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J Appl Physiol (August 29, 2003). doi:10.1152/japplphysiol.00323.2003
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Submitted on April 1, 2003
Accepted on August 25, 2003

Does ACE inhibition enhance endurance performance and muscle energy metabolism in rats?

Lahoucine Bahi1, Nathalie Koulmann2, Herve Sanchez2, Iman Momken1, Vladimir Veksler1, Andre-Xavier Bigard2, and Renee Ventura-Clapier1*

1 Faculte de Pharmacie, U-446 INSERM, 92 296, Chatenay-Malabry, France
2 Unite de Bioenergetique, Departement des Facteurs Humains, CRSSA, 38702, La Tronche, France

* To whom correspondence should be addressed. E-mail: Renee.Ventura{at}cep.u-psud.fr.

The renin-angiotensin-aldosterone system (RAAS) 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. 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 to 12 weeks with an ACE inhibitor perindopril (2 mg/kg/day) 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 (perindopril 57±5 min vs 55±6 min in 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 in 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 octanoyl-carnitine 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.




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