Expiratory flow limitation is the pathophysiologic hallmark of chronic obstructive pulmonary disease (COPD), but dyspnea (breathlessness) is its most prominent and distressing symptom. Acute dynamic lung hyperinflation, which refers to the temporary increase in operating lung volumes above their resting value, is a key mechanistic consequence of expiratory flow limitation, and has serious mechanical and sensory repercussions. It is associated with excessive loading and functional weakness of inspiratory muscles, and with restriction of normal VT expansion during exercise. There is a strong correlation between the intensity of dyspnea at a standardized point during exercise, the end-expiratory lung volume, and the increased ratio of inspiratory effort to volume displacement (i.e., esophageal pressure relative to maximum: Vt as a % of predicted VC). This increased effort–displacement ratio in COPD crudely reflects the neuromechanical dissociation of the respiratory system that arises as a result of hyperinflation. The corollary of this is that any intervention that reduces end-expiratory lung volume will improve effort–displacement ratios and alleviate dyspnea. In flow-limited patients, bronchodilators act by improving dynamic airway function, thus enhancing lung emptying and reducing lung hyperinflation. Long-acting bronchodilators have recently been shown to reduce hyperinflation during both rest and exercise in moderate to severe COPD. This lung deflation allows greater Vt expansion for a given inspiratory effort during exercise with consequent improvement in dyspnea and exercise endurance.