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)

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.

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.

Adipose tissue (AT)-derived cytokines are proposed to contribute to obesity-associated vascular insulin resistance. We tested the hypothesis that voluntary physical activity and diet restriction-induced maintenance of body weight would both result in decreased AT inflammation and concomitant improvements in insulin-stimulated vascular relaxation in the hyperphagic, obese Otsuka Long-Evans Tokushima fatty (OLETF) rat. Rats (aged 12 wk) were randomly assigned to sedentary (SED; n ϭ 10), wheel running (WR; n ϭ 10), or diet restriction (DR; n ϭ 10; fed 70% of SED) for 8 wk. WR and DR rats exhibited markedly lower adiposity (7.1 Ϯ 0.4 and 15.7 Ϯ 1.1% body fat, respectively) relative to SED (27 Ϯ 1.2% body fat), as well as improved blood lipid profiles and systemic markers of insulin resistance. Reduced adiposity in both WR and DR was associated with decreased AT mRNA expression of inflammatory genes (e.g., MCP-1, TNF-␣, and IL-6) and markers of immune cell infiltration (e.g., CD8, CD11c, and F4/80). The extent of these effects were most pronounced in visceral AT compared with subcutaneous and periaortic AT. Markers of inflammation in brown AT were upregulated with WR but not DR. In periaortic AT, WR-and DR-induced reductions in expression and secretion of cytokines were accompanied with a more atheroprotective gene expression profile in the adjacent aortic wall. WR, but not DR, resulted in greater insulin-stimulated relaxation in the aorta; an effect that was, in part, mediated by a decrease in insulin-induced endothelin-1 activation in WR aorta. Collectively, we show in OLETF rats that lower adiposity leads to less AT and aortic inflammation, as well as an exercise-specific improvement in insulin-stimulated vasorelaxation. calorie restriction; exercise; gene expression; inflammation; obesity MORE THAN ONE-THIRD OF AMERICANS are obese (38), and the causes underlying the obesity epidemic appear to be largely related to physical inactivity and overnutrition, a set of behaviors increasingly prevalent in our society (5-7, 11, 57). Cumulative evidence indicates that obesity is an important contributor to the development of whole body insulin resistance, Type 2 diabetes, and cardiovascular disease (21). A critical link between obesity and its associated metabolic and cardiovascular diseases is thought to be chronic low-grade systemic inflammation (21). In this regard, recent studies implicate adipose tissue (AT) as a local and systemic source of inflammatory cytokines that may be involved in the instigation of vascular insulin resistance and atherosclerosis associated with obesity (12, 13, 19, 20, 31, 33-36, 45, 46, 51, 55, 56). Indeed, excessive lipid accumulation and enlargement of adipocytes in obesity are associated with infiltration of immune cells into AT, contributing to AT inflammation and subsequent secretion of proinflammatory cytokines (52). A deeper understanding of the influence of lifestyle modifications on AT inflammation and vascular insulin resistance may lead to more effective strategies aimed at prevent...

Circulating microparticles (MPs) are biological vectors of information within the cardiovascular system that elicit both deleterious and beneficial effects on the vasculature. Acute exercise has been shown to alter MP concentrations, probably through a shear stress-dependent mechanism, but evidence is limited. Therefore, we investigated the effect of exercise intensity on plasma levels of CD34 and CD62E MPs in young, healthy men and women. Blood samples were collected before, during and after two energy-matched bouts of acute treadmill exercise: interval exercise (10 × 1 min intervals at ∼95% of maximal oxygen uptake V̇O2max) and continuous exercise (65% V̇O2max). Continuous exercise, but not interval exercise, reduced CD62E MP concentrations in men and women by 18% immediately after exercise (from 914.5 ± 589.6 to 754.4 ± 390.5 MPs μl ; P < 0.05), suggesting that mechanisms underlying exercise-induced CD62E MP dynamics are intensity dependent. Furthermore, continuous exercise reduced CD62E MPs in women by 19% (from 1030.6 ± 688.1 to 829.9 ± 435.4 MPs μl ; P < 0.05), but not in men. Although interval exercise did not alter CD62E MPs per se, the concentrations after interval exercise were higher than those observed after continuous exercise (P < 0.05). Conversely, CD34 MPs did not fluctuate in response to short-duration acute continuous or interval exercise in men or women. Our results suggest that exercise-induced MP alterations are intensity dependent and sex specific and impact MP populations differentially.