Adaptive mTOR inhibition guided by real‑time recovery signals offers a way to keep the civilization‑survival dial in the range where autophagy is upregulated without sacrificing the anabolic capacity needed for tissue repair. High heart‑rate variability (HRV) and deep sleep reflect a parasympathetic state that activates AMPK, which in turn phosphorylates TSC2 and suppresses mTORC1 activity, promoting autophagy and stress resistance [1][2]. Conversely, low HRV signals a sympathetic dominance that favors mTORC1‑driven protein synthesis for wound healing and immune defense [3]. By dosing rapamycin only when wearable‑derived HRV exceeds a personalized threshold (e.g., >70 ms RMSSD) and skipping doses when HRV falls below that threshold, we predict that intermittent mTORC1 suppression will be timed to periods when the organism is already biased toward survival mode, thereby amplifying autophagy without triggering the compensatory rebound that occurs with constant inhibition [4][5]. We can test this hypothesis in a crossover trial with two arms: (1) fixed low‑dose rapamycin (3 mg weekly) and (2) HRV‑adaptive rapamycin (same weekly total dose but administered only on days when overnight HRV exceeds the individual’s 75th percentile). Primary outcomes will be changes in circulating LC3‑II/I ratio (autophagy marker) and myofibrillar protein synthesis rate measured by deuterated leucine incorporation after a standardized resistance‑exercise bout. Secondary outcomes include lean‑mass change, illness‑free days, and self‑reported recovery scores. We expect the adaptive arm to show a ≥20 % greater increase in autophagy markers and no significant difference in muscle‑protein synthesis compared with the fixed arm, while the fixed arm may show a blunted synthetic response due to chronic mTORC1 suppression [6][7]. A falsifiable outcome would be that the adaptive regimen fails to elevate autophagy above baseline or reduces muscle‑protein synthesis relative to fixed dosing, indicating that recovery‑linked timing does not uncouple the two processes. Beyond the simple dial metaphor, we propose that HRV‑linked AMPK activation creates a bistable switch: when AMPK activity crosses a threshold, it not only inhibits mTORC1 but also deacetylates FOXO3 via increased NAD+ synthesis, reinforcing autophagy‑gene expression independently of rapamycin [8]. This mechanistic layer predicts that measuring mitochondrial acetyl‑FOXO3 levels will serve as a pharmacodynamic biomarker for successful adaptive dosing. If adaptive dosing does not alter acetyl‑FOXO3 despite HRV‑guided rapamycin intake, the proposed AMPK‑FOXO3 circuit would be insufficient to explain the observed effects, prompting a revision of the model. Safety monitoring will focus on opportunistic infection rates and lipid panel changes, as previous work shows that intermittent rapamycin preserves immune competence while still modulating inflammation [4][5]. We will also collect nocturnal skin‑temperature variability, which correlates with mitochondrial uncoupling and may provide an orthogonal corroboration of the survival‑mode signal. A secondary analysis will test whether combining HRV and temperature thresholds improves predictive power for autophagy activation, using a multivariable logistic regression model. If the combined metric outperforms HRV alone, it would support the hypothesis that multiple parasympathetic readouts converge on a common AMPK‑FOXO3 axis. Conversely, if neither metric predicts changes in autophagic flux, the civilizational‑survival dial framework would need refinement to incorporate additional nutrient‑sensing layers such as leucine‑triggered Rag GTPase activity.