This study investigated the effects of high-intensity training, with or without induced metabolic alkalosis, on lactate transporter (MCT1 and MCT4) and sodium-bicarbonate cotransporter (NBC) content in rat skeletal muscles. Male Wistar rats performed high-intensity training on a treadmill 5x/wk for 5 wk, receiving either sodium bicarbonate (ALK-T) or a placebo (PLA-T) prior to each training session, and were compared to a group of control rats (CON). MCT1, MCT4 and NBC content was measured by Western blotting in soleus and extensor digitorum longus (EDL) skeletal muscles. Citrate synthase (CS), phosphofructokinase (PFK) activities, and muscle buffer capacity (m), were also evaluated. Following training, CS and PFK activities were significantly higher in the soleus only (P<0.05), whereas m was significantly higher in both soleus and EDL (P<0.05). MCT1 (PLA-T: 30%, ALK-T: 23%) and NBC contents (PLA-T: 85%, ALK-T: 60%) increased significantly only in the soleus following training (P<0.01). MCT4 content in the soleus was significantly greater in ALK-T (115%), but not PLA-T compared to CON. There was no significant change in protein content in the EDL. Finally, NBC content was only related to MCT1 content in soleus (r = 0.53, P<0.01). In conclusion, these results suggest that MCT1, MCT4 and NBC undergo fibre-specific adaptive changes in response to high-intensity training and that induced alkalosis has a positive effect on training-induced changes in MCT4 content. The correlation between MCT1 and NBC expression suggests that lactate transport may be facilitated by NBC in oxidative skeletal muscle, which may in turn favor better muscle pH regulation.