The premise that lung function can regulate chest wall mobility is an accepted concept. Descriptions of the primary and accessory respiratory structures do not usually include spinal components as a part of these classifications. The case for including these components as a part of the respiratory mechanism and their role in the development of dyspnea and chest wall rigidity in chronic obstructive pulmonary disease (COPD) is reviewed. Mechanical impairment of the chest wall is a contributing factor in the prognosis of COPD. Reducing this impairment improves prognosis. Because spinal manipulation and soft-tissue therapy increase joint mobility and decrease muscle hypertonicity, respectively, applying these interventions to the chest wall in COPD could reduce chest wall rigidity, thereby improving breathing mechanics. Improvements in breathing mechanics reduce the work of the respiratory muscles and delay the onset of dyspnea. Exercise capacity is reliant on the ability to overcome activity-limiting dyspnea, which usually occurs prior to maximum exercise capacity being reached. Delaying the onset of dyspnea permits more exercise to be performed before dyspnea develops. Spinal manipulation and soft-tissue therapy have the potential to deliver such a delay. Because exercise tolerance is considered to be a strong predictor of quality of life and survival in COPD, any increase in exercise capacity would therefore improve prognosis for the disease.