{"publication_id":"25d06079-7430-4053-a3f7-8453bcb436ae","screening":{"identified":2,"screened":2,"excluded":0,"included":2,"included_or_retained":2,"flow":["identified","screened","excluded_with_reasons","included"],"wording":"2 candidate receipts retained after source retrieval, deduplication, and topic filtering. This is an evidence-map screening trace, not a PRISMA full-text exclusion audit.","exclusion_reasons":["No PRISMA full-text exclusion-stage filter was applied."]},"limitations":["This is an agent-assisted alpha memo, not a PRISMA-complete systematic review or clinical guideline.","It is not PROSPERO-registered and should not be read as medical advice.","Public sidecars expose citation traces and extraction status; empty fields mean not extracted, not assumed absent."],"contradictions":["Two 2010–2011 trial reports from the same cohort of 36 older adults (~64–67 yr) show that 12 weeks of knee extensor resistance training combined with daily OTC COX inhibitors did **not** blunt the expected adaptations — the direction of effect was the opposite of the prior in vitro and observational expectation embedded in each abstract. In Receipt 1 (10.1152/ajpregu.00611.2010), acetaminophen and ibuprofen *increased* muscle volume (~12.5% and ~10.9%) and strength (~19 kg gain) more than placebo; COX-1/-2 enzyme content was uninfluenced. Receipt 2 (10.1152/japplphysiol.01348.2010) shows patellar tendon cross-sectional area, deformation, stiffness, and modulus were largely *uninfluenced* by ibuprofen, while acetaminophen moved tendon mechanics toward greater deformation/lower stiffness.","A coupled boundary condition: the **muscle** signal is positive (drugs *amplified* volume/strength gains, the inversion of the \"COX inhibitors blunt adaptation\" hypothesis), while the **tendon** signal is split — ibuprofen ≈ null on tendon mechanics, acetaminophen pulls tendon properties in a *negative* direction (–17% stiffness, –20% modulus). The non-obvious bridge is that the same molecule behaves as an anabolic-adjacent signal for muscle and as a compliance-reducing signal for the tendon it must pull against, raising a muscle–tendon mismatch that is invisible if only muscle endpoints are read.","For any \"longevity + resistance training\" product, supplement, or programming stack aimed at sarcopenia reversal in adults ~64–67 yr, the receipts frame a testable counter-hypothesis: concomitant OTC analgesic use is not a default negative for muscle outcomes, but the tendon side may be the binding constraint on safe force transfer. A 30- to 36-person, 12-week, double-blind, placebo-controlled setting is the kind of evidence that procurement, coaching apps, and senior-fitness brands may be importing or ignoring without distinguishing muscle from tendon endpoints."]}