Background: Contracting skeletal muscle produces reactive oxygen species (ROS) originating from both mitochondrial and cytosolic sources. The use of non-specific antioxidants, such as vitamins C and E, during exercise has produced inconsistent results in terms of exercise performance. Consequently, the effects of the mitochondrial-targeted coenzyme Q10, named Mitoquinone (MitoQ) on exercise responses are currently under investigation.
Methods: In this study, we conducted a meta-analysis to quantitatively synthesize research assessing the impact of MitoQ on aerobic endurance performance and exercise-induced oxidative damage. PubMed, Web of Science, and SCOPUS databases were used to select articles from inception to January 16th of 2024. Inclusion criteria were MitoQ supplementation must be compared with a placebo group, showing acute exercise responses in both; for crossover designs, at least 14 d of washout was needed, and exercise training can be concomitant to MitoQ or placebo supplementation if the study meets the other inclusion criteria points. The risk of bias was evaluated through the Critical Appraisal Checklist (JBI).
Results: We identified eight studies encompassing a total sample size of 188 subjects. Our findings indicate that MitoQ supplementation effectively reduces exercise-induced oxidative damage (SMD: -1.33; 95% CI: -2.24 to -0.43). Furthermore, our findings indicate that acute and/or chronic MitoQ supplementation does not improve endurance exercise performance (SMD: -0.50; 95% CI: -1.39 to 0.40) despite reducing exercise-induced oxidative stress. Notably, our sensitivity analysis reveals that MitoQ may benefit subjects with peripheral artery disease (PAD) in improving exercise tolerance.
Conclusion: While MitoQ effectively reduces exercise-induced oxidative damage, no evidence suggests that aerobic exercise performance is enhanced by either acute or chronic MitoQ supplementation. However, acute MitoQ supplementation may improve exercise tolerance in subjects with PAD. Future research should investigate whether MitoQ supplementation concurrent with exercise training (e.g., 4-16 weeks) alters adaptations induced by exercise alone and using different doses.
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http://dx.doi.org/10.1186/s40798-024-00741-5 | DOI Listing |
Ophthalmic Genet
January 2025
Department of Ophthalmology, Stein Eye Institute at UCLA, Los Angeles, California, USA.
Purpose: To assess the impact of MitoQ, a mitochondria-targeted antioxidant, on viability of human corneal endothelial cell (hCEnC) lines expressing mutations associated with congenital hereditary endothelial dystrophy (CHED) and Fuchs endothelial corneal dystrophy type 4 (FECD4).
Methods: wildtype () and mutant () hCEnC lines were created to express either variant 2 (V2) or variant 3 (V3) by stable transduction of hCEnC-21T with lentiviruses containing either or one of the following mutations: V2 (V3) mutants c.374 G>A (c.
Anim Reprod Sci
February 2025
Key Laboratory for Animal Science of National Ethnic Affairs Commission, Southwest Minzu University, Chengdu 610041, China; Key Laboratory of Qinghai-Tibetan Plateau Animal Genetic Resource Reservation and Exploitation of Ministry of Education, Southwest Minzu University, Chengdu 610041, China. Electronic address:
Low-temperature preservation of yak semen during transportation and conservation is crucial to accelerate yak breeding. The effects of low-temperature cooling on yak semen quality, however, are poorly understood. This study aimed to determine the dose-dependent effect of mitochondria-targeted antioxidant "MitoQ" on the motility, oxidative status, and mitochondrial function of yak semen during low-temperature preservation.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran. Electronic address:
Objective: The present study investigated the preventive effect of MitoQ supplementation and endurance training (ET) on the TLR4/CREB/ NF-κβ signaling pathway, antioxidant indices, and behaviors in C6-induced glioblastoma (GBM) in rats.
Methods: 60 male Wistar rats were randomly divided into five groups (n = 12); Sham, Tumor, MitoQ, ET, and MitoQ + ET. Rats in the training groups performed endurance training (5 days per week), and MitoQ at the dose of 250 µM/L daily was administered in drinking water for 8 weeks.
Theriogenology
January 2025
Laboratory of Theriogenology, College of Veterinary Medicine, Chungnam National University, Daejeon, 34134, Republic of Korea. Electronic address:
Oxidative stress caused by excess reactive oxygen species (ROS) is one of the main causes of low efficiency in in vitro production of embryos. These ROS can cause mitochondrial dysfunction and apoptosis, resulting in poor embryo development. Therefore, to prevent mitochondrial damage and apoptosis caused by ROS, we investigated the effects of mitoquinone (MitoQ), a mitochondrial-targeted antioxidant, on the in vitro culture (IVC) of porcine embryos.
View Article and Find Full Text PDFFree Radic Biol Med
November 2024
Key Laboratory of Environmental Toxicology of Anhui Higher Education Institutes, Anhui Medical University, Hefei, China; Department of Toxicology, Anhui Medical University, Hefei, China. Electronic address:
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