In COPD-only patients, lacking severe metabolic dysregulation, acute exercise stressors (mechanical strain, oxidative stress, transient hypoxia) may dominate the post-exercise molecular landscape, activating EGR1 through MAPK/ERK and AP-1 pathways, resulting in maintained or slightly increased expression despite functional improvement. The gene discussed is EGR1; the disease is chronic obstructive pulmonary disease.