The therapeutic value of physical exercise for mental health is widely acknowledged yet mechanistically underspecified. This paper formalizes the Exercise–ECS–Attachment Axis—a unified mechanistic pathway demonstrating that moderate-intensity aerobic exercise (60–75% HRmax) functions as a biological solvent for the vlPAG-mediated Shame Lock (Paper 6) through targeted upregulation of N-arachidonoylethanolamine (Anandamide/AEA) and functional downregulation of Fatty Acid Amide Hydrolase (FAAH).1,2 Drawing on converging evidence from exercise physiology, endocannabinoid pharmacology, PAG columnar neuroscience, and Polyvagal Theory, we demonstrate that the exercise-induced AEA surge activates CB1 receptors in the amygdala and PAG, inhibiting defensive glutamate release and creating a temporal window of safety signaling sufficient to re-engage the Ventral Vagal Complex (VVC) for social engagement.3,4,5 The pathway is further reinforced by a synergistic AEA–Oxytocin loop that bridges individual regulation to relational re-engagement.6 Critically, this paper introduces the Exercise Resistance Phenotype—a blunted endocannabinoid response documented in PTSD populations7—as a diagnostic marker within the SADA-Entropy framework (Paper 3). We further differentiate exercise response by ABM attachment profile: Architect (dlPAG-dominant), Radar (lPAG-dominant), and Special Forces (vlPAG-dominant), demonstrating that generic exercise prescription produces asymmetric outcomes across profiles. The Exercise–ECS–Attachment Axis constitutes the primary non-pharmacological implementation mechanism for Phase 1 of the SADA Recalibration Protocol (Paper 4).