RESUMEN
PURPOSE: We aimed to determine the effects of different intensities of acute exercise on Hcy plasma levels, and the exercise-induced changes in Hcy liver metabolism. METHOD: First, thirty-two Wistar rats were randomly submitted to an acute bout of swimming exercise carrying a load of 2% (n=8), 4% (n=8) and 6% (n=8) of their total body weight attached in their tail. Control rats remained rested (n=8). Blood samples were taken from tail vein for plasma S-containing amino acids determination before (Rest) and post, 1, 2, 3, 4, 6, and 10h after acute swimming exercise. Second, 56 exercised rats (4% loads) were euthanized before (Rest) and1, 2, 3, 4, 6, and 10h after acute swimming exercise. Blood and liver samples were collected for amino acids and keys genes involved in the Hcy metabolism assay. RESULTS: Acute exercise increases (P<0.05) plasma Hcy concentration in an intensity-dependent manner (rest 7.7±0.8; 6% load 13.8±3.6; 4% load 12.2±2.9±and 2% load 10.1±2.6, µmol/L); this increase is transient and does not promote hyperhomocysteinemia (<15µmol/L).Exercise-induced increased plasma Hcywas accompanied by the decreased liver S-adenosylmethionine/S-adenosylhomocysteine ratio and elevated MAT1a mRNA content. Acute exercise also caused elevated mRNA of key enzymes of transsulfuration (CBS) and remethylation (BHMT and the MTRR). CONCLUSION: Our data provided evidence that acute exercise increases plasma Hcy concentration due to the augmented requirement for methylated compounds that increases liver SAM consumption. Also, Hcy remethylation and transsulfuration are coordinately regulated to maintain methyl balance.