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This Article Full Text Full Text (PDF) All Versions of this Article: 556/1/297    most recent jphysiol.2003.058222v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Juel, C. Articles by Dela, F. Search for Related Content PubMed PubMed Citation Articles by Juel, C. Articles by Dela, F.

¹ Copenhagen Muscle Research Centre, University of Copenhagen, Denmark² The August Krogh Institute, University of Copenhagen, Denmark³ Department of Medical Physiology, The Panum Institute, University of Copenhagen, Denmark

Lactate is released from skeletal muscle in proportion to glucose uptake rates, and it leaves the cells via simple diffusion and two monocarboxylate transporter proteins, MCT1 and MCT4. In reponse to endurance training MCT1 – and possibly MCT4 – content in muscle increases. The MCTs have not previously been measured in patients with type 2 diabetes (Type 2), and the response to strength training is unknown. Ten Type 2 and seven healthy men (Control) strength-trained one leg (T) 3 times a week for 6 weeks while the other leg remained untrained (UT). Each session lasted no more than 30 min. After strength training, muscle biopsies were obtained and an isoglycaemic, hyperinsulinaemic clamp, combined with arterial and femoral venous catheterization of both legs, was carried out. During hyperinsulinaemia lactate release was always increased in T versus UT legs. MCT1 was lower (P<0.05) and MCT4 similar in Type 2 versus Control. With training, MCT1 content always increased, while MCT4 only increased in Control. Conclusions: MCT1 content in skeletal muscle in Type 2 is lower compared with healthy men. Strength training increases MCT1 content in healthy men and in Type 2, thus normalizing the content in Type 2.

(Received 17 December 2003; accepted after revision 13 January 2004; first published online 14 January 2004)
Corresponding author F. Dela: Department of Medical Physiology, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK 2200 Copenhagen N, Denmark.  Email: f.dela{at}mfi.ku.dk

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