New Findings r What is the central question of this study?What is the effect of acute endurance exercise on circulating angiogenic cell (CAC) and microparticle (MP)

MicroRNAs (miRNAs) are short, noncoding RNAs that influence biological processes by regulating gene expression after transcription. It was recently discovered that miRNAs are released into the circulation (ci-miRNAs) where they are highly stable and can act as intercellular messengers to affect physiological processes. This review provides a comprehensive summary of the studies to date that have investigated the effects of acute exercise and exercise training on ci-miRNAs in humans. Findings indicate that specific ci-miRNAs are altered in response to different protocols of acute and chronic exercise in both healthy and diseased populations. In some cases, altered ci-miRNAs correlate with fitness and health parameters, suggesting causal mechanisms by which ci-miRNAs may facilitate adaptations to exercise training. However, strong data supporting such mechanisms are lacking. Thus, a purpose of this review is to guide future studies by discussing current and novel proposed roles for ci-miRNAs in adaptations to exercise training. In addition, substantial, fundamental gaps in the field need to be addressed. The ultimate goal of this research is that an understanding of the roles of ci-miRNAs in physiological adaptations to exercise training will one day translate to therapeutic interventions.

Antioxidants have been shown to improve endothelial function and cardiovascular outcomes. However, the effects of antioxidants on exercise training-induced vascular adaptations remain elusive. General acting antioxidants combined with exercise have not impacted circulating angiogenic cells (CACs). We investigated whether mitochondria-specific antioxidant (MitoQ) supplementation would affect the response to 3 weeks of endurance exercise training on CD3 , CD3 /CD31 , CD14 /CD31 , CD31 , CD34 /VEGFR2 and CD62E peripheral blood mononuclear cells (PBMCs), muscle mitochondrial capacity, and maximal oxygen uptake (VO2 max ) in healthy men aged 22.1 ± 0.7 years, with a body mass index of 26.9 ± 0.9 kg m , and 24.8 ± 1.3% body fat. Analysis of main effects revealed that training induced 33, 105 and 285% increases in CD14 /CD31 , CD62E and CD34 /VEGFR2 CACs, respectively, and reduced CD3 /CD31 PBMCs by 14%. There was no effect of MitoQ on CAC levels. Also independent of MitoQ supplementation, exercise training significantly increased quadriceps muscle mitochondrial capacity by 24% and VO2 max by roughly 7%. In conclusion, endurance exercise training induced increases in multiple CAC types, and this adaptation is not modified by MitoQ supplementation. Furthermore, we demonstrate that a mitochondrial-targeted antioxidant does not influence skeletal muscle or whole-body aerobic adaptations to exercise training.

Endothelial dysfunction and inflammation are characteristics of subclinical atherosclerosis and may increase through progressive menopausal stages. Evaluating endothelial responses to acute exercise can reveal underlying dysfunction not apparent in resting conditions. The purpose of this study was to investigate markers of endothelial function and inflammation before and after acute exercise in healthy low-active perimenopausal (PERI) and late postmenopausal (POST) women. Flow-mediated dilation (FMD), CD31/CD42b and CD62E endothelial microparticles (EMPs), and the circulating inflammatory factors monocyte chemoattractant protein 1 (MCP-1), interleukin 8 (IL-8), and tumor necrosis factor-α (TNF-α) were measured before and 30 min after acute exercise. Before exercise, FMD was not different between groups (PERI: 6.4 ± 0.9% vs. POST: 6.5 ± 0.8%, P = 0.97); however, after acute exercise PERI tended to improve FMD (8.5 ± 0.9%, P = 0.09), whereas POST did not (6.2 ± 0.8%, P = 0.77). Independent of exercise, we observed transient endothelial dysfunction in POST with repeated FMD measures. There was a group × exercise interaction for CD31/CD42b EMPs (P = 0.04), where CD31/CD42b EMPs were similar before exercise (PERI: 57.0 ± 6.7 EMPs/μl vs. POST: 58.5 ± 5.3 EMPs/μl, P = 0.86) but were higher in POST following exercise (PERI: 48.2 ± 6.7 EMPs/μl vs. POST: 69.4 ± 5.3 EMPs/μl, P = 0.023). CD62E EMPs were lower in PERI compared with POST before exercise (P < 0.001) and increased in PERI (P = 0.04) but did not change in POST (P = 0.68) in response to acute exercise. After acute exercise, MCP-1 (P = 0.055), TNF-α (P = 0.02), and IL-8 (P < 0.001) were lower in PERI but only IL-8 decreased in POST (P < 0.001). Overall, these data suggest that perimenopausal and late postmenopausal women display different endothelial and inflammatory responses to acute exercise.

Maximal exercise induces a robust CAC response encompassing both progenitor and nonprogenitor cell types, with these effects differing between men and women for CD62E and CD14/CD31 cell types and the potential influence of menstrual cycle phase and contraceptive use.