Developmental knockdown of neuronal Raptor (mTORC1 component) reduced embryonic survival but didn't impact adult mortality, while neuronal mTOR knockdown increased adult mortality despite normal embryonic development. Both interventions significantly decreased growth rates, body weight, fat mass, blood glucose levels, and exercise capacity in mice. This neuronal specificity reveals a critical paradox in mTOR biology. While systemic rapamycin treatment consistently extends lifespan across species, selectively reducing mTOR signaling in neurons during development appears to create metabolic dysfunction that could undermine healthspan benefits. The finding that mTORC1 reduction may confer post-birth survival advantages suggests timing and tissue specificity are crucial factors in mTOR's longevity effects. This challenges the assumption that mTOR reduction is universally beneficial and highlights why clinical translation of mTOR-based interventions remains complex. The neuronal control of whole-body metabolism through mTOR signaling represents an important mechanistic insight, but the reduced exercise capacity and metabolic dysfunction observed here suggest that blanket mTOR inhibition strategies may need refinement to avoid compromising physical function while pursuing longevity benefits.