Division of Angiology, Heart and Vessel Department, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Institute of Sport Sciences, University of Lausanne, Lausanne, Switzerland.
Acta Physiol (Oxf). 2021 Oct;233(2):e13700. doi: 10.1111/apha.13700. Epub 2021 Jun 19.
The optimal exercise intensity to improve endothelial function remains unclear, as well as whether the addition of hypoxia could potentiate this function. Therefore, the aim of this study was to compare the effects of different exercise intensities in normoxia and hypoxia on vascular reactivity and nitric oxide (NO) bioavailability in mice.
C57BL/6 mice underwent treadmill running three times per week, for 4 weeks at either low, maximal or supramaximal intensity in normoxia or hypoxia (inspire oxygen fraction = 0.13). Vascular reactivity and expression of genes and proteins involved in NO production/bioavailability were assessed in aorta using isolated vessel tension experiments, RT-qPCR and western blot, respectively. Circulating NO metabolites and pro-/antioxidant markers were measured.
Hypoxic exercise improved both acetylcholine-induced vasorelaxation and phenylephrine-induced vasoconstriction compared to normoxic exercise, independently of intensity. In hypoxia, a higher acetylcholine-induced vasorelaxation was observed with high intensities (supramaximal and maximal) compared to low intensity. Exercise protocols modulated endothelial nitric oxide synthase (eNOS) and α1-adrenergic receptor (α -AR) mRNA level, but not superoxide dismutase 3 (SOD3) and p47phox. No significant differences were observed for protein expression of α -AR, total eNOS, phosphorylated eNOS, SOD isoforms and p47phox. However, plasma SOD and catalase activities were significantly increased in hypoxic supramaximal compared to hypoxic low intensity, while concentration of nitrotyrosine significantly decreased. The latter was also observed in hypoxic maximal and supramaximal compared to the same intensities in normoxia.
Hypoxic high-intensity exercise increases NO bioavailability and improves vascular function, opening promising clinical perspectives for cardiovascular disease prevention.
提高内皮功能的最佳运动强度仍不清楚，此外，缺氧是否能增强这种功能也不清楚。因此，本研究旨在比较常氧和缺氧条件下不同运动强度对小鼠血管反应性和一氧化氮（NO）生物利用度的影响。
C57BL/6 小鼠每周进行 3 次跑步机跑步运动，4 周分别在常氧或低氧（吸入氧分数=0.13）下进行低强度、最大强度或超最大强度运动。采用离体血管张力实验、RT-qPCR 和 Western blot 分别评估主动脉血管反应性以及参与 NO 产生/生物利用度的基因和蛋白的表达。测量循环中 NO 代谢产物和促/抗氧化标志物。
与常氧运动相比，低氧运动独立于强度改善了乙酰胆碱诱导的血管舒张和去甲肾上腺素诱导的血管收缩。在低氧条件下，与低强度相比，高强度（超最大强度和最大强度）观察到更高的乙酰胆碱诱导的血管舒张。运动方案调节内皮型一氧化氮合酶（eNOS）和α1-肾上腺素能受体（α -AR）mRNA 水平，但不调节超氧化物歧化酶 3（SOD3）和 p47phox。α -AR、总 eNOS、磷酸化 eNOS、SOD 同工酶和 p47phox 的蛋白表达没有明显差异。然而，与低氧低强度相比，在低氧超最大强度时血浆 SOD 和过氧化氢酶活性显著增加，而硝基酪氨酸浓度显著降低。在低氧最大强度和超最大强度时与常氧时相同强度相比，也观察到了这一现象。
低氧高强度运动增加了 NO 的生物利用度，改善了血管功能，为心血管疾病的预防提供了有前景的临床前景。
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