Effect of six weeks ubiquinol supplementation on mitochondrial respiratory function and exercise capacity in healthy males

Jarred P Acton; Nehal S Alsharif; Jack W Bond; Stuart P Cocksedge; Abbie G Mclellan; Donald L Peden; Mark P Funnell; Hannah F Dugdale; Lewis J James; Richard A Ferguson; Tom Clifford; Stephen J Bailey

doi:10.1007/s00421-026-06275-w

Effect of six weeks ubiquinol supplementation on mitochondrial respiratory function and exercise capacity in healthy males

Jarred P Acton
, Nehal S Alsharif
, Jack W Bond
, Stuart P Cocksedge
, Abbie G Mclellan
, Donald L Peden
, Mark P Funnell
, Hannah F Dugdale
, Lewis J James
, Richard A Ferguson
, Tom Clifford
, Stephen J Bailey

Centre for Healthcare and Community Transformation

Loughborough University
King Abdulaziz University
Norwegian School of Sport Sciences
NIHR Nottingham Biomedical Research Centre
NIHR ARC East Midlands
University Hospitals of Leicester NHS Trust
University of Leicester

Research output: Contribution to journal › Article › peer-review

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Abstract

Coenzyme Q10 (CoQ ) is an integral component of the mitochondrial electron transfer system. Most studies have administered the oxidised form of CoQ (ubiquinone) and observed no effects on mitochondrial respiratory function or endurance exercise performance. The reduced form of CoQ , ubiquinol (UQH ), has greater bioavailability than ubiquinone, but the effects of UQH supplementation on mitochondrial respiratory function and exercise capacity are unclear. Fifty-four healthy, recreationally active males were randomised to receive either 300 mg·day UQH or placebo (PLA) for 6 weeks in a double-blind independent-group design. Before and after the supplementation period, skeletal muscle mitochondrial respiration variables and protein content of the mitochondrial leak proteins, adenine nucleotide translocase1 + 2 (ANT1 + 2) and uncoupling protein-3 (UCP-3), were assessed. In addition, participants completed a severe-intensity cycle test to exhaustion to assess time to the limit of tolerance (T ) and oxygen uptake (V̇O ) kinetics. Compared to pre-supplementation and PLA, UQH supplementation increased plasma [CoQ ] (P < 0.05), and lowered inverse respiratory control ratio (Pre-PLA: 0.064 ± 0.034 vs. Post-PLA: 0.072 ± 0.026; Pre- UQH : 0.073 ± 0.039 vs. Post-UQH : 0.044 ± 0.019; P < 0.05), suggestive of improved oxidative phosphorylation coupling efficiency. There were no differences in ANT1 + 2 or UCP-3 protein content post-supplementation compared to pre-supplementation between groups (P > 0.05). End-exercise V̇O , change in V̇O between 2 min and end-exercise, and T were not different between groups post-supplementation (P > 0.05). Six-weeks UQH supplementation increased plasma [CoQ ] and oxidative phosphorylation coupling efficiency, but did not alter mitochondrial leak proteins, T or V̇O kinetics during severe-intensity exercise in healthy, active males. [Abstract copyright: © 2026. The Author(s).]

Original language	English
Pages (from-to)	(In-Press)
Number of pages	16
Journal	European Journal of Applied Physiology
Volume	(In-Press)
Early online date	6 Jun 2026
DOIs	https://doi.org/10.1007/s00421-026-06275-w
Publication status	E-pub ahead of print - 6 Jun 2026

Bibliographical note

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted CC BY
use, you will need to obtain permission directly from the copyright holder.

Funding

We are thankful to all participants that volunteered to take part in the study. This is a summary of independent research match funded by Kaneka Pharma Europe and Loughborough University, carried out at the National Institute for Health and Care Research (NIHR) Leicester Biomedical Research Centre (BRC). The views expressed are those of the author(s) and not necessarily those of the NIHR or the UK Department of Health of Health and Social Care.

Funders
National Institute for Health and Care Research
Loughborough University
NIHR Imperial Biomedical Research Centre
National Institute for Health Research (NIHR) Leicester Biomedical Research Centre

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Coenzyme Q10
Dietary supplement
Exercise performance
Mitochondrial respiratory efficiency
V̇O kinetics

ASJC Scopus subject areas

Orthopedics and Sports Medicine
Public Health, Environmental and Occupational Health
Physiology (medical)

Access to Document

10.1007/s00421-026-06275-wLicence: CC BY

Cocksedge2026VoRFinal published version, 2.29 MBLicence: CC BY

Cite this

Acton, J. P., Alsharif, N. S., Bond, J. W., Cocksedge, S. P., Mclellan, A. G., Peden, D. L., Funnell, M. P., Dugdale, H. F., James, L. J., Ferguson, R. A., Clifford, T., & Bailey, S. J. (2026). Effect of six weeks ubiquinol supplementation on mitochondrial respiratory function and exercise capacity in healthy males. European Journal of Applied Physiology, (In-Press), (In-Press). Advance online publication. https://doi.org/10.1007/s00421-026-06275-w

Acton, JP, Alsharif, NS, Bond, JW, Cocksedge, SP, Mclellan, AG, Peden, DL, Funnell, MP, Dugdale, HF, James, LJ, Ferguson, RA, Clifford, T & Bailey, SJ 2026, 'Effect of six weeks ubiquinol supplementation on mitochondrial respiratory function and exercise capacity in healthy males', European Journal of Applied Physiology, vol. (In-Press), pp. (In-Press). https://doi.org/10.1007/s00421-026-06275-w

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abstract = "Coenzyme Q10 (CoQ ) is an integral component of the mitochondrial electron transfer system. Most studies have administered the oxidised form of CoQ (ubiquinone) and observed no effects on mitochondrial respiratory function or endurance exercise performance. The reduced form of CoQ , ubiquinol (UQH ), has greater bioavailability than ubiquinone, but the effects of UQH supplementation on mitochondrial respiratory function and exercise capacity are unclear. Fifty-four healthy, recreationally active males were randomised to receive either 300 mg·day UQH or placebo (PLA) for 6 weeks in a double-blind independent-group design. Before and after the supplementation period, skeletal muscle mitochondrial respiration variables and protein content of the mitochondrial leak proteins, adenine nucleotide translocase1 + 2 (ANT1 + 2) and uncoupling protein-3 (UCP-3), were assessed. In addition, participants completed a severe-intensity cycle test to exhaustion to assess time to the limit of tolerance (T ) and oxygen uptake ({\.V}O ) kinetics. Compared to pre-supplementation and PLA, UQH supplementation increased plasma [CoQ ] (P < 0.05), and lowered inverse respiratory control ratio (Pre-PLA: 0.064 ± 0.034 vs. Post-PLA: 0.072 ± 0.026; Pre- UQH : 0.073 ± 0.039 vs. Post-UQH : 0.044 ± 0.019; P < 0.05), suggestive of improved oxidative phosphorylation coupling efficiency. There were no differences in ANT1 + 2 or UCP-3 protein content post-supplementation compared to pre-supplementation between groups (P > 0.05). End-exercise {\.V}O , change in {\.V}O between 2 min and end-exercise, and T were not different between groups post-supplementation (P > 0.05). Six-weeks UQH supplementation increased plasma [CoQ ] and oxidative phosphorylation coupling efficiency, but did not alter mitochondrial leak proteins, T or {\.V}O kinetics during severe-intensity exercise in healthy, active males. [Abstract copyright: {\textcopyright} 2026. The Author(s).]",

keywords = "Coenzyme Q10, Dietary supplement, Exercise performance, Mitochondrial respiratory efficiency, {\.V}O kinetics",

author = "Acton, \{Jarred P\} and Alsharif, \{Nehal S\} and Bond, \{Jack W\} and Cocksedge, \{Stuart P\} and Mclellan, \{Abbie G\} and Peden, \{Donald L\} and Funnell, \{Mark P\} and Dugdale, \{Hannah F\} and James, \{Lewis J\} and Ferguson, \{Richard A\} and Tom Clifford and Bailey, \{Stephen J\}",

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AU - Acton, Jarred P

AU - Alsharif, Nehal S

AU - Bond, Jack W

AU - Cocksedge, Stuart P

AU - Mclellan, Abbie G

AU - Peden, Donald L

AU - Funnell, Mark P

AU - Dugdale, Hannah F

AU - James, Lewis J

AU - Ferguson, Richard A

AU - Clifford, Tom

AU - Bailey, Stephen J

N1 - Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted CC BY use, you will need to obtain permission directly from the copyright holder.

PY - 2026/6/6

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N2 - Coenzyme Q10 (CoQ ) is an integral component of the mitochondrial electron transfer system. Most studies have administered the oxidised form of CoQ (ubiquinone) and observed no effects on mitochondrial respiratory function or endurance exercise performance. The reduced form of CoQ , ubiquinol (UQH ), has greater bioavailability than ubiquinone, but the effects of UQH supplementation on mitochondrial respiratory function and exercise capacity are unclear. Fifty-four healthy, recreationally active males were randomised to receive either 300 mg·day UQH or placebo (PLA) for 6 weeks in a double-blind independent-group design. Before and after the supplementation period, skeletal muscle mitochondrial respiration variables and protein content of the mitochondrial leak proteins, adenine nucleotide translocase1 + 2 (ANT1 + 2) and uncoupling protein-3 (UCP-3), were assessed. In addition, participants completed a severe-intensity cycle test to exhaustion to assess time to the limit of tolerance (T ) and oxygen uptake (V̇O ) kinetics. Compared to pre-supplementation and PLA, UQH supplementation increased plasma [CoQ ] (P < 0.05), and lowered inverse respiratory control ratio (Pre-PLA: 0.064 ± 0.034 vs. Post-PLA: 0.072 ± 0.026; Pre- UQH : 0.073 ± 0.039 vs. Post-UQH : 0.044 ± 0.019; P < 0.05), suggestive of improved oxidative phosphorylation coupling efficiency. There were no differences in ANT1 + 2 or UCP-3 protein content post-supplementation compared to pre-supplementation between groups (P > 0.05). End-exercise V̇O , change in V̇O between 2 min and end-exercise, and T were not different between groups post-supplementation (P > 0.05). Six-weeks UQH supplementation increased plasma [CoQ ] and oxidative phosphorylation coupling efficiency, but did not alter mitochondrial leak proteins, T or V̇O kinetics during severe-intensity exercise in healthy, active males. [Abstract copyright: © 2026. The Author(s).]

AB - Coenzyme Q10 (CoQ ) is an integral component of the mitochondrial electron transfer system. Most studies have administered the oxidised form of CoQ (ubiquinone) and observed no effects on mitochondrial respiratory function or endurance exercise performance. The reduced form of CoQ , ubiquinol (UQH ), has greater bioavailability than ubiquinone, but the effects of UQH supplementation on mitochondrial respiratory function and exercise capacity are unclear. Fifty-four healthy, recreationally active males were randomised to receive either 300 mg·day UQH or placebo (PLA) for 6 weeks in a double-blind independent-group design. Before and after the supplementation period, skeletal muscle mitochondrial respiration variables and protein content of the mitochondrial leak proteins, adenine nucleotide translocase1 + 2 (ANT1 + 2) and uncoupling protein-3 (UCP-3), were assessed. In addition, participants completed a severe-intensity cycle test to exhaustion to assess time to the limit of tolerance (T ) and oxygen uptake (V̇O ) kinetics. Compared to pre-supplementation and PLA, UQH supplementation increased plasma [CoQ ] (P < 0.05), and lowered inverse respiratory control ratio (Pre-PLA: 0.064 ± 0.034 vs. Post-PLA: 0.072 ± 0.026; Pre- UQH : 0.073 ± 0.039 vs. Post-UQH : 0.044 ± 0.019; P < 0.05), suggestive of improved oxidative phosphorylation coupling efficiency. There were no differences in ANT1 + 2 or UCP-3 protein content post-supplementation compared to pre-supplementation between groups (P > 0.05). End-exercise V̇O , change in V̇O between 2 min and end-exercise, and T were not different between groups post-supplementation (P > 0.05). Six-weeks UQH supplementation increased plasma [CoQ ] and oxidative phosphorylation coupling efficiency, but did not alter mitochondrial leak proteins, T or V̇O kinetics during severe-intensity exercise in healthy, active males. [Abstract copyright: © 2026. The Author(s).]

KW - Coenzyme Q10

KW - Dietary supplement

KW - Exercise performance

KW - Mitochondrial respiratory efficiency

KW - V̇O kinetics

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DO - 10.1007/s00421-026-06275-w

M3 - Article

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SN - 1439-6319

VL - (In-Press)

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JO - European Journal of Applied Physiology

JF - European Journal of Applied Physiology

ER -

Effect of six weeks ubiquinol supplementation on mitochondrial respiratory function and exercise capacity in healthy males

Abstract

Bibliographical note

Funding

UN SDGs

Keywords

ASJC Scopus subject areas

Access to Document

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