Abstract
Background and Aim: Mitochondria play an important role in signaling and metabolic
pathways in skeletal muscle. In this study, the effects of MitoQ supplementation alone and
in combination with endurance training (ET) or high-intensity interval training (HIIT) were
investigated in relation to the process of mitochondrial quality control in the gastrocnemius
muscle of male rats.
Methods: Animals were assigned into 6 groups (n = 7): Control, MitoQ, ET, ET + MitoQ, HIIT,
and HIIT + MitoQ. The gene and protein expression were quantified using real-time polymerase
chain reaction (2-ΔΔCT) and Western blot analysis, respectively. Statistical analysis was performed
using one-way analysis of variance.
Results: ET significantly increased protein expression of dynamin-related protein 1 (DRP1) and
mitofusin1 (MFN1) and gene expression of optic atrophy Type 1 (Opa1) in skeletal muscle, when
compared to the control group (p < 0.001). HIIT only increased MFN1 protein expression compared
to the control group (p < 0.0001). MitoQ in combination with HIIT significantly increased protein
expression of DRP1 and MFN1 compared to MitoQ alone (p < 0.01).
Conclusion: In sum, exercise training can affect mitochondrial dynamics by changing the factors
involved in the fission and fusion process, and ET can improve training capacity in skeletal muscle
by modulating expression of OPA1 and MFN1. While MitoQ supplementation alone did not
significantly alter the mitochondrial fission-fusion process, its combination with HIIT appeared
to elevate the expression of DRP1, suggesting a potential synergistic effect that warrants further
investigation. Future studies should delve into the mechanisms by which MitoQ and exerciseinduced
stress affect mitochondrial quality control, particularly in the context of redox modulation
and signaling pathways that govern mitochondrial plasticity.
Relevance for Patients: Combining MitoQ with exercise training may enhance mitochondrial
function, potentially improving muscle health in patients.
DOI: http://doi.org/10.36922/jctr.24.00044
Author affiliation
1Physiology Research Center, Institute of Neuropharmacology, Department of Physiology and Pharmacology, Afzalipour School of Medicine,
Kerman University of Medical Sciences, Kerman, Iran
2Cardiovascular Research Center, Institute of Basic and Clinical Physiology Sciences,
Kerman University of Medical Sciences, Kerman, Iran
3Endocrinology and Metabolism Research Center, Institute of Basic and Clinical
Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran
4Gastroenterology and Hepatology Research Center, Institute of
Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran
5Department of Physical Education, Faculty of
Medicine and Physiology Research Center, Kerman University of Medical Sciences, Kerman, Iran
*Corresponding author:
Beydolah Shahouzehi
Gastroenterology and Hepatology Research
Center, Institute of Basic and Clinical
Physiology Sciences, Kerman University of
Medical Sciences, Kerman, Iran
Email: bshahouzehi@gmail.com
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