We explored the mechanism(s) of increased aromatic amino acids concentrations in liver cirrhosis using Phe and Tyr isotope infusions in male patients with compensated cirrhosis (five in Child Class A, three in B) and in eight matched healthy controls, both in post-absorptive and fed states. After a baseline period, a standard liquid mixed-meal was fed continuously over 4-hr. Both a "plasma" and an intracellular (ic) model were employed. In the patients, steady-state Phe and Tyr concentrations were 30%-50% greater, and rates of Phe appearance (Ra) (plasma model), Tyr Ra, and Phe hydroxylation (both models), were 25%- >100% greater than in controls in both states. Meal ingestion increased (p<0.05 or less vs. basal) Phe and Tyr concentrations, Phe and Tyr Ra, Phe hydroxylation, and % Tyr Ra not deriving from Hy in both groups. Hy and Tyr Ra remained >50% greater (p<0.04 -p<0.01) in patients, whereas Phe Ra was more modestly increased. Phe utilization for protein synthesis increased similarly in both groups. Tyr clearance was normal, whereas Phe clearance tended to be lower (p=0.09, ic model) in the patients. In summary, in compensated liver cirrhosis studied under fasted and fed states: 1) Tyr Ra is increased; 2) Phe hydroxylation and Phe Ra (plasma model) are increased: 3) Tyr clearance is normal; 4) Phe clearance is slightly decreased. In conclusion, in cirrhosis increased total tyrosine Ra and hydroxylation contribute to fasting and post-meal hypertyrosinemia, whereas the mechanism(s) responsible for the hyperphenylalaninemia may include both increased production and decreased disposal.