Effect of AMPK activation on acute exercise‐induced monocarboxylate transporter (MCT) 1 and MCT4 mRNA expression in skeletal muscle

We examined the mechanism on acute exercise‐induced MCT1 and MCT4 mRNA expression in skeletal muscle. The rats were subjected to a bout of high‐intensity intermittent swimming (HIS) or low‐intensity prolonged swimming exercise (LIS). The HIS rats swam for fifteen 20‐second with a weight equal to 18% of their body weight. The LIS rats swam without load in two 3h sessions separated by 45min of rest. HIS elevated the phosphorylation of 5 fAMP‐activated prtein kinase (pAMPK), calcium/calmodulin‐dependent kinase II (pCaMKII), and p38 mitogen‐activated protein kinase (pMAPK), which are characterized upstream modulators of transcriptional regulation. LIS elevated pAMPK, whereas pCaMKII and pMAPK were not altered. MCT1 and MCT4 mRNA were transiently upregulated by HIS and LIS. Direct exposure of epitrochlearis to 0.5mM 5‐aminoimidazole‐4‐carboxamide‐1‐ƒÀ‐d‐ribonucleoside (AICAR) or 1mM caffeine increased both MCT1 and MCT4 mRNA. When 1mM caffeine‐induced pAMPK was inhibited by dantrolene, neither MCT1 nor MCT4 mRNA was increased. The present findings suggest that, irrespective of exercise intensity, acute exercise may upregulate MCT1 and MCT4 mRNA expression, through AMPK‐mediated pathway in skeletal muscle.