This study used an integrative experimental model in humans to investigate whether muscle angiogenic factors are differentially modulated by exercise stimuli eliciting different degrees of mechanical and metabolic stress. In a randomized crossover design, twelve men performed two low‑volume high-intensity exercise regimens, including short sprint intervals (SSI) or long sprint intervals (LSI) inducing pronounced mechanical/metabolic stress, and a high‑volume moderate‑intensity continuous exercise protocol (MIC) inducing mild but prolonged mechanical/metabolic stress. Gene and protein expression of angioregulatory factors was determined in vastus lateralis muscle samples obtained before and after exercise. Exercise upregulated muscle VEGF mRNA to a greater extent in LSI and MIC compared to SSI. Analysis of angioregulatory factors sensitive to shear stress revealed more marked exercise-induced VEGF‑R2 mRNA responses in MIC than SSI, as well as greater PECAM‑1 and eNOS mRNA responses in LSI than SSI. No apparent exercise‑induced phosphorylation of shear stress‑sensory proteins VEGF‑R2^Tyr1175, PECAM‑1^Tyr713 and eNOS^Ser1177 was observed despite robust elevations in femoral artery shear stress. Exercise evoked greater mRNA responses of the mechanical stretch sensor MMP9 in SSI than MIC. Exercise‑induced mRNA responses of the metabolic stress sensor HIF‑1α were more profound in LSI than SSI. These results suggest that low-volume high-intensity exercise transcriptionally activates angiogenic factors in a mechanical/metabolic stress‑dependent manner. Furthermore, the angiogenic potency of low-volume high-intensity exercise appears similar to that of high‑volume moderate‑intensity exercise, but only on condition of eliciting severe mechanical/metabolic stress. We conclude that the angiogenic stimulus produced by exercise depends on both magnitude and protraction of myocellular homeostatic perturbations.

中文翻译：

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运动诱导的人体骨骼肌机械和代谢应激对血管生成因子的抑制性调节。

这项研究在人体中使用了一个综合性实验模型，研究了运动刺激引起不同程度的机械和代谢压力时，肌肉血管生成因子是否受到不同的调节。在随机交叉设计中，十二名男子进行了两种低容量的高强度运动方案，包括短冲刺间隔（SSI）或长冲刺间隔（LSI）引起明显的机械/代谢压力，以及大容量的中强度连续锻炼协议（MIC）会引起轻度但长时间的机械/代谢压力。测定运动前后的股外侧肌样本中血管调节因子的基因和蛋白表达。与SSI相比，在LSI和MIC中锻炼上调了肌肉VEGF mRNA的表达。对剪应力敏感的血管调节因子的分析显示，与SSI相比，MIC在运动诱导的VEGF-R2 mRNA反应中表现更为明显，而在LSI中，PECAM-1和eNOS mRNA的反应则高于SSI。没有明显的运动引起的切应力感测蛋白VEGF-R2的磷酸化^Tyr1175，PECAM-1 ^Tyr713和eNOS ^Ser1177尽管股动脉的切应力明显升高，但仍能观察到。运动引起的SSI机械拉伸传感器MMP9的mRNA反应比MIC更大。运动导致的代谢应激传感器HIF-1α的mRNA反应在LSI中比SSI更为明显。这些结果表明，小剂量高强度运动以机械/代谢应激依赖性方式转录激活血管生成因子。此外，小容量高强度运动的血管生成潜能似乎与大容量中强度运动的相似，但仅在引起严重的机械/代谢应激的情况下。我们得出结论，运动产生的血管生成刺激取决于肌细胞稳态干扰的大小和持续时间。