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This Article Full Text Full Text (PDF) All Versions of this Article: 561/2/647    most recent jphysiol.2004.073411v1 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 Google Scholar Google Scholar Articles by Constantin-Teodosiu, D. Articles by Greenhaff, P. L Search for Related Content PubMed PubMed Citation Articles by Constantin-Teodosiu, D. Articles by Greenhaff, P. L

¹ Centre for Integrated Systems Biology and Medicine, School of Biomedical Sciences, The University of Nottingham Medical School, Nottingham NG7 2UH, UK

While lowering muscle glycogen availability to an extent that would reduce muscle pyruvate formation during intense exercise, we investigated the importance of muscle pyruvate availability to pyruvate dehydrogenase complex (PDC) activation during intense exercise in human skeletal muscle. The present study demonstrated that regardless of whether pre-exercise muscle glycogen content was at a habitual resting concentration (412 ± 30 mmol (kg dry muscle)^–1) or depleted (60 ± 3 mmol (kg dry muscle)^–1), the increase in PDC activation from its resting value (5.46 ± 0.96 and 3.67 ± 0.34 nmol acetyl-CoA min^–1 (mg protein)^–1, respectively) during 10 min of exercise at 75% of the maximum rate of oxygen consumption (12.82 ± 1.72 and 13.24 ± 1.42 nmol acetyl-CoA min^–1 (mg protein)^–1, respectively) was the same, despite pyruvate accumulation during exercise being 3-fold lower in the glycogen depleted state (0.34 ± 0.04 and 0.11 ± 0.06 mmol (kg dry muscle)^–1, P < 0.001). However, as a result of the reduction in pyruvate availability, calculated flux through the PDC reaction was at least 2-fold lower in the glycogen depleted state compared with normal (21.81 ± 2.62 and 9.41 ± 0.63 nmol acetyl-CoA min^–1 (mg protein)^–1, respectively; P < 0.001). It is therefore pertinent to conclude that whilst muscle pyruvate availability appears to be important to the rate of flux through the PDC reaction during in vivo contraction, it is not of primary importance to the control of PDC activation under these conditions, which is probably principally regulated by muscle calcium availability. The proposed central role of pyruvate in muscle PDC activation during in vivo contraction may therefore have been over stated.

(Received 6 August 2004; accepted after revision 5 October 2004; first published online 7 October 2004)
Corresponding author D. Constantin-Teodosiu: Centre for Integrated Systems Biology and Medicine, School of Biomedical Sciences, The University of Nottingham Medical School, Nottingham NG7 2UH, UK. Email: tim.constantin{at}nottingham.ac.uk