Title of article :
Does exercise training interfere with the effects of -carnitine supplementation?
Author/Authors :
Reury F. P. Bacurau، نويسنده , , Francisco Navarro، نويسنده , , Reinaldo A. Bassit، نويسنده , , Marcela O. Meneguello، نويسنده , , Ronaldo V. T. Santos، نويسنده , , André L. R. Almeida، نويسنده , , L. u?s F. B. P. Costa Rosa، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2003
Pages :
5
From page :
337
To page :
341
Abstract :
Objective We investigated the effect of -carnitine supplementation on carnitine content in muscle fiber, glucose, and fatty acid metabolism and on performance in trained rats. Methods Male Wistar rats received a daily dose of 28 mg/kg, intragastrically, during the last 4 wk of a 6-wk moderate-intensity training program. The contents of carnitine and coenzyme A were evaluated in muscle fiber and its capacity to metabolize labeled glucose, oleate, and pyruvate. The ergogenic effect of the amine was assessed by the evaluation of time until exhaustion in an exercise session. The results were analyzed by analysis of variance and Tukey’s post hoc test, and significance was set at P < 0.05. Results In our model, carnitine supplementation increased time until exhaustion (14.0%), similar to that observed for trained rats, but the effect was even greater (30.3% increase) in the supplemented and trained rats. Carnitine supplementation increased oleate decarboxylation (17% for sedentary rats and 119% for trained rats) and decreased glucose (29.7% and 45% for sedentary and trained rats, respectively) and [2-14C ]-pyruvate (45.9% and 61% for sedentary and trained rats, respectively) decarboxylation. The flux of [1-14C]-pyruvate through the Krebs cycle increased by 32% and 70% for supplemented sedentary and trained rats, respectively. The training protocol also increased [1-14C]-pyruvate decarboxylation by 32%. The cytosolic content of free, long-chain, and short-chain acyl-carnitine increased in the soleus muscle obtained from supplemented sedentary rats by 28%, 117%, and 16%, respectively, and 99%, 205%, and 32% for the muscle from supplemented trained rats. Conclusions This study showed that carnitine supplementation increases fatty acid oxidation in skeletal muscle by a mechanism that includes increasing total carnitine content in soleus muscle mitochondria and the total content of acyl-carnitine. The most interesting finding was that the effect of supplementation was even greater in trained rats that had received 3-wk supplementation of carnitine.
Keywords :
acyl-carnitine , Mitochondrial metabolism , acetyl coenzyme A , substrateoxidation , Krebs cycle
Journal title :
Nutrition
Serial Year :
2003
Journal title :
Nutrition
Record number :
717945
Link To Document :
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