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Effects of High Intensity Interval Training and Aging on Cardiac Muscle Apoptosis Markers in C57bl/6 Mice Publisher



Soori R1 ; Ghram A1, 2 ; Zare Shahneh M1 ; Choobineh S1 ; Costa PB3 ; Voltarelli FA4
Authors

Source: Sport Sciences for Health Published:2021


Abstract

Background: Apoptosis is a specific form of programmed cell death that plays an important role in tissue homeostasis and also occurs during aging. In addition, exercise training may alter apoptosis-related signaling in muscles, including the cardiac muscle. However, the effects of high-intensity interval training (HIIT) on apoptosis markers in the heart have not yet been studied. Thus, the aim of the present study was to investigate the effects of HIIT on Bcl-2 and Bax expression protein levels in young and old cardiac muscles. Methods: Four and 24-month old C57BL/6J mice were used as our young adult and old groups, respectively. Animals were randomly assigned to four groups: young control (YC), young trained (YT), old control (OC), and old trained (OT). The trained groups performed HIIT 5 sessions per week for 4 weeks. RNA extraction and synthesis of cDNA was performed, and Bax and Bcl2 heart gene levels were determined by RT-PCR analysis. Results: Training induced significant increases in Bcl-2 gene expression in YT group comparing to the YC group (p = 0.010) and in OT group comparing to OC group (p = 0.002). Training induced non-significant decrease (p > 0.05) in Bax gene expression and in Bax/Bcl-2 ratio in YT group comparing to the YC group and in OT group comparing to OC group. Aging showed no significant effect in Bcl-2 gene expression, Bax gene expression, and Bax/Bcl-2 ratio in CY group comparing to the OC group and in YT group comparing to OT group (p > 0.05). Conclusion: In conclusion, 4 weeks of HIIT increased Bcl-2 level for young and old heart muscles, and no effect of aging was revealed, indicating that HIIT ameliorated anti-apoptotic signaling in the young and old heart of mice. © 2020, Springer-Verlag Italia S.r.l., part of Springer Nature.