Abstract 18108: Extreme Physical Activity Reverses Beneficial Vascular Effects of Moderate Physical Activity. Study in an Animal Model
Introduction: Moderate aerobic exercise reduces atherosclerotic burden. However, recent data show increased cardiovascular disease burden and mortality in the most trained individuals.
Aim: To assess vascular remodeling after very high intensity training.
Methods: Wistar rats underwent very high (INT, 60min 60cm/s, n=20) or moderate intensity (MOD, 45min 35cm/s, n=20) treadmill training for 16 weeks. Sedentary rats (SED n=20) served as controls. Morphologic analyses were performed in descending thoracic aorta and intramyocardial arteries. Aortic wall oxidative stress was quantified with dihydroethidium (DHE). In vivo functional remodeling was assessed in a hemodynamic study. Ex vivo vascular reactivity to acetilcholine (Ach), phenylephrine (Phe) and KCl was studied in intact- and denuded-endothelium conditions.
Results: INT promoted increased aorta wall thickness, elastin fiber disorganization and disruptions in tunica media compared to MOD and SED. Lumen of intramyocardial arteries was narrower and tunica media was thicker in INT rats (Fig A). An in vivo hemodynamic study showed a higher pulse pressure in the INT group (Fig B), suggesting a stiffer aorta. MOD exercise improved ex vivo endothelial function by increasing Ach-mediated vasodilatation and reducing Phe vasoconstriction response; INT exercise did not provide further benefits (Fig C). Conversely, Phe response was increased in endothelium deanuded aorta of the INT group (Fig D); increased response to KCl in the INT group confirmed tunica media hypereactivity. DHE staining was increased in the tunica media of the INT group.
Conclusions: While moderate exercise improves vascular function, high intensity exercise blunts it by increasing vascular wall thickness and stiffness, and by inducing tunica media hipereactivity. Oxidative stress likely mediates these effects. Our findings provide important insights into increased atherosclerotic burden in very high trained individuals.
Author Disclosures: C. Rubies: None. M. Batlle: None. N. Castillo: None. A.P. Dantas: None. M. Sitges: None. J. Brugada: None. L. Mont: None. E. Guasch: None.
- © 2015 by American Heart Association, Inc.