Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, C054

Oral Communications

Effects of Mitochondrial Antioxidant (MitoQ) Supplementation and Endurance Exercise Training on Endothelial Microparticles and Endothelial Cell Integrity

D. D. Shill1,2, T. B. Willingham3,2, W. M. Southern2, K. K. McCully2, J. M. Hagberg1, N. T. Jenkins2

1. School of Public Health - Department of Kinesiology, University of Maryland, College Park, Maryland, United States. 2. Department of Kinesiology, University of Georgia, Athens, Georgia, United States. 3. NHLBI, National Institutes of Health, Bethesda, Maryland, United States.

Antioxidants and chronic exercise are viable options to mitigate deleterious reactive oxygen species (ROS) and improve endothelial function, but the efficacy of non-specific antioxidants to elicit beneficial vascular effects, alone or during exercise training, remains inconsistent. MitoQ, a mitochondria-specific antioxidant, has been shown to elicit favorable changes in the vasculature [1, 2]. The impact of chronic exercise with and without MitoQ on training-induced vascular adaptations, and related functional consequences in the endothelium, are not fully understood. Endothelial microparticles (EMPs) are shed from the endothelium in response to activation and apoptosis, facilitating intercellular communication. Thus, using in vivo and in vitro complementary studies, we investigated the effects of MitoQ on endothelial cell integrity. As previously reported [3], 20 healthy men (22.1±0.7 yr) performed 3 weeks of aerobic cycle training at 50-70% maximal oxygen uptake (VO2max) for 45-60 min, with and without MitoQ supplementation (n=10/group). For the current study, blood samples were analyzed for plasma levels of EMPs derived from apoptotic endothelial cells (CD31+/CD42b-) and two subpopulations of activated endothelial cells (CD54+/CD45-, CD62E+). In vitro, ROS were assessed in human umbilical vein endothelial cells pretreated with and without MitoQ before exposure to Antimycin-A for 24hr. Data are presented as mean ± SEM and were analyzed using a 2-factor repeated measures ANOVA. A group x time interaction was observed for EMPs derived from apoptotic endothelial cells after training (P=0.06). MitoQ supplementation reduced CD31+/CD42b- EMPs by 27% after training (18.1±2.7 to 13.3±1.8 EMPs/µl; n=10; P=0.06), whereas no change was observed in the placebo group (14.0±2.0 to 16.1±2.4 EMPs/µl; n=10; P>0.05). Circulating levels of CD54+/CD45- EMPs, derived from activated endothelial cells, were unaltered by exercise training or MitoQ administration (P>0.05). Independent of MitoQ supplementation, circulating levels of CD62E+ EMPs from activated endothelial cells were reduced by 30% (70.6±9.3 to 49.8±6.3 EMPs/µl; n=20; P<0.05 for main effect of training). In vitro, pretreating endothelial cells with MitoQ reduced ROS production by 15% (n=3; P<0.05). In summary, short-term endurance exercise training reduces endothelial cell activation with or without MitoQ supplementation. The addition of MitoQ supplementation during training may increase endothelial integrity by reducing endothelial cell apoptosis. MitoQ reduces Antimycin-A induced ROS production in endothelial cells.

Where applicable, experiments conform with Society ethical requirements