Effects of high-intensity training on MCT1, MCT4, and NBC expressions in rat skeletal muscles: influence of chronic metabolic alkalosis.
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 5 times/wk for 5 wk, receiving either sodium bicarbonate (ALK-T) or a placebo (PLA-T) prior to each training session, and were compared with 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) and phosphofructokinase (PFK) activities and muscle buffer capacity (betam) were also evaluated. Following training, CS and PFK activities were significantly higher in the soleus only (P < 0.05), whereas betam 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 with CON. There was no significant change in protein content in the EDL. Finally, NBC content was related only to MCT1 content in soleus (r = 0.50, P < 0.01). In conclusion, these results suggest that MCT1, MCT4, and NBC undergo fiber-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.
Thomas
Claire
C
Université Montpellier 1, UFR Médecine EA701, F-34295, Montpellier, France. thomasclaire@wanadoo.fr
Bishop
David
D
Moore-Morris
Tom
T
Mercier
Jacques
J
D000471:Alkalosis / Q000139:chemically induced / Q000378:metabolism*; D000818:Animals; D002908:Chronic Disease; D002950:Citrate (si)-Synthase / Q000378:metabolism; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D027501:Monocarboxylic Acid Transporters / Q000378:metabolism*; D009124:Muscle Proteins / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000378:metabolism*; D010732:Phosphofructokinase-1 / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology; D005082:Physical Exertion / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D017693:Sodium Bicarbonate; D027982:Sodium-Bicarbonate Symporters / Q000378:metabolism*; D027981:Symporters / Q000378:metabolism*; D000099233:Monocarboxylate Transport Protein 1
D002950:Citrate (si)-Synthase; D019344:Lactic Acid; D027501:Monocarboxylic Acid Transporters; D009124:Muscle Proteins; D010732:Phosphofructokinase-1; D017693:Sodium Bicarbonate; D027982:Sodium-Bicarbonate Symporters; D027981:Symporters; D000099233:Monocarboxylate Transport Protein 1; C516342:Slc16a3 protein, rat; C422004:Slc4a4 protein, rat; C068652:1-phosphofructokinase