Heat stress adversely affects poultry production and meat quality, leading to economic losses. This study aimed to investigate the effects of adding tributyrin on growth performance, meat quality, muscle oxidative status, and gut microbiota of Taihe silky fowls under cyclic heat stress (CHS) conditions. In this study, 120-day-old Taihe silky fowls (male) were randomly divided into six dietary treatments. These treatments included a normal control treatment (NC, fed a basal diet), a heat stress control treatment (HS, fed a basal diet), and HS control treatments supplemented with 0.04%, 0.08%, 0.16%, and 0.32% tributyrin, respectively. The NC treatment group was kept at 24 ± 1 °C, while the HS treatment birds were exposed to 34 ± 1 °C for 8 h/d for 4 weeks. Results showed that CHS decreased growth performance and compromised the meat quality of broilers (p < 0.05). However, tributyrin supplementation improved ADG and FCR in broilers exposed to CHS (p < 0.05). Additionally, tributyrin supplementation resulted in increased shear force value and GSH-Px activity, as well as a decrease in drip loss, ether extract content, and MDA content of the breast muscle in broilers under CHS (p < 0.05). Furthermore, tributyrin supplementation up-regulated the mRNA expressions of Nrf2, NQO1, HO-1, SOD, and GSH-Px of the breast muscle in broilers exposed to CHS (p < 0.05). Based on these positive effects, the study delved deeper to investigate the impact of 0.16% tributyrin supplementation (HS + 0.16%T) on the cecum microbiota. The HS + 0.16%T treatment showed an increase in the relative abundance of Rikenellaceae_RC9_gut_group (p < 0.05) and a trend towards an increase in Lactobacillus (p = 0.096) compared to the HS treatment. The results indicate that supplementation successfully improved the growth performance and meat quality of Taihe silky fowls. Furthermore, tributyrin supplementation, particularly at levels of 0.16%, improved meat quality by enhancing muscle antioxidant capacity, which is believed to be associated with activation of the Nrf2 signaling pathway.