Submitted on November 3, 2008
Revised on April 9, 2009
Accepted on April 30, 2009
Decreased muscle ACE activity enhances functional response to endurance training in rats, without change in muscle oxidative capacity or contractile phenotype
Estelle Habouzit1, Hélène Richard1, Hervé Sanchez1, Bernard Serrurier1, Rachel Monnet2, Nathalie Koulmann3, Renee Ventura-Clapier4, and Xavier Bigard1*
1 CRSSA
2 Centre de Recherches du Service de Sante des Armees
3 Centre de Recherches du Service de Santes Arm
4 U-769 Inserm; IFR-141
* To whom correspondence should be addressed. E-mail: xavier_bigard{at}yahoo.fr.
In the present study, we tested the hypothesis that chronic ACE inhibition could improve the training-induced improvement in endurance exercise performance, and that this could be related to enhanced skeletal muscle metabolic efficiency. Female Wistar rats were assigned to four groups comprising animals either maintained sedentary or endurance trained (Sed and Tr, respectively), and treated or nor for 10 weeks with an ACE inhibitor, perindopril (2 mg.kg-1.day-1) (Per and Ctr, respectively) (n=8 each). Trained rats underwent a 8-wk treadmill training protocol that consisted of 2h/day running at 30 m/min on a 8% decline. Before and one week before the end of experimental conditioning, the running time to exhaustion of rats was measured on a treadmill. The training program led to an increase in endurance time, higher in Tr-Per than in Tr-Ct group (125% in Tr-Ct vs. 183% in Tr-Per groups, P<0.05). Oxidative capacity, measured in saponin-permeabilized fibers of slow soleus and fast plantaris muscles increased with training, but less in Tr-Per than in Tr-Ctr rats. The training-induced increase in citrate synthase activity also was less in soleus from Tr-Per than Tr-Ctr rats. The training-induced increase in the percentage of the type IIa isoform of myosin heavy chain (MHC) (45%, P<0.05) and type IIx MHC (25%, P<0.05), associated with decreased type IIb MHC (34%, P<0.05) was minimized by perindopril administration. These findings demonstrate that the enhancement in physical performance observed in perindopril-treated animals cannot be explained by changes in mitochondrial respiration and/or MHC distribution within muscles involved in running exercise.
