The effects of training on the monocarboxylate transporter (mct1) in skeletal muscles and the heart

Themonocarboxylate transporter l (MCT1) protein is found in both red and white skeletal muscles as well as in the heart. Concentrations of MCT1 are however graded among these tissues as follows: heart > red muscle > white muscle. Since training decreases circulating lactate concentrations and increases lactate transport in isolated vesicles we examined the effects of treadmill training on MCT1 in metabolically heterogeneous skeletal muscles (soleus, EDL, and red and white gastrocnemius) and in the heart. Animals trained 3 weeks on a motor driven treadmill (21 m/min, 12% grade 4 x Ih/wk) or remained sedentary. Skeletal muscles and hearts were analyzed for MCT1, via western blotting, and citrate synthase activity at the end of each week of training. MCT1 content was not changed in any of the skeletal muscles examined, nor did training increase the citrate synthase activity in the skeletal muscles. In contrast, MCT1 content was increased 35% in the heart (P<0.05). Most of the changes occurred within the first week of training. Concurrently, no changes were observed in heart citrate synthase activity. Thus, mild exercise which does not result in marked improvements in the oxidative capacities of skeletal muscles or the heart, does increase markedly the MCT1 content in heart but not in skeletal muscle. Therefore, it appears that MCTI expression is more easily induced in the heart than in skeletal muscles, and it also implies that lactate uptake by the heart can be increased rapidly independent of any concomitant changes in the oxidative capacities in this tissue.