We examine herein the contribution of V‐ATPase activity to the energy budget of aerobically developing embryos of Artemia franciscana and discuss the results in the context of quiescence under anoxia. ³¹P‐NMR analysis indicates that intracellular pH and NTP levels are unaffected by acute incubation of dechorionated embryos with the V‐ATPase inhibitor, bafilomycin A₁. Bafilomycin A₁ also has no significant effect on oxygen consumption by isolated mitochondria. Taken together, these data indicate that bafilomycin does not affect energy‐producing pathways in the developing embryo. However, the V‐ATPase inhibitor exhibits a concentration‐dependent inhibition of oxygen consumption in aerobic embryos. A conservative analysis of respirometric data indicates that proton pumping by the V‐ATPase, and processes immediately dependent on this activity, constitutes approximately 31% of the aerobic energy budget of the preemergent embryo. Given the complete absence of detectable Na⁺K⁺‐ATPase activity during the first hours of aerobic development, it is plausible that the V‐ATPase is performing a role in both the acidification of intracellular compartments and the energization of plasma membranes. Importantly, the high metabolic cost associated with maintaining these diverse proton gradients requires that V‐ATPase activity be downregulated under anoxia in order to attain the almost complete metabolic depression observed in the quiescent embryo.