Altering the pattern of electrical activity delivered to the muscle can change muscle contractile properties. The changes are caused by modifications in gene expression, and several regulatory mechanisms have been suggested to participate in the excitation-transcription coupling. We have focused on a group of muscle specific helix-loop-helix transcription factors that are master regulators of differentiation into muscle cells during development. These factors are also expressed in the adult, and interestingly the levels of myoD is expressed at higher levels in fast than in slow muscles, while myogenin displays the reciprocal pattern. We find that both factors are dependent on electrical stimulation, such that myogenin is induced by patterns leading to slow contractile properties in fast muscles. Effects on myoD protein-levels in the opposite direction where, however, only altered after prolonged stimulation, suggesting that changes in its protein levels could not cause the changes in contractile phenotype. MyoD can, however, be inactivated by phosphorylation at T115, and we show that the fraction of phosphorylated myoD is increased by slow-patterned activity. When a T115A mutated, constitutively active form of myoD is over expressed, a shift in form type I to type II was observed. Wild type myoD had little effect on normally active slow muscles, probably because it is phosphorylated: it had effects similar to the mutated form in inactive muscles. When myogenin was over expressed an increase in oxidative capacity typical of slow muscles were observed. We suggest that the myoD/myogenin balance is important for linking muscle activity and fiber type specific expression in adults.