Esophageal peristalsis consists of initial inhibition (relaxation) followed by excitation (contraction), both of which move sequentially in the aboral direction. Initial inhibition results in receptive relaxation and bolus-induced luminal distension, which allows propulsion by the contraction with minimal resistance to flow. Similar to the contraction wave, luminal distension has unique waveform characteristics in normal subjects; both are modulated by bolus volume, bolus viscosity, and posture, suggesting a possible cause-and-effect relationship between the two. Distension contraction plots in patients with dysphagia with normal bolus clearance [high-amplitude esophageal contractions (HAECs), esophagogastric junction outflow obstruction (EGJOO), and functional dysphagia (FD)] reveal two major findings: 1) unlike normal subjects, there is luminal occlusion distal to bolus during peristalsis in certain patients, i.e., with type 3 achalasia and nonobstructive dysphagia; and 2) bolus travels through a narrow lumen esophagus during peristalsis in patients with HAECs, EGJOO, and FD. Aforementioned findings indicate a relative dynamic obstruction to the bolus flow during peristalsis and reduced distensibility of esophageal wall in the bolus segment of the esophagus. We speculate that a normal or supernormal contraction wave pushing bolus against resistance is the mechanism of dysphagia sensation in significant number of patients. Representations of distension and contraction, combined with objective measures of flow timing and distensibility are complementary to the current scheme of classifying esophageal motility disorders based solely on the characteristics of contraction phase of peristalsis. Better understanding of the distensibility of the bolus-containing segment of the esophagus during peristalsis will lead to the development of novel medical and surgical therapies in the treatment of dysphagia in significant number of patients.