As human pluripotent stem cells (hPSCs) exit pluripotency they were incorrectly thought to switch from aerobic glycolytic to an oxidative phosphorylation based metabolism. Through C13-metabolic analysis we show that metabolic switching occurs only during mesendoderm differentiations. Aerobic glycolysis is maintained and essential during early ectoderm specification. Therefore metabolic switching is not a required event for exit from pluripotency. MYC/MYCN binds to the promoters of key metabolic genes whose elevated expression establishes aerobic glycolysis in hPSCs, and is lost during mesendoderm formation but can be re-established by ectopically restoring MYC activity. Knockdown of MYC/MYCN within hPSCs results in the loss of aerobic glycolysis and induces a spontaneous differentiation to mesendoderm but not ectoderm. In nascent ectoderm, sustained MYCN activity maintains the transcription of 'switch' genes that are required for lineage commitment. We also show that tricarboxylic acid cycle flux is upregulated to support biosynthetic precursors production in hPSCs and ectoderm. This study identifies MYC/MYCN as developmental regulators that couple metabolism to pluripotency and cell fate determination.