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Original Article

Korean J Physiol Pharmacol 2020; 24(1): 53-68

Published online January 1, 2020 https://doi.org/10.4196/kjpp.2020.24.1.53

Copyright © The Korean Journal of Physiology & Pharmacology.

Interaction of genetic background and exercise training intensity on endothelial function in mouse aorta

Seung Kyum Kim1,*, Joshua J. Avila2, and Michael P. Massett2

1Department of Sports Science, Seoul National University of Science and Technology, Seoul 01811, Korea, 2Department of Health and Kinesiology, Texas A&M University, College Station, TX, USA

Correspondence to:*Seung Kyum Kim
E-mail: skkim7@seoultech.ac.kr

Received: July 17, 2019; Revised: October 18, 2019; Accepted: November 7, 2019

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


The purpose of this study was to characterize the genetic contribution to endothelial adaptation to exercise training. Vasoreactivity was assessed in aortas from four inbred mouse strains (129S1, B6, NON, and SJL) after 4 weeks of moderate intensity continuous exercise training (MOD), high intensity interval training (HIT) or in sedentary controls (SED). Intrinsic variations in endothelium-dependent vasorelaxation (EDR) to acetylcholine (ACh) as well as vasocontractile responses were observed across SED groups. For responses to exercise training, there was a significant interaction between mouse strain and training intensity on EDR. Exercise training had no effect on EDR in aortas from 129S1 and B6 mice. In NON, EDR was improved in aortas from MOD and HIT compared with respective SED, accompanied by diminished responses to PE in those groups. Interestingly, EDR was impaired in aorta from SJL HIT compared with SED. The transcriptional activation of endothelial genes was also influenced by the interaction between mouse strain and training intensity. The number of genes altered by HIT was greater than MOD, and there was little overlap between genes altered by HIT and MOD. HIT was associated with gene pathways for inflammatory responses. NON MOD genes showed enrichment for vessel growth pathways. These findings indicate that exercise training has non-uniform effects on endothelial function and transcriptional activation of endothelial genes depending on the interaction between genetic background and training intensity.

Keywords: Endothelium, Exercise, Gene expression profiling, Inbred mouse strain