Effects of exercise and L-arginine on ventricular remodeling and oxidative stress.
OBJECTIVE
Our aim was to characterize the changes in messenger RNA (mRNA) abundance, protein, and activity levels of the enzymatic antioxidants, superoxide dismutase (SOD), glutathione peroxidase, and catalase by exercise training combined with L-arginine after myocardial infarction (MI).


METHODS
L-Arginine (1 g x kg(-1) x d(-1)) and N(G)-nitro-L-arginine methyl ester (L-NAME; 10 mg x kg(-1) x d(-1)) were administered in drinking water for 8 wk. Sprague-Dawley rats were randomized to the following groups: sham-operated control (Sham); MI sedentary (Sed); MI exercise (Ex); MI sedentary + L-arginine (Sed + LA); MI exercise + L-arginine (Ex + LA); MI sedentary + L-NAME (Sed + L-NAME); and MI exercise + L-NAME (Ex + L-NAME).


RESULTS
The glutathione peroxidase, catalase, and gp91(phox) mRNA levels were comparable among all the groups. The SOD mRNA level was significantly increased in the Ex group (5.43 +/- 0.87) compared with the Sed group (1.74 +/- 0.29), whereas this effect was pronouncedly down-regulated by the L-NAME intervention (2.51 +/- 1.17, P < 0.05). The protein levels of SOD in the Sed and Ex groups were both significantly decreased with the administration of L-NAME. The protein levels of catalase were significantly higher in the Ex and Ex + LA groups than that in the Sed, Sed + LA, and L-NAME-treated groups. The collagen volume fraction was significantly lowered by the exercise and/or L-arginine treatment when compared with the Sed group. Fractional shortening was significantly preserved in the trained groups compared with their corresponding sedentary groups with or without drug treatments. However, the beneficial effect was not further improved by L-arginine treatment.


CONCLUSIONS
Our results suggest that exercise training exerts antioxidative effects and attenuates myocardial fibrosis in the MI rats. These improvements, in turn, alleviate cardiac stiffness and preserve post-MI cardiac function. In addition, L-arginine appears to have no additive effect on cardiac function or expression of enzymatic antioxidants.
Xu
Xiaohua
X
Laboratory of Cardiovascular Research, University of Texas at San Antonio, San Antonio, TX 78249, USA.
Zhao
Weiyan
W
Lao
Shunhua
S
Wilson
Bryan S
BS
Erikson
John M
JM
Zhang
John Q
JQ
D000818:Animals; D001120:Arginine / Q000008:administration & dosage / Q000235:genetics / Q000378:metabolism*; D004452:Echocardiography; D004791:Enzyme Inhibitors / Q000008:administration & dosage / Q000378:metabolism; D005609:Free Radicals / Q000037:antagonists & inhibitors; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology / Q000534:rehabilitation; D019331:NG-Nitroarginine Methyl Ester / Q000008:administration & dosage / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects* / Q000235:genetics; D010805:Physical Conditioning, Animal / Q000502:physiology*; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000187:drug effects; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D017422:Sequence Analysis, DNA; D016019:Survival Analysis; D020257:Ventricular Remodeling / Q000187:drug effects* / Q000235:genetics
D004791:Enzyme Inhibitors; D005609:Free Radicals; D012333:RNA, Messenger; D001120:Arginine; D019331:NG-Nitroarginine Methyl Ester