Article Title



Zach J. Hutchison, McKenna A. Tharpe, Alex M. Barnett, Braxton A. Linder, Meral N. Culver, Michael D. Brown, FACSM, Andreas N. Kavazis, FACSM, Austin T. Robinson. Auburn University, Auburn, AL.

Background: Cardiovascular disease (CVD) is characterized by endothelial dysfunction and heightened oxidative stress. Additionally, there are well documented racial disparities in endothelial function and CVD. MitoQ, a mitochondrial specific antioxidant, improves vascular function in rodents and healthy older adults by scavenging excess reactive oxygen species (ROS). However, the role of MitoQ in attenuating racial disparities in vascular function is unknown. Therefore, as part of an ongoing clinical trial (NCT04334135), we evaluated endothelial function and ROS in healthy adults pre- and post-acute MitoQ (or placebo) supplementation and performed a preliminary racial comparison. Methods: Seventeen participants (eight males, age: 28±10 years, BMI 25±4 kg/m2, BP 110±12/66±6 mmHg, Mean±SD) were randomly assigned to placebo or MitoQ (100-160mg, depending on body mass). Participants reported as White, Black, or biracial based on parental race. Using a cross design, experimental sessions were separated by a ≥72-hour washout period. Measures were performed before and 60 minutes after ingestion of MitoQ or placebo capsules. We assessed brachial blood pressure (oscillometric) and brachial artery flow mediated dilation (FMD) via ultrasound. We placed an intravenous catheter to assess whole blood ROS levels via electronic paramagnetic resonance. To investigate treatment x time interactions, we performed 2-way ANOVA and ANCOVA. Results: Irrespective of treatment, systolic blood pressure decreased with time (p<0.01). We did not find treatment x time interactions for brachial FMD % (pre placebo: 7.1±4% to post placebo: 6.4±4% vs pre MitoQ: 6.0±4% to post MitoQ: 6.9±4%, p=0.61), brachial shear stress area under the curve (AUC) during reactive hyperemia (p=0.30), or brachial FMD normalized to shear AUC (p=0.46). Additionally, there was not a treatment x time interaction for blood ROS (p=0.67). We identified a trend for a treatment x race interaction (p=0.058) for [post-pre] ∆FMD whereby MitoQ resulted in a negative ∆FMD only in White adults. However, when we included pre-treatment FMD as a covariate for ∆FMD, this trend was attenuated (p=0.193). Conclusion: While additional data are needed, our preliminary findings indicate that acute MitoQ supplementation does not influence vascular function or oxidative stress in healthy adults.

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