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Gene expression of myogenic factors and phenotype-specific markers in electrically stimulated muscle of paraplegics

¹Department of Molecular Muscle Biology, Copenhagen Muscle Research Centre, Righospitalet, University of Copenhagen, Copenhagen, Denmark; ²Department of Physiology, University College London, London, United Kingdom; ³Department of Biomedical Sciences, Consiglio Nazionalle delle Ricerche Centre of Muscle Biology and Physiopathology, University of Padua, Padua, Italy; ⁴Centre for Spinal Cord Injured, Neuroscience Centre, Rigshospitalet, Copenhagen, Denmark; and ⁵Sports Medicine Research Unit, Bispebjerg Hospital, Copenhagen, Denmark

Submitted 18 October 2004 ; accepted in final form 1 March 2005

The transcription factors myogenin and MyoD have been suggested to be involved in maintaining slow and fast muscle-fiber phenotypes, respectively, in rodents. Whether this is also the case in human muscle is unknown. To test this, 4 wk of chronic, low-frequency electrical stimulation training of the tibialis anterior muscle of paraplegic subjects were used to evoke a fast-to-slow transformation in muscle phenotype. It was hypothesized that this would result from an upregulation of myogenin and a downregulation of MyoD. The training evoked the expected mRNA increase for slow fiber-specific markers myosin heavy chain I and 3-hydroxyacyl-CoA dehydrogenase A, whereas an mRNA decrease was seen for fast fiber-specific markers myosin heavy chain IIx and glycerol phosphate dehydrogenase. Although the slow fiber-specific markers citrate synthase and muscle fatty acid binding protein did not display a significant increase in mRNA, they did tend to increase. As hypothesized, myogenin mRNA was upregulated. However, contrary to the hypothesis, MyoD mRNA also increased, although later than myogenin. The mRNA levels of the other myogenic regulatory factor family members, myogenic factor 5 and myogenic regulatory factor 4, and the myocyte enhancer factor (MEF) family members, MEF-2A and MEF-2C, did not change. The results indicate that myogenin is indeed involved in the regulation of the slow oxidative phenotype in human skeletal muscle fibers, whereas MyoD appears to have a more complex regulatory function.

spinal cord; low-frequency stimulation; fast-to-slow transition; metabolic genes; myosin heavy chain

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