These myogenic deficits are aggravated by the COPD systemic milieu (oxidative/inflammatory stress, hypoxemia, corticosteroid exposure, and comorbidities), which blunts myogenic transcription programs (e.g., TNF-α/myostatin effects on MyoD/myogenin) and can directly impair muscle precursor cell differentiation, particularly during acute exacerbations [15,16,84,85,86,87]. Here, MYOD1 is linked to chronic obstructive pulmonary disease.