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Whether a deficiency in muscle repair and regeneration may exist in the lower limb muscles of COPD patients remains debatable. We hypothesized that the negative regulator myotastin may inhibit muscle regeneration potential in sarcopenic COPD patients. In vastus lateralis (VL) of control subjects and severe COPD patients with and without sarcopenia, satellite cells (SC) were identified (immunofluorescence, anti-Pax7 and anti-myf5): activated (Pax7+ and myf5+), quiescent/regenerative potential (Pax7+ and myf-5-), and total SC, nuclear activation (TUNEL assay), and muscle fiber type (morphometry, hybrid fibers), muscle damage, muscle regeneration markers (Pax7, myf-5, myogenin, and myoD), and myostatin levels were identified. Compared to control subjects and normal body composition COPD, in the VL of sarcopenic COPD patients, myostatin protein levels, activated SC, hybrid fibers, TUNEL-positive cells, internal nuclei, and total abnormal fraction were significantly increased, while quadriceps muscle strength, numbers of Pax7+ and myf-5- and slow- and fast-twitch muscle fiber areas decreased. In VL of sarcopenic and non-sarcopenic COPD patients, TUNEL-positive cell counts were greater, whereas expression of muscle regeneration markers was lower than in controls. Myostatin may have interfered with the process of muscle cell proliferation early on during the regeneration process, thus leading to poor muscle growth and development following injury in COPD patients with sarcopenia. This may be another relevant mechanism of muscle mass loss in COPD. Method: CIBERES, FIS 18/00075 (FEDER), SEPAR 2018, and unrestricted grant from Menarini SA 2018.