in a pre-clinical mini-swine model of pressure overload-induced HF.