Rethinking dyspnea in pulmonary rehabilitation: from respiratory load and interoceptive processing to biofeedback and neurofeedback.

Dyspnea in chronic obstructive pulmonary disease (COPD) is often treated as the perceptual consequence of altered airflow, lung volume, gas exchange, or work of breathing. Yet breathlessness is not a unitary symptom or a direct readout of pulmonary dysfunction. It comprises at least three partially dissociable sensations-air hunger, breathing effort, and chest tightness-with distinct physiological triggers and affective salience. Current models suggest that conscious breathlessness emerges from the interaction of respiratory motor drive, corollary discharge, sensory afferent feedback, central integration, and higher-order interoceptive inference. In COPD, this framework helps explain why dyspnea may diverge from spirometric impairment and why symptom burden can remain high despite appropriate treatment. This Perspective develops a hypothesis-generating conceptual model for pulmonary rehabilitation, rather than a systematic or scoping review. We argue that respiratory biofeedback may be relevant not only because it can modify breathing pattern, but also because it may help test whether changing perceived control, autonomic regulation, and affective responses to respiratory signals can influence rehabilitation-relevant outcomes. Our recent pilot trial in late-stage COPD is compatible with this interpretation, but it did not directly test cognitive-affective mechanisms of action. From this perspective, neurofeedback should not be considered an established treatment for dyspnea, but a plausible future translational research question for selected highly symptomatic patients. Extension of this framework beyond COPD to other chronic respiratory diseases requires condition-specific validation.