Background: We evaluated associations of CT-defined sarcopenia and myosteatosis with complicated acute left-sided colonic diverticulitis (ALCD) and their incremental discrimination beyond clinical characteristics and inflammatory markers. Methods: This retrospective single-center cohort included 164 adults hospitalized with CT-confirmed ALCD. L3 skeletal muscle index (SMI) and attenuation classified patients as having neither abnormality, CT-defined sarcopenia only, myosteatosis only, or both abnormalities. Complicated ALCD was defined as World Society of Emergency Surgery (WSES) CT stage ≥ 1A. Multivariable logistic regression and bootstrap internal validation of discrimination and calibration were performed. An additional sensitivity analysis used WSES stage ≥ 1B. Results: Complicated ALCD occurred in 93/164 patients (56.7%). Proportions differed across the four phenotypes (34.7%, 48.0%, 61.5% and 78.4%; overall p < 0.001). A separate analysis showed a positive trend with the number of muscle abnormalities (0, 1 or 2; p < 0.001). After adjustment, myosteatosis alone (aOR, 4.27; 95% CI, 1.34–13.62) and both abnormalities (aOR, 9.27; 95% CI, 2.85–30.17) remained independently associated with complicated ALCD, whereas CT-defined sarcopenia alone did not. Adding muscle phenotypes to a clinical reference model containing age, sex, ASA class, ACCI, WBC and CRP increased the apparent AUC from 0.837 to 0.877 (apparent ΔAUC, 0.040; 95% CI, 0.004–0.078). Optimism-corrected AUCs were 0.812 and 0.845 (corrected ΔAUC, 0.033). The phenotype-extended clinical model had an optimism-corrected calibration slope of 0.806, indicating residual overfitting. Associations for myosteatosis and the combined phenotype were also observed using WSES stage ≥ 1B. Twelve-month CT-confirmed repeat attacks occurred in 11/121 evaluable patients (9.1%), without phenotype differences (p = 0.553). Conclusions: Myosteatosis and the combined phenotype were associated with complicated ALCD and added discriminatory information beyond the clinical reference model. Residual overfitting and the absence of external validation limit clinical application; clinical net benefit remains unestablished.