Hypoxia episodes have been generally studied over the last decade for their lethal consequences in coastal areas, which are nurseries for several fish species. The possible long-lasting effects of non-lethal hypoxia exposures at larval stage are, however, poorly documented. We investigated the long-lasting phenotypic impact of an experimental exposure to moderate hypoxia (40 % air saturation) between 30 and 38 days post-hatching in European sea bass (Dicentrarchus labrax). At the juvenile stage, our data indicate that this early hypoxia exposure impacted on juvenile growth rate but not on hypoxia tolerance. Growth depression was associated with a regulation of metabolism as suggested by a decrease in blood glycaemia, a decreased hepatic expression of the glucose transporter glut2 and of acaca involved in fatty acid synthesis as well as an increased hepatic expression of glycolytic ldh-a, which is a target gene of hypoxia inducible factors (HIFs). Interestingly, while fish were not exposed to hypoxia, the cellular oxygen sensor egln3 gene, which is also a target of HIFs, exhibited higher expression level in the hepatic tissue of juveniles that have experienced hypoxia at larval stage. Even if further studies are needed to evaluate the functional significance of such effects and to decipher the underlying molecular mechanisms, the present data evidence that early life exposure to a hypoxia event has long-lasting impact on sea bass juvenile physiology.