Recovery Capacity Theory proposes that biological resilience depends not only on energy availability, structural integrity, information processing, or damage burden, but also on the timing, completeness, and reserve capacity of repair. The framework introduces recovery half-life, temporal oxidative debt, and repair reserve capacity as measurable variables describing how biological systems return to baseline following stress. Using the mitochondrial PRDX3–TRX2–GRX2–SRX network as an initial mechanistic model, the manuscript explores how recovery kinetics may influence aging, frailty, mitochondrial dysfunction, neurodegeneration, chronic illness, and stress intolerance. Sulfur metabolism, glutathione dynamics, reactive sulfur species, circadian timing, and reserve architecture are integrated into a broader resilience framework. The manuscript is intended as an evidence-led and explicitly falsifiable synthesis designed to generate testable predictions rather than establish clinical claims. The central proposal is that future biology may benefit from measuring recovery curves and reserve capacity in addition to traditional static biomarkers.