A brief review of the literature concerning the synthesis of phosphatidylcholine and phosphatidylethanolamine in muscle suggests that the cytidine pathways are replaced by the recently proposed acyl-specific de novo and salvage glycerolphosphodiester pathways ( Infante, 1984) in fully differentiated muscle. An analysis of published data suggests an impaired synthesis of 4,7,10,13,16,19-docosahexaenoic phosphatidylcholine, at the level of de novo sn-3-glycerolphosphorylcholine synthesis, as the primary defect in Duchenne and ( dy) murine muscular dystrophies. This phosphatidylcholine species is postulated to be required for optimum sarcoplasmic Ca 2+ transport activity. It is proposed that this impairment initiates the secondary series of events which lead to the observed pathology of these diseases. Based on some predictions of the hypothesis, potential diagnosis and treatments are suggested.