Materials, Vol. 18, Pages 972: The Low-Cycle Fatigue Behavior of a High-Strength Low-Alloy Steel Subjected to Tempforming

Escrito el 21/02/2025
Anastasiia Dolzhenko

Materials, Vol. 18, Pages 972: The Low-Cycle Fatigue Behavior of a High-Strength Low-Alloy Steel Subjected to Tempforming

Materials doi: 10.3390/ma18050972

Authors: Anastasiia Dolzhenko Pavel Dolzhenko Valeriy Dudko Rustam Kaibyshev Andrey Belyakov

The developed microstructures and their deformation behavior were studied in a high-strength low-alloy steel subjected to tempforming, i.e., tempering followed by large-strain rolling at temperatures of 823 K or 923 K. Tempforming has been recently proposed as an advanced treatment for low-alloy steels in order to substantially increase their impact toughness at low temperatures. However, the mechanical properties, especially the fatigue behavior, of tempformed steels have not been studied in sufficient detail. The present study, therefore, is focused on the strengthening mechanisms of the tempformed steel, placing particular emphasis on the low-cycle fatigue behavior. Tempforming resulted in a lamellar-type microstructure with a high dislocation density and dispersed Cr23C6 carbide particles. The size of the latter particles increased from 25 nm to 40 nm with an increase in tempforming temperature. The transverse grain size and dislocation density comprised 550 nm and 2.6 × 1015 m−2 after tempforming at 823 K or 865 nm and 1.8 × 1015 m−2 after processing at 923 K, respectively. Tempforming led to significant strengthening, which was attributed to high-density dislocations arranged in low-angle subboundaries. The yield strength of 1140 MPa or 810 MPa was observed for the steel samples tempformed at 823 K or 923 K, respectively. The low-cycle fatigue behavior depended on the plastic strain amplitude, which, in turn, was controlled by the previous strengthening under tempforming conditions besides the total strain amplitude. An increase in the plastic strain amplitude promoted fatigue softening that was caused by a decrease in the dislocation density as a result of subgrain coalescence.