Bahi L, Koulmann N, Sanchez H, Momken I, Veksler V, Bigard A X, Ventura-Clapier R
Cardiologie Cellulaire et Moléculaire, Institut National de la Santé et de la Recherche Médicale unité-446, 92296 Châtenay-Malabry, France.
J Appl Physiol (1985). 2004 Jan;96(1):59-64. doi: 10.1152/japplphysiol.00323.2003. Epub 2003 Aug 29.
The renin-angiotensin-aldosterone system plays an important role in the hydroelectrolytic balance, blood pressure regulation, and cell growth. In some studies, the insertion (I) allele of the angiotensin-converting enzyme (ACE) gene, associated with a lower ACE activity, has been found in excess frequency in elite endurance athletes, suggesting that decreased ACE activity could be involved in endurance performance (Myerson S, Hemingway H, Budget R, Martin J, Humphries S, and Montgomery H. J Appl Physiol 87: 1313-1316, 1999). To test this hypothesis, we evaluated whether ACE inhibition could be associated with improved endurance performance and muscle oxidative capacity in rats. Eight male Wistar rats were treated for 10-12 wk with an ACE inhibitor, perindopril (2 mg.kg-1.day-1), and compared with eight control rats. Endurance time was measured on a treadmill, and oxidative capacity and regulation of mitochondrial respiration by substrates were evaluated in saponin-permeabilized fibers of slow soleus and fast gastrocnemius muscles. Endurance time did not differ between groups (57 +/- 5 min for perindopril vs. 55 +/- 6 min for control). Absolute and relative (to body weight) left ventricular weight was 20% (P < 0.01) and 12% (P < 0.01) lower, respectively, in the treated group. No difference in oxidative capacity, mitochondrial enzyme activities, or mitochondrial regulation by ADP was observed in soleus or gastrocnemius. Mitochondrial respiration with glycerol 3-phosphate was 17% higher in gastrocnemius (P < 0.03) and with octanoylcarnitine 14% greater in soleus (P < 0.01) of treated rats. These results demonstrate that ACE inhibition was not associated with improved endurance time and maximal oxidative capacity of skeletal muscles. This suggests that ACE activity has no implication in endurance capacity and only minor effects on mitochondrial function in sedentary animals.
肾素-血管紧张素-醛固酮系统在水电解质平衡、血压调节及细胞生长过程中发挥着重要作用。在一些研究中，已发现血管紧张素转换酶（ACE）基因的插入（I）等位基因与较低的ACE活性相关，且在优秀耐力运动员中出现的频率过高，这表明ACE活性降低可能与耐力表现有关（迈尔森S、海明威H、巴杰特R、马丁J、汉弗莱斯S和蒙哥马利H。《应用生理学杂志》87: 1313 - 1316，1999）。为验证这一假设，我们评估了ACE抑制是否与大鼠耐力表现的改善及肌肉氧化能力有关。八只雄性Wistar大鼠用ACE抑制剂培哚普利（2毫克·千克⁻¹·天⁻¹）治疗10 - 12周，并与八只对照大鼠进行比较。在跑步机上测量耐力时间，并在慢比目鱼肌和快腓肠肌的皂素通透纤维中评估氧化能力及底物对线粒体呼吸的调节。两组之间的耐力时间无差异（培哚普利组为57 ± 5分钟，对照组为55 ± 6分钟）。治疗组的绝对左心室重量和相对（相对于体重）左心室重量分别降低了20%（P < 0.01）和12%（P < 0.01）。在比目鱼肌或腓肠肌中，未观察到氧化能力、线粒体酶活性或ADP对线粒体调节的差异。治疗组大鼠的腓肠肌中以3 - 磷酸甘油为底物的线粒体呼吸高出17%（P < 0.03），比目鱼肌中以辛酰肉碱为底物的线粒体呼吸高出14%（P < 0.01）。这些结果表明，ACE抑制与骨骼肌耐力时间的改善及最大氧化能力无关。这表明ACE活性与耐力能力无关，且对久坐不动动物的线粒体功能仅有轻微影响。
