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Normal swallow‐induced contraction of the esophagus is called primary peristalsis. Following closure of the UES and entry of the bolus into the esophagus, a progressive circumferential contraction begins in the upper esophagus and passes distally along the esophageal body to reach the relaxed LES. The LES then contracts in sequence. The velocity of the peristaltic wave varies between 2.5 and 5 cm/s along the esophagus in a bimodal fashion [160–162] (Figure 5.9). The duration of normal swallow‐induced contraction is less than 7 s, and contraction amplitudes rarely exceed 200 mmHg [163]. Figure 5.10 shows these events as recorded by both conventional and high‐resolution manometry.

Figure 5.9 Velocity of the peristaltic wave front along the esophagus. The bimodal velocity was apparent using axial reconstructions of pressure data. The two modes represent propagation through the proximal striated muscle and distal smooth muscle regions, with deceleration near the lower esophageal sphincter. There is no break in velocity in the smooth muscle region.

Source: Clouse RA, Diamant NE. Motor function of the esophagus. In: Johnson LR, ed. Physiology of the Gastrointestinal Tract, 4th ed; 2006. © 2006, Elsevier.

For peristalsis to progress distally, the proximal esophagus needs to contract before the distal esophagus at any point along the esophagus. This is ensured by esophageal inhibition, which ensures a latency gradient progressing from proximally towards the distal esophagus. The following are key factors that contribute to the latency gradient: (i) sequential firing of preganglionic efferent vagal nerve; (ii) varying discharge latency to firing of vagal efferent fibers [164]; (iii) shorter latency to contraction in the proximal esophageal muscle compared to distally [165, 166]; and (iv) gradient of cholinergic and nitrergic nerves and neurotransmitters along the esophagus [166].

Esophageal shortening of 2–2.5 cm also occurs with swallow‐induced contraction. This is mediated by longitudinal muscle contraction, which proceeds distally at 2–4 cm/s slightly in advance of the circular muscle contraction [167–169] or very close to it [169–171]. The onset, peak, and duration of circular and longitudinal muscle contraction are precisely coordinated throughout the esophagus [172, despite different neural control of the two muscle layers [173]. Longitudinal muscle contraction augments circular muscle contraction and reduces stress on the esophageal wall [174]. Simultaneous circular and longitudinal muscle contraction stiffens the esophageal wall and augments contraction to better propel a bolus. Longitudinal muscle contraction thins the distal esophageal wall, allowing distal accommodation of the bolus as it moves forward. Axial stretch induces distal esophageal and LES relaxation as well as deglutitive inhibition, potentially by activating mechanosensitive inhibitory motor neurons, resulting in NO‐mediated inhibition in the distal esophagus [175–177]. Swallow‐induced UES elevation also stretches the esophagus longitudinally, with similar results [172]. Coordination of the longitudinal and circular muscle layers is partly a function of cholinergic innervation, which can be abnormal in spastic disorders such as nutcracker esophagus [178, 179].

Of interest, the amplitude of the circular muscle contraction shows a consistent decrease in a short segment 4–6 cm below the UES. This is termed the transition zone, the region where striated (segment 1) and smooth muscle (segments 2 and 3) have interspersed and/or innervation changes from the RLN proximally to the more distal vagal branches. There are two other troughs in amplitude: one separating the smooth muscle segment into two (segment 2, segment 3) and the other separating the distal smooth muscle segment from the LES [160, 162, 180]. It is not known if these findings are due to separate neuromuscular units governed by output from subunits in the SPG, or by peripheral intramural mechanisms within regional differences in muscle or nerve. If central, it raises the possibility that SPG control of the esophagus may be grouped into distinct functional subunits defined by sphincters and contracting segments.

The contraction amplitude determines the efficacy of bolus propulsion and esophageal emptying, with this efficacy decreasing as amplitude decreases [181]. At a threshold of 30 mmHg, incomplete bolus transit is identified with a sensitivity of 85% and specificity of 66% [182]. Gravity facilitates transport, especially of liquids, and distal contraction amplitude can decrease in the more upright position [183].