Sweat can leave lasting chemical damage in aged skin after conditioning breaks
Extracellular covalent adduct accumulationIn susceptible photoaged human skin, sweat-derived urea may chemically modify extracellular proteins, leaving damage despite restored sweating.
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HERETICAL: In susceptible photoaged skin, retained sweat becomes a chemically damaging exposure after maintenance interruption creates superficial microerosions. Sweat-derived urea supplies cyanate that carbamylates exposed, slowly replaced extracellular proteins. Resuming conditioning restores secretion but renews the chemical exposure, so normal isolated sweating coexists with persistent loss of mechanical and repair competence. The stored state is covalent protein modification, not continuing inflammation or diminished conditioning. Preventing this modification would stabilize SPV_12 and prevent escalation of SPV_11.
At sweat concentrations, temperatures and exposure durations actually measured during bounded interruption and resumption, isotopically labelled sweat urea produces labelled homocitrulline in extracellular proteins of aged human skin explants, accompanied by impaired mechanical recovery.
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Removing urea from otherwise composition-matched artificial sweat prevents both outcomes; adding it back restores them. Exposure cessation fails to restore function within the declared recovery window despite uninterrupted repair time. Absence of sufficient adduct formation at realistic exposure falsifies this mechanism before clinical testing and favors the repair-restart rival.
Repeated friction erases skin repair progress and sustains failure after maintenance gaps predicts instead: With cumulative thermal exposure, friction dose, sweat chemistry and systemic support matched, distributing friction into frequent interruptions prolongs recovery more than concentrating the same dose outside one protected repair interval.
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Serial imaging must show actual loss of newly established epithelial coverage after interruptions. Providing one sufficiently long protected interval restores barrier and subsequent joint-challenge performance without increasing conditioning dose. Recovery should occur without any necessary change in protein-carbamylation burden, separating this mechanism from IH_Q_L3_M_G4_5_01.