Chronic electrical stimulation increases MCT1 and lactate uptake in red and white skeletal muscle

Am J Physiol. 1997 Aug;273(2 Pt 1):E239-46. doi: 10.1152/ajpendo.1997.273.2.E239.

Abstract

We examined whether chronic stimulation of red and white rat muscles increased the concentrations of the monocarboxylate transporter MCT1. Red and white tibialis anterior (RTA and WTA, respectively) and extensor digitorum longus (EDL) muscles were chronically stimulated via the peroneal nerve for 7 days. Stimulated and contralateral control muscles were examined for MCT1 content, L-lactate uptake, lactate dehydrogenase (LDH) isoforms, and muscle fiber composition. MCT1 was 1.5 times greater in stimulated RTA, 3 times greater in stimulated WTA, and 1.9 times greater in stimulated EDL compared with respective control muscles (P < 0.05). L-Lactate uptake increased in all stimulated muscles (P < 0.05), and this was highly correlated with the increase in MCT1 (r = 0.96). The heart-type LDH (H-LDH) subunits also increased in all stimulated muscles (P < 0.05). The H-LDH subunits correlated highly with MCT1 in the muscles (r = 0.83). There was no change in muscle-type LDH subunits (P > 0.05). There were negligible alterations in muscle fiber composition in the stimulated muscles, suggesting that the increase in MCT1 was independent of changes in muscle fiber composition. These studies are the first to demonstrate that chronic muscle contraction increases MCT1 concentrations in both red and white skeletal muscles.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carrier Proteins / metabolism*
  • Electric Stimulation
  • Hindlimb
  • Isoenzymes
  • L-Lactate Dehydrogenase / metabolism
  • Lactic Acid / metabolism*
  • Male
  • Monocarboxylic Acid Transporters
  • Muscle Fibers, Skeletal / metabolism
  • Muscle, Skeletal / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Time Factors

Substances

  • Carrier Proteins
  • Isoenzymes
  • Monocarboxylic Acid Transporters
  • Lactic Acid
  • L-Lactate Dehydrogenase