High-intensity Interval training enhances mobilization/functionality of endothelial progenitor cells and depressed shedding of vascular endothelial cells undergoing hypoxia.

PURPOSE

Exercise training improves endothelium-dependent vasodilation, whereas hypoxic stress causes vascular endothelial dysfunction. Monocyte-derived endothelial progenitor cells (Mon-EPCs) contribute to vascular repair process by differentiating into endothelial cells. This study investigates how high-intensity interval (HIT) and moderate-intensity continuous (MCT) exercise training affect circulating Mon-EPC levels and EPC functionality under hypoxic condition.

METHODS

Sixty healthy sedentary males were randomized to engage in either HIT (3-min intervals at 40 and 80 % VO for five repetitions, n = 20) or MCT (sustained 60 % VO, n = 20) for 30 min/day, 5 days/week for 6 weeks, or to a control group (CTL) that did not received exercise intervention (n = 20). Mon-EPC characteristics and EPC functionality under hypoxic exercise (HE, 100 W under 12 % O) were determined before and after HIT, MCT, and CTL.

RESULTS

The results demonstrated that after the intervention, the HIT group exhibited larger improvements in VO, estimated peak cardiac output (Q), and estimated peak perfusions of frontal cerebral lobe (Q) and vastus lateralis (Q) than the MCT group. Furthermore, HIT (a) increased circulating CD14/CD16/CD34/KDR (Mon-1 EPC) and CD14/CD16/CD34/KDR (Mon-2 EPC) cell counts, (b) promoted the migration and tube formation of EPCs, (c) diminished the shedding of endothelial (CD34/KDR/phosphatidylserine) cells, and (d) elevated plasma nitrite plus nitrate, stromal cell-derived factor-1, matrix metalloproteinase-9, and vascular endothelial growth factor-A concentrations at rest or following HE, compared to those of MCT. In addition, Mon-1 and -2 EPC counts were directly related to VO and estimated peak Q, Q, and Q.

CONCLUSIONS

HIT is superior to MCT for improving hemodynamic adaptation and Mon-EPC production. Moreover, HIT effectively enhances EPC functionality and suppresses endothelial injury undergoing hypoxia.