Combination of Coenzyme Q10 Intake and Moderate Physical Activity Counteracts Mitochondrial Dysfunctions in a SAMP8 Mouse Model
Open accessAbstract
Aging skeletal muscles are characterized by a progressive decline in muscle mass and muscular strength. Such muscular dysfunctions are usually associated with structural and functional alterations of skeletal muscle mitochondria. The senescence‐accelerated mouse‐prone 8 (SAMP8) model, characterized by premature aging and high degree of oxidative stress, was used to investigate whether a combined intervention with mild physical exercise and ubiquinol supplementation was able to improve mitochondrial function and preserve skeletal muscle health during aging. 5‐month‐old SAMP8 mice, in a presarcopenia phase, have been randomly divided into 4 groups (n = 10): untreated controls and mice treated for two months with either physical exercise (0.5 km/h, on a 5% inclination, for 30 min, 5/7 days per week), ubiquinol 10 (500 mg/kg/day), or a combination of exercise and ubiquinol. Two months of physical exercise significantly increased mitochondrial damage in the muscles of exercised mice when compared to controls. On the contrary, ubiquinol and physical exercise combination significantly improved the overall status of the skeletal muscle, preserving mitochondrial ultrastructure and limiting mitochondrial depolarization induced by physical exercise alone. Accordingly, combination treatment while promoting mitochondrial biogenesis lowered autophagy and caspase 3‐dependent apoptosis. In conclusion, the present study shows that ubiquinol supplementation counteracts the deleterious effects of physical exercise‐derived ROS improving mitochondrial functionality in an oxidative stress model, such as SAMP8 in the presarcopenia phase.
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Improvements from ubiquinol supplementation can be further enhanced by combination with physical exercise in SAMP8 mouse models.
“Finally, these improvements can be further enhanced by the combination of physical exercise and ubiquinol supplementation, as recently reported in in vivo studies carried out on SAMP8 mouse models [96].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [96]
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- Authors
- Andreani, C., Bartolacci, C., Guescini, M., Battistelli, M., Stocchi, V., Orlando, F., Provinciali, M., Amici, A., Marchini, C., Tiano, L., Orlando, P., & Silvestri, S.
- Affiliations
- Università di Camerino (IT)
- University of Urbino (IT)
- Istituto Nazionale di Riposo e Cura per Anziani (IT)
- Marche Polytechnic University (IT)
- Corresponding author
- Orlando, P.
- ORCID
- Venue
- Oxidative Medicine and Cellular Longevity
- Publisher
- Wiley
- Published
- 2018-01
- Volume
- 2018
- Issue
- 1
- Pages
- 8936251-8936251
- ISSN
- 1942-0994 (ISSN-L)
- 1942-0900
- PMC
- PMC6220380
- OpenAlex
- W2898337428
- Cited by
- 37
- References
- 100
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 4 · 2023: 4 · 2022: 6 · 2021: 4 · 2020: 3 · 2019: 7 · 2017: 1
- FWCI
- 1.25
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Università Politecnica delle Marche (Università Politecnica delle Marche) (submittedVersion)
- CINECA IRIS Institutional Research information system (University of Urbino) (submittedVersion, cc-by-nc-nd)
- Unicam Scientific Publications (University of Camerino) (submittedVersion, other-oa)
- Funders
- Fondazione Umberto Veronesi
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Keywords
- coenzyme Q10, moderate-intensity exercise, mitochondrial dysfunction, skeletal muscle aging, pre-sarcopenia, oxidative stress, mitochondrial biogenesis, autophagy, caspase-3-dependent apoptosis, mitochondrial depolarization, reactive oxygen species
- MeSH terms
- Animals, Autophagy, Cell Survival, Disease Models, Animal, Flow Cytometry, Mitochondria, Muscle, Physical Conditioning, Animal, Ubiquinone, Blotting, Western, Oxidative Stress, Mitochondrial Diseases, Mice
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