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Korean Circ J. 2018 Nov;48(11):1014-1024. English. Original Article. https://doi.org/10.4070/kcj.2018.0084
Rao Z , Wang S , Bunner WP , Chang Y , Shi R .
School of Kinesiology, Shanghai University of Sport, Shanghai, China. raoz17@ecu.edu
Sport Health and Rehabilitation Center, China Institute of Sport Science, Beijing, China.
Department of Kinesiology, East Carolina University, Greenville, NC, USA.
Hunan University of Technology, Zhuzhou, China.
Abstract

Background and Objectives

Intense exercise (IE) induced myocardial fibrosis (MF) showed contradictory findings in human studies, making the relationship between IE and the development of MF unclear. This study aims to demonstrate exercise induced MF is associated with cardiac damage, and inflammation is essential to the development of exercise induced MF.

Methods

Sprague-Dawley rats were submitted to daily 60-minutes treadmill exercise sessions at vigorous or moderate intensity, with 8-, 12-, and 16-week durations; time-matched sedentary rats served as controls. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum cardiac troponin I (cTnI) concentration. After completion of the exercise protocol rats were euthanized. Biventricular morphology, ultrastructure, and collagen deposition were then examined. Protein expression of interleukin (IL)-1β and monocyte chemotactic protein (MCP)-1 was evaluated in both ventricles.

Results

After IE, right but not left ventricle (LV) MF occurred. Serum cTnI levels increased and right ventricular damage was observed at the ultrastructure level in rats that were subjected to long-term IE. Leukocyte infiltration into the right ventricle (RV) rather than LV was observed after long-term IE. Long-term IE also increased protein expression of pro-inflammation factors including IL-1β and MCP-1 in the RV.

Conclusions

Right ventricular damage induced by long-term IE is pathological and the following inflammatory response is essential to the development of exercise induced MF.

Copyright © 2019. Korean Association of Medical Journal Editors.