Goto Chikara, Higashi Yukihito, Kimura Masashi, Noma Kensuke, Hara Keiko, Nakagawa Keigo, Kawamura Mitsutoshi, Chayama Kazuaki, Yoshizumi Masao, Nara Isao
Physical Therapy Health Sciences, School of Medicine, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan.
Circulation. 2003 Aug 5;108(5):530-5. doi: 10.1161/01.CIR.0000080893.55729.28. Epub 2003 Jul 21.
Aerobic exercise enhances endothelium-dependent vasodilation in hypertensive patients, patients with chronic heart failure, and healthy individuals. However, it is unclear how the intensity of exercise affects endothelial function in humans. The purpose of the present study was to determine the effects of different intensities of exercise on endothelium-dependent vasodilation in humans.
We evaluated the forearm blood flow responses to acetylcholine, an endothelium-dependent vasodilator, and isosorbide dinitrate, an endothelium-independent vasodilator, before and after different intensities of exercise (mild, 25% VO2max; moderate, 50% VO2max; and high, 75% VO2max; bicycle ergometers, 30 minutes, 5 to 7 times per week for 12 weeks) in 26 healthy young men. Forearm blood flow was measured using a mercury-filled Silastic strain-gauge plethysmograph. Twelve weeks of moderate-intensity exercise, but not mild- or high-intensity exercise, significantly augmented acetylcholine-induced vasodilation (7.5+/-2.4 to 11.4+/-5.8 mL/min per 100 mL tissue; P<0.05). No intensity of aerobic exercise altered isosorbide dinitrate-induced vasodilation. The administration of NG-monomethyl-L-arginine, a nitric oxide synthase inhibitor, abolished the moderate-intensity exercise-induced augmentation of the forearm blood flow response to acetylcholine. High-intensity exercise increases plasma concentrations of 8-hydroxy-2'-deoxyguanosine (from 6.7+/-1.1 to 9.2+/-2.3 ng/mL; P<0.05) and serum concentrations of malondialdehyde-modified low-density lipoprotein (from 69.0+/-19.5 to 82.4+/-21.5 U/L; P<0.05), whereas moderate exercise tended to decrease both indices of oxidative stress.
These findings suggest that moderate-intensity aerobic exercise augments endothelium-dependent vasodilation in humans through the increased production of nitric oxide and that high-intensity exercise possibly increases oxidative stress.
有氧运动可增强高血压患者、慢性心力衰竭患者及健康个体的内皮依赖性血管舒张功能。然而，运动强度如何影响人体内皮功能尚不清楚。本研究的目的是确定不同强度运动对人体内皮依赖性血管舒张的影响。
我们评估了26名健康年轻男性在不同强度运动（轻度，25%最大摄氧量；中度，50%最大摄氧量；高强度，75%最大摄氧量；自行车测力计，30分钟，每周5至7次，共12周）前后，对内皮依赖性血管舒张剂乙酰胆碱和非内皮依赖性血管舒张剂硝酸异山梨酯的前臂血流反应。使用充汞的硅橡胶应变片体积描记器测量前臂血流。12周的中等强度运动，而非轻度或高强度运动，显著增强了乙酰胆碱诱导的血管舒张（每100 mL组织从7.5±2.4增至11.4±5.8 mL/min；P<0.05）。有氧运动的任何强度均未改变硝酸异山梨酯诱导的血管舒张。一氧化氮合酶抑制剂NG-单甲基-L-精氨酸的给药消除了中等强度运动诱导的前臂血流对乙酰胆碱反应的增强。高强度运动增加了血浆8-羟基-2'-脱氧鸟苷浓度（从6.7±1.1增至9.2±2.3 ng/mL；P<0.05）和血清丙二醛修饰的低密度脂蛋白浓度（从69.0±19.5增至82.4±21.5 U/L；P<0.05），而中等强度运动则倾向于降低氧化应激的这两个指标。
这些发现表明，中等强度有氧运动通过增加一氧化氮的产生增强人体内皮依赖性血管舒张，而高强度运动可能增加氧化应激。
