Abstract

To elucidate the mechanism of dynamic strain aging (DSA) causing serrations in the tensile curves of an fcc austenitic Fe-18Mn-0.55C (wt.%) twinning-induced plasticity (TWIP) steel, many tensile tests were performed by varying both tensile temperature (203−323 K) and initial strain rate (ε˙ini = 1 × 10−2 − 1 × 10−4/s). At the ranges of tensile temperature and ε˙ini adopted in this study, only type A serrations appeared, and a critical engineering strain (ec) for serrations decreased with increasing tensile temperature and with decreasing ε˙ini. For the short-range diffusion model based on C-Mn complex, the activation energy value (QreC) for the reorientation of C in C-Mn complex was calculated by ab-initio simulation. The QreC value was ~2.4 eV for the fcc austenite matrix, and 0.60 eV and 0.18 eV for the hcp stacking fault depending on diffusion path. There was no intersection between staying time (ts) and reorientation time (tre) calculated using the QreC values. This indicates that DSA is not caused by the reorientation of C-Mn complexes. In addition, ec revealed no dependency on the concentration of vacancy (Va). Therefore, DSA causing type A serrations is not explained by short-range diffusion models based on C-Mn and C-Va complexes. DSA is elucidated by the dislocation arrest model, which belongs to the long-range diffusion model. The measured activation energy (0.85 eV) corresponding to the activation energy (0.57−1.00 eV) for dislocation pipe diffusion of C and C-segregated dislocations in atom probe tomography (APT) maps support the occurrence of long-range C diffusion.

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