The molecular mechanisms of muscle atrophy in chronic obstructive pulmonary disease are poorly understood. In wasted animals, muscle mass is regulated by several AKT - related signalling pathways. Purposes: To measure the protein expression of AKT, FoxO-1, -3, atrogin-1 and the phosphophrylated form of AKT, p70^S6K GSK-3 and 4EBP1 and the mRNA expression of atrogin-1, MuRF1, FoxO-1,-3 in the quadriceps of 12 patients with chronic obstructive pulmonary disease with muscle atrophy and 10 healthy controls. Five patients with chronic obstructive pulmonary disease with preserved muscle mass were subsequently recruited and were compared with 6 patients with low muscle mass. Methods: were measured the quadriceps by Western blot and quantitative PCR, respectively. Results: The levels of atrogin-1 and MuRF1 mRNA and of phosphorylated AKT and 4E-BP1 and FoxO-1 proteins were increased in chronic obstructive pulmonary disease patients with muscle atrophy compared to healthy controls while atrogin-1, p70^S6K, GSK-3 and FoxO-3 protein levels were similar. Chronic obstructive pulmonary disease patients with muscle atrophy showed an increased expression of p70^S6K, GSK-3 and 4E-BP1 compared to chronic obstructive pulmonary disease patients with preserved muscle mass. Conclusion: An increase in atrogin-1 and MuRF1 mRNA and FoxO-1 protein content was observed in the quadriceps chronic obstructive pulmonary disease patients. The transcriptional regulation of atrogin-1 and MuRF1 may occur via FoxO-1 but independently of AKT. The overexpression of the muscle hypertrophic signalling pathways found in chronic obstructive pulmonary disease patients with muscle atrophy could represent an attempt to restore muscle mass.