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Purpose <p>Dietary supplements are recognized for their ability to diminish physical exercise-induced muscle damage by either enhancing antioxidants or reducing inflammation. However, no specific mechanism has been developed to reduce muscle damage as they can blunt the antioxidant response. Therefore, this study aimed to investigate the effect of ubiquinol (CoQH2) on reducing oxidative stress in the muscle overuse model.</p> Methods <p>Wistar rats (60-day-old males) were randomized into non-exercised and overuse groups, subdivided into the vehicle (control) and CoQH2-supplemented groups. After treadmill adaptation, the maximum velocity (Vmax) was measured. The overuse group was subjected to exercise for 21 successive days at three different intensities: low intensity (without inclination, 50–60&#xa0;min, 60% of Vmax), moderate intensity (10% inclination, 40–60&#xa0;min, 80% of Vmax), and high intensity (inclination -10% until exhaustion, 80% of Vmax). CoQH2 (500&#xa0;mg·kg<sup>−1</sup>) was administered daily by gavage. Twenty-four hours after the last exercise session, animals were euthanized, followed by blood and extensor digitorum longus&#xa0;harvested. The contractile measurements were measured using a force transducer acquisition system (Fort 10 WPI, Transduction Laboratories Co). Oxidative stress parameters were measured [hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), glutathione (GSH) and glutathione disulfide (GSSG), malondialdehyde-thiobarbituric acid (MDA–TBA), and protein carbonylation].</p> Results <p>CoQH<sub>2</sub> supplementation reduced feed intake, while body mass and water consumption were not altered. The maximum muscle force was significantly increased in overuse-exposed animals. Overuse protocol induced lymphoplasmacytic infiltrate and synovial cell hyperplasia in the muscle–tendon region. The overuse group exhibited elevated levels of hydrogen peroxide and protein carbonylation in both EDL muscle and serum. The antioxidant effects of CoQH₂ were only demonstrated on serum protein carbonylation, while CoQH₂ supplementation did not impact other redox state parameters.</p> Conclusion <p>These results suggest that CoQH₂ supplementation exerts a targeted antioxidant function on oxidative protein damage in serum without altering the muscle redox balance. While CoQH₂ did not affect muscle carbonylation or other redox parameters, it demonstrated protection specifically against serum protein oxidation in the overuse model. This selective antioxidant effect suggests that CoQH₂ may have specific effects, suggesting further investigation for potential therapeutic application.</p>

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Effects of solubilized ubiquinol supplementation on redox markers after experimental muscle overuse

  • 期刊论文

  • 发表日期：

    2025年5月8日

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  • Anand Thirupathi,
  • Franciane F. Vasconcellos,
  • Ana C. Macedo,
  • Luis F. B. Marqueze,
  • Amanda K. Costa,
  • João V. Peixoto,
  • Bruna Isadora Pilger,
  • Caroline B. Vaz de Paula,
  • Lúcia Noronha,
  • Eduardo B. B. Cunha,
  • Katya Naliwaiko,
  • Luiz C. Fernandes,
  • Ricardo A. Pinho

摘要

Purpose

Dietary supplements are recognized for their ability to diminish physical exercise-induced muscle damage by either enhancing antioxidants or reducing inflammation. However, no specific mechanism has been developed to reduce muscle damage as they can blunt the antioxidant response. Therefore, this study aimed to investigate the effect of ubiquinol (CoQH2) on reducing oxidative stress in the muscle overuse model.

Methods

Wistar rats (60-day-old males) were randomized into non-exercised and overuse groups, subdivided into the vehicle (control) and CoQH2-supplemented groups. After treadmill adaptation, the maximum velocity (Vmax) was measured. The overuse group was subjected to exercise for 21 successive days at three different intensities: low intensity (without inclination, 50–60 min, 60% of Vmax), moderate intensity (10% inclination, 40–60 min, 80% of Vmax), and high intensity (inclination -10% until exhaustion, 80% of Vmax). CoQH2 (500 mg·kg−1) was administered daily by gavage. Twenty-four hours after the last exercise session, animals were euthanized, followed by blood and extensor digitorum longus harvested. The contractile measurements were measured using a force transducer acquisition system (Fort 10 WPI, Transduction Laboratories Co). Oxidative stress parameters were measured [hydrogen peroxide (H2O2), glutathione (GSH) and glutathione disulfide (GSSG), malondialdehyde-thiobarbituric acid (MDA–TBA), and protein carbonylation].

Results

CoQH2 supplementation reduced feed intake, while body mass and water consumption were not altered. The maximum muscle force was significantly increased in overuse-exposed animals. Overuse protocol induced lymphoplasmacytic infiltrate and synovial cell hyperplasia in the muscle–tendon region. The overuse group exhibited elevated levels of hydrogen peroxide and protein carbonylation in both EDL muscle and serum. The antioxidant effects of CoQH₂ were only demonstrated on serum protein carbonylation, while CoQH₂ supplementation did not impact other redox state parameters.

Conclusion

These results suggest that CoQH₂ supplementation exerts a targeted antioxidant function on oxidative protein damage in serum without altering the muscle redox balance. While CoQH₂ did not affect muscle carbonylation or other redox parameters, it demonstrated protection specifically against serum protein oxidation in the overuse model. This selective antioxidant effect suggests that CoQH₂ may have specific effects, suggesting further investigation for potential therapeutic application.