Acute Exercise-Induced Oxidative Stress Does Not Affect Immediate or Delayed Precursor Cell Mobilization in Healthy Young Males

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.

Keywords: acute exhaustive exercise; apoptosis; endothelial; hematopoietic; mesenchymal; oxidative stress index; stem cell mobilization; total oxidative capacity.

Figure 1

Gating strategy of mononuclear cells (MNCs), circulating angiogenic precursor cells (CACs), circulating non-angiogenic precursor cells (nCACs), mesenchymal precursor cells (MPCs), endothelial cells (ECs), and apoptotic MNCs as representative example of gating of apoptotic subsets. Numbers in boxes represent % of parent population.

Figure 2

Total oxidative capacity (TOC) values (A), TAC values (B), and TOC/TAC ratio (C; n = 18). Values are mean ± SD. Differences from baseline are indicated by ^*, with ^**p < 0.01, ^****p < 0.0001. Differences between the two interventions are indicated by ^#, with ^##p < 0.01, ^###p < 0.001.

Figure 3

Total number of MNCs (A) and number of apoptotic MNCs (B) in cells/ml blood (n = 18). Values are mean ± SD. Differences from baseline are indicated by ^*, with ^*p < 0.05, ^***p < 0.001, and ^****p < 0.0001.

Figure 4

Total number of CACs (A) and number of apoptotic CACs (B) in cells/ml blood (n = 18). Values are mean ± SD. Differences from baseline are indicated by ^*, with ^*p < 0.05, ^**p < 0.01, and ^****p < 0.0001.

Figure 5

Total number of nCACs (A) and number of apoptotic nCACs (B) in cells/ml blood (n = 18). Values are mean ± SD.

Figure 6

Total number of MPCs (A) and number of apoptotic MPCs (B) in cells/ml blood (n = 18). Values are mean ± SD.

Figure 7

Total number of ECs (A) and number of apoptotic ECs (B) in cells/ml blood (n = 18). Values are mean ± SD. Differences from baseline are indicated by ^*, with ^***p < 0.001. Differences between the two interventions are indicated by ^#, with ^#p < 0.05.