The mechanism of dynamic strain aging for type A serrations in tensile flow curves of Fe-18Mn-0.55C (wt.%) twinning-induced plasticity steel

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 (e_c) 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 (Q_re ^C) for the reorientation of C in C-Mn complex was calculated by ab-initio simulation. The Q_re ^C 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 (t_s) and reorientation time (t_re) calculated using the Q_re ^C values. This indicates that DSA is not caused by the reorientation of C-Mn complexes. In addition, e_c 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.