In the course of work in which the phosphorylase kinase (PhK)-deficient mouse was used as a model of a defined inherited myopathy, we measured the PhK activity in regenerated autografts of normal whole extensor digitorum longus (EDL) muscles. Initially, no PhK activity was found for up to 71 days after grafting. A more sensitive assay technique revealed PhK activity in regenerated normal grafts from 43 days after grafting, but the levels never reached those found in ungrafted normal muscle. PhK activity was also reduced in normal EDL muscles following either: denervation, or tenotomy, or denervation and devascularisation, or denervation, devascularisation and tenotomy, but the reduction was never as great as that observed in grafted muscle of equivalent age. PhK activity was also reduced in the tibialis anterior (TA) muscles of the myopathic C57B1/10 mdx strain of mouse, in which the skeletal muscles undergo persistent bouts of degeneration and regeneration, whilst retaining their vascular and nervous connections. It was concluded that the loss of PhK activity in grafted muscle is due to a combination of the effects of denervation, tenotomy and regeneration which occur on grafting.