Heart failure (HF) is a slow progressive syndrome characterized by low cardiac output and peripheral metabolic, biochemical and histological alterations. Protein loss and reduced protein turnover occur with aging, but the consequences of CHF superimposed on the normal aging response are unknown. This study has two objectives. Firstly to determine if there was a difference between older aged match controls and those with stable heart failure (i.e., ischemic pathology) in whole body protein turnover and secondly, whether protein metabolism in liver and skeletal muscle protein turnover is impacted by CHF. We measured the whole body protein synthesis rate with a U-¹⁵N labeled algal protein hydrolysate in 10 patients with CHF and 10 age matched controls. The muscle fractional synthesis rate of lateral vastus muscle was determined with U-¹³C alanine on muscle biopsies obtained by a standard percutaneous needle biopsy technique. The fractional synthesis rates of five plasma proteins of hepatic origin (fibrinogen, complement C-3, ceruloplasmin, transferrin and VLDL Apoliprotein B-100 was determined using ²H₅ L-phenylalanine as the tracer. Results: Whole body protein synthesis rate was reduced in the CHF patients (3.09 ± 0.19 vs 2.25 ± 0.71 g prot. kg^-1.d^-1, p <0.05) as was the muscle fractional synthesis rate (3.02+0.58 vs 1.33 + 0.71 %. d^-1, p<0.05) and of VLDL Apoliprotein B-100 (265 + 25 vs 197 + 16 %. d^-1, p<0.05). The CHF patients were hyperinsulinemic (9.6 ± 3.1 vs 47.0 + 7.8 µU/ml, p<0.01). The results were compared against those found with bed rest. Conclusions: (1) Protein turnover is depressed in CHF patients, both skeletal muscle and liver are impacted. (2) The results are similar to those found with bed rest suggesting that the inactivity associated is a factor in the depressed protein metabolism.