Non-technical summary Circulating angiogenic cells (CACs) repair and maintain the vascular endothelium. CACs are responsive to lifestyle factors such as diet and physical activity. For example, their capacity to regenerate the endothelium is impaired in cardiovascular disease patients, whereas exercise training can improve CAC function. In this study, we examined the effects of a high-fat meal with and without prior endurance exercise on several molecular aspects of CAC function, including levels of reactive oxygen species (ROS), nitric oxide (NO), intracellular lipids, and gene expression. Our results indicated that the high-fat meal induced significant oxidative stress (i.e. ROS production) in the CACs that expressed the cell surface protein CD31. However, when subjects performed a single bout of exercise on the prior day, the meal had no effect on ROS in CD31 + cells. Therefore, we concluded that prior exercise prevents the oxidative stress induced by a high-fat meal in CD31 + CACs.Abstract We hypothesized that prior exercise would prevent postprandial lipaemia (PPL)-induced increases in intracellular reactive oxygen species (ROS) in three distinct circulating angiogenic cell (CAC) subpopulations. CD34 + , CD31 + /CD14 − /CD34 − , and CD31 + /CD14 + /CD34 − CACs were isolated from blood samples obtained from 10 healthy men before and 4 h after ingesting a high fat meal with or without ∼50 min of prior endurance exercise. Significant PPL-induced increases in ROS production in both sets of CD31 + cells were abolished by prior exercise. Experimental ex vivo inhibition of NADPH oxidase activity and mitochondrial ROS production indicated that mitochondria were the primary source of PPL-induced oxidative stress. The attenuated increases in ROS with prior exercise were associated with increased antioxidant gene expression in CD31 + /CD14 − /CD34 − cells and reduced intracellular lipid uptake in CD31 + /CD14 + /CD34 − cells. These findings were associated with systemic cardiovascular benefits of exercise, as serum triglyceride, oxidized low density lipoprotein-cholesterol, and plasma endothelial microparticle concentrations were lower in the prior exercise trial than the control trial. In conclusion, prior exercise completely prevents PPL-induced increases in ROS in CD31 + /CD14 − /CD34 − and CD31 + /CD14 + /CD34 − cells. The mechanisms underlying the effects of exercise on CAC function appear to vary among specific CAC types.

We investigated the influence of acute and chronic endurance exercise on levels of intracellular nitric oxide (NO), superoxide (O₂·⁻), and expression of genes regulating the balance between these free radicals in CD34⁺ and CD34⁻ peripheral blood mononuclear cells (PBMCs; isolated by immunomagnetic cell separation). Blood samples were obtained from age- and body mass index (BMI)-matched endurance-trained (n = 10) and sedentary (n = 10) men before and after 30 min of exercise at 75% maximal oxygen uptake (·VO(₂max)). Baseline levels of intracellular NO (measured by DAF-FM diacetate) and O₂·⁻ (measured by dihydroethidium) were 26% (P < 0.05) and 10% (P < 0.05) higher, respectively, in CD34⁺ PBMCs from the sedentary group compared with the endurance-trained group. CD34⁺ PBMCs from the sedentary group at baseline had twofold greater inducible nitric oxide synthase (iNOS) mRNA and 50% lower endothelial NOS (eNOS) mRNA levels compared with the trained group (P < 0.05). The baseline group difference in O₂·⁻ was eliminated by acute exercise. Experiments with apocynin indicated that the training-related difference in O₂·⁻ levels was explained by increased NADPH oxidase activity in the sedentary state. mRNA levels of additional angiogenic and antioxidant genes were consistent with a more angiogenic profile in CD34⁺ cells of trained subjects. CD34⁻ PBMCs, examined for exploratory purposes, also displayed a more angiogenic mRNA profile in trained subjects, with vascular endothelial growth factor (VEGF) and eNOS being more highly expressed in trained subjects. Overall, our data suggest an association between the sedentary state and increased nitro-oxidative stress in CD34⁺ cells.

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