Research Paper Volume 12, Issue 20 pp 20226—20234
Aerobic exercise induces tumor suppressor p16INK4a expression of endothelial progenitor cells in human skeletal muscle
- 1 Laboratory of Regenerative Medicine in Sports Science, School of Physical Education and Sports Science, South China Normal University, Guangzhou, China
- 2 Laboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan
- 3 Laboratory of Exercise Nutrition, National Taichung University of Education, Taichung, Taiwan
- 4 Department of Anesthesiology, Far East Memorial Hospital, New Taipei, Taiwan
- 5 Department of Physical Medicine and Rehabilitation, Taipei Veterans General Hospital and National Yang Ming University, Taipei, Taiwan
- 6 Department of Chest Medicine, Taipei Veterans General Hospital and National Yang Ming University, Taipei, Taiwan
- 7 Chinese Medicine, Hualien Tzu Chi Hospital, Tzu Chi Medical Foundation, Tzu Chi University, Hualien, Taiwan
- 8 College of Sports Science and Technology, Mahidol University, Bangkok, Thailand
- 9 Department of Kinesiology and Health Education, The University of Texas at Austin, TX 78712, USA
Received: March 9, 2020 Accepted: July 7, 2020 Published: October 26, 2020https://doi.org/10.18632/aging.103763
How to Cite
Copyright: © 2020 Wu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Aerobic exercise induces oxidative stress and DNA damage, nevertheless, lowers cancer incidence. It remains unclear how genetic stability is maintained under this condition. Here, we examined the dynamic change of the tumor suppressor p16INK4a in cells of skeletal muscle among young men following 60-min of aerobic cycling at 70% maximal oxygen consumption (V̇O2max). Rg1 (5 mg, an immunostimulant ginsenoside) and placebo (PLA) were supplemented 1 h before exercise. Data from serial muscle biopsies shows unchanged p16INK4a+ cells after exercise followed by a considerable increase (+21-fold) in vastus lateralis muscle 3 h later. This increase was due to the accumulation of endothelial progenitor cells (p16INK4a+/CD34+) surrounding myofibers and other infiltrated nucleated cells (p16INK4a+/CD34-) in necrotic myofibers. During the Rg1 trial, acute increases of p16INK4a+ cells in the muscle occurred immediately after exercise (+3-fold) and reversed near baseline 3 h later. Rg1 also lowered IL-10 mRNA relative to PLA 3 h after exercise. Post-exercise increases in VEGF mRNA and CD163+ macrophages were similar for PLA and Rg1 trials. Conclusion: The marked increases in p16INK4a protein expression of endothelial progenitor cells in skeletal muscle implicates a protective mechanism for maintaining genetic stability against aerobic exercise. Rg1 accelerates resolution of the exercise-induced stress response.