Cardiac hypertrophy is stimulated by altered training intensity and correlates with autophagy modulation in male Wistar rats

Julia Windi Gunadi; Vita Murniati Tarawan; Iwan Setiawan; Ronny Lesmana; Roro Wahyudianingsih; Unang Supratman

doi:10.1186/s13102-019-0121-0

Cardiac hypertrophy is stimulated by altered training intensity and correlates with autophagy modulation in male Wistar rats

BMC Sports Sci Med Rehabil. 2019 Jun 10:11:9. doi: 10.1186/s13102-019-0121-0. eCollection 2019.

Authors

Julia Windi Gunadi¹, Vita Murniati Tarawan², Iwan Setiawan², Ronny Lesmana^{2

3

4}, Roro Wahyudianingsih⁵, Unang Supratman⁶

Affiliations

¹ 1Department of Physiology, Faculty of Medicine, Maranatha Christian University, Bandung, Indonesia.
² 2Physiology Division, Department of Biomedical Science, Faculty of Medicine, Universitas Padjadjaran, Bandung, Indonesia.
³ 3Division of Biological Activity, Central Laboratory, Universitas Padjadjaran, Bandung, Indonesia.
⁴ 4Center of Excellence in Higher Education for Pharmaceutical Care Innovation, Universitas Padjadjaran, Bandung, Indonesia.
⁵ 5Department of Anatomy Pathology, Faculty of Medicine, Maranatha Christian University, Bandung, Indonesia.
⁶ 6Department of Chemistry, Faculty of Mathematics and Natural Sciences, Universitas Padjadjaran, Bandung, Indonesia.

Abstract

Background: The mechanism for cardiac hypertrophy process that would be a benefit for improvement of cardiovascular endurance needed to be investigated throughly. Specific intensity of training may play a role for homeostasis process in cardiac during training. In the present study, we examine the effect of different intensity of treadmill training on cardiac hypertrophy process and autophagy related gene expression in male wistar rats.

Methods: Three different intensities of treadmill training were conducted on 15 male wistar rats (Low Intensity: 10 m/minute, Moderate Intensity: 20 m/minute, and High Intensity: 30 m/minute) compared to 5 sedentary rats as control. Training duration was 30 min per day, frequency was 5 days per week, during 8 weeks period. Heart weight and heart weight/body weight ratio were measured after the experiments. Left ventricle myocardium was taken for microscopic analysis with HE staining. mRNA was extracted from left ventricle myocardium for examining αMHC and autophagy related gene expression (PIK3CA, mTOR, LC3, p62) using semi quantitative PCR.

Results: We observed that altered training intensity might stimulate cardiac hypertrophy process. MI and HI training increased heart weight and heart weight/body weight ratio. This finding is supported by microscopic result in which cardiac hypertrophy was found in MI and HI, with focal fibrosis in HI, and increased αMHC gene expression in MI (p < 0.05) and HI (p = 0.076). We also observed decreased PIK3CA (LI 0.8 fold, MI 0.9 fold), mTOR (LI 0.9 fold, MI 0.9 fold), LC3 (LI 0.9 fold, MI 0.8 fold, HI 0.8 fold), and p62 (LI 0.8 fold, MI 0.9 fold) compared to control. Interestingly, we found increased mTOR (HI 1.1 fold) and p62 (HI 1.1 fold) compared to control.

Conclusion: Training with different intensity creates different cardiac hypertrophy process based on heart weight and heart weight/body weight ratio, microscopic examination and autophagy related gene expression.

Keywords: Autophagy; Cardiac hypertrophy; LC3; PIK3CA; Training; mTOR; p62; αMHC.