Iranian Journal of Basic Medical Sciences (Aug 2022)

Effects of different-intensity exercise and creatine supplementation on mitochondrial biogenesis and redox status in mice

  • Seyhan Taskin,
  • Hakim Celik,
  • Seniz Demiryurek,
  • Sibel Turedi,
  • Abdullah Taskin

DOI
https://doi.org/10.22038/ijbms.2022.65047.14321
Journal volume & issue
Vol. 25, no. 8
pp. 1009 – 1015

Abstract

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Objective(s): Dietary supplementation combined with exercise may potentiate the beneficial effects of exercise by reducing exercise-induced oxidative stress and improving mitochondrial quality and capacity. In this study, the effects of creatine monohydrate (CrM) supplementation with low and high-intensity exercise on mitochondrial biogenesis regulators, Nrf2 anti-oxidant signaling pathway and muscle damage levels were investigated. Materials and Methods: Balb/c male mice were divided into six experimental groups: control, control+CrM, high-intensity exercise, high-intensity exercise+CrM, low-intensity exercise, and low-intensity exercise+CrM. Mice were given CrM supplementation and at the same time, low and high-intensity exercise was applied to the groups on the treadmill at 30min/5day/8week. Then, mitochondrial biogenesis marker (PGC-1α, NRF-1, TFAM), Nrf2 and HO-1 protein expressions, total oxidant-anti-oxidant status level, and histopathological changes were investigated in serum and muscle tissue. Results: Exercise intensity and CrM supplementation were found to be effective factors in mitochondrial biogenesis induction via the PGC-1α signaling pathway. Nrf2 and HO-1 protein levels increased with exercise intensity, and this result was directly related to serum oxidative stress markers. In addition, CrM supplementation was effective in reducing exercise-induced muscle damage. Conclusion: This combination induced skeletal muscle adaptations, including mitochondrial biogenesis and enhanced anti-oxidant reserves. This synergistic effect of dietary supplementation with low-intensity exercise may be valuable as a complement to treatment, especially in diseases caused by mitochondrial dysfunction.

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