Document Type : Original Article
Authors
1 Department of Sport Physiology, CT. C., Islamic Azad University, Tehran, Iran
2 Department of Physical Education and Sport Sciences, Dez. C., Islamic Azad University, Dezful, Iran
3 Department of Physical Education and Sport Sciences, Khod. C., Islamic Azad University, Khodabandeh, Iran
Abstract
Background: One global issue is population ageing and its associated consequences. This study aims to examine how endurance training and MitoQ supplementation can affect atrophy and mitochondrial dynamic signaling in the heart tissue of old rats.
Methods: In the present study, 28 male Wistar rats were divided into four groups, each with seven rats. The groups were: control, endurance training, MitoQ supplementation, and endurance training combined with MitoQ supplementation. In the training groups, the rats performed endurance training 5 days a week for 8 weeks. Also, MitoQ supplementation was administered in drinking water (250 μM) for 8 weeks. Western blotting and the real-time PCR method (2-DDCt) were used to measure the variables. The data were analyzed statistically using two-way ANOVA.
Results: The group that received ET+MitoQ had a much lower level of NF-κB gene expression than the control group, which was a significant difference (p = 0.04). Also, this group had significantly lower MuRF gene expression than the control group (p = 0.002). The ET group also showed significantly reduced MuRF gene expression compared to the control group (p = 0.04). In addition, the ET group showed a significant decrease in FIS1 protein expression compared to the control group (p = 0.04).
Conclusion: The combination of exercise training and MitoQ can have anti-inflammatory and subsequently anti-atrophic effects on cardiac tissue in aged rats. In addition, MitoQ supplementation alone may change mitochondrial dynamics in aged heart tissue. An increase in Drp1 expression (removing damaged mitochondria) and a reduction in Mfn1 expression (reducing oxidative stress) can have a protective effect on the aged cardiac muscle.
Keywords
Main Subjects
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