Dual Role of Mobile Interstitials in Defect Kinetics: From Retardation to Acceleration

Abstract

Mobile interstitial atoms redistribute while defects migrate, complicating prediction of defect kinetics and leading to contradictory reports of acceleration and retardation. We formulate defect activation in a grand-canonical ensemble at fixed interstitial chemical potential and define a pathway free-energy landscape $ΔG(Λ;T,μ)$ and the corresponding activation free energy $ΔG^{\ddagger}$. We compute these quantities using both hyperplane-constrained thermodynamic integration via a mean force relation and a two-state chemical-potential integration, denoted TSCPI. The latter requires sampling only the initial and transition states; a single chemical-potential integration then yields $ΔG^{\ddagger}(T,μ)$ across a wide $μ$ range, enabling rapid mapping over temperature and chemical potential. Applied to vacancy diffusion in FCC, BCC, and HCP metals with H (including in plane and cross plane diffusion in Zr) and in BCC W with He, both free energy routes agree with diffusion coefficients from molecular dynamics mean square displacements. The resulting maps reveal regimes of suppression and enhancement, including a crossover from suppression to enhancement with increasing hydrogen concentration. A site occupancy analysis links barrier shifts to state dependent site spectrum changes and transferable interstitial interaction terms.