Abstract
Exercise is known to acutely and transiently mobilize precursor cells to the peripheral blood. To date, the underlying mechanisms have not yet been fully elucidated and we hypothesized that exercise-induced oxidative stress could be a mobilizing agent, either directly or via circulating apoptotic cells as mediators. The aim of the study was to assess the effect of acute exercise-induced oxidative stress on numbers of circulating angiogenic precursor cells (CACs), circulating non-angiogenic precursor cells (nCACs), mesenchymal precursor cells (MPCs), mature endothelial cells (ECs), and mononuclear cells (MNCs), as well as their apoptotic subsets. Healthy, young males (n = 18, age: 24.2 ± 3.5 years) completed two identical, standardized incremental cycling tests. The first, un-supplemented control test was followed by a 7-day-long supplementation of vitamin C (1,000 mg/day) and E (400 I.U./day), immediately preceding the second test. Blood samples were collected before, directly after, 30, 90, 180, and 270 min after exercise, and aforementioned circulating cell numbers were determined by flow cytometry and a hematology analyzer. Additionally, total oxidative capacity (TOC) and total antioxidative capacity (TAC) were measured in serum at all timepoints. Antioxidative supplementation abolished the exercise-induced increase in the oxidative stress index (TOC/TAC), and reduced baseline concentrations of TOC and TOC/TAC. However, it did not have any effect on CACs, nCACs, and MPC numbers or the increase in apoptotic MNCs following exercise. Our results indicate that exercise-induced oxidative stress is neither a main driver of lymphocyte and monocyte apoptosis, nor one of the mechanisms involved in the immediate or delayed mobilization of precursor cells.
Highlights
Several studies have shown that an acute stimulus of maximal exercise can elicit a transitory increase in endothelial precursor cells (EPCs; Koutroumpi et al, 2012; Silva et al, 2012; De Biase et al, 2013; Boppart et al, 2015) as well as mature endothelial cells (ECs; Shaffer et al, 2006; Niemiro et al, 2017), hematopoietic precursor cells (HPCs; De Lisio and Parise, 2013; Boppart et al, 2015), and mesenchymal precursor cells (MPCs; Ramírez et al, 2006; Boppart et al, 2015) present in the peripheral blood
Agha et al (2018) found the increase in CD34+ HPC numbers after vigorous cycling to be reduced upon blockage of β1- and β2-adrenergic receptors, which further solidifies the role of sympathetic stress in exercise-induced stem cell mobilization
The present study investigated the effects of exercise-induced oxidative stress on circulating numbers of circulating angiogenic precursor cells (CACs), nCACs, MPCs, ECs, and their apoptotic subsets after an acute bout of incremental cycling
Summary
Several studies have shown that an acute stimulus of maximal exercise can elicit a transitory increase in endothelial precursor cells (EPCs; Koutroumpi et al, 2012; Silva et al, 2012; De Biase et al, 2013; Boppart et al, 2015) as well as mature endothelial cells (ECs; Shaffer et al, 2006; Niemiro et al, 2017), hematopoietic precursor cells (HPCs; De Lisio and Parise, 2013; Boppart et al, 2015), and mesenchymal precursor cells (MPCs; Ramírez et al, 2006; Boppart et al, 2015) present in the peripheral blood. Identifying the factors responsible for this exercise-induced rise in circulating stem and progenitor cell numbers may contribute to a better understanding of the known health benefits of exercise in general and may help to better tailor training regimens Several mechanisms, such as activation of the sympathetic nervous system, increased shear stress, or a shift in the redox balance have already been proposed in literature (MoebiusWinkler et al, 2011; Kröpfl et al, 2014; Emmons et al, 2016; Kröpfl et al, 2020) but a thorough investigation of the possible players at hand, how they interact and to which extent each of them contributes to the final mobilization has long been lacking. Contrary to their initial hypothesis of increased shear stress correlating with increased mobilization, they found blood flow restriction to even reduce the exercise-induced increase in circulating EPCs
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