The mechanism against entry of gastric content into the pharynx during high-intensity vocalization such as seen among professional singers is not known. We hypothesized that phonation-induced upper esophageal sphincter (UES) contraction enhances the pressure barrier against entry of gastroesophageal contents into pharynx. To determine and compare the effect of phonation on luminal pressures of the esophagus and its sphincters, we studied 17 healthy volunteers (7 male, 10 female) by concurrent high-resolution manometry and voice analysis. We tested high-and low-pitch vowel sounds. Findings were verified in six subjects by UES manometry using a water-perfused sleeve device. Eight of the volunteers (2 male, 6 female) had concurrent video fluoroscopy with high-resolution manometry and voice recording. Fluoroscopic images were analyzed for laryngeal movement. To define the sex-based effect, subgroup analysis was performed. All tested phonation frequencies and intensities induced a significant increase in UES pressure (UESP) compared with prephonation pressure. The magnitude of the UESP increase was significantly higher than that of the distal esophagus, the lower esophageal sphincter (LES), and the stomach. Concurrent videofluoroscopy did not show posterior laryngeal movement during phonation, eliminating a purely mechanical cause for phonation-induced UESP increase. Subgroup analysis demonstrated phonation-induced UESP increases in males that were significantly greater than those of females. Phonation induces a significant increase in UESP, suggesting the existence of a phonation-induced UES contractile reflex. UESP increase due to this reflex is significantly higher than that of the distal esophagus, LES, and stomach. The phonation-induced UESP increase is influenced by sex.upper esophageal sphincter ANATOMIC CONTINUITY OF THE stomach and lung necessitates the existence of elaborate defense mechanisms for prevention of retrograde aspiration. In the past several years our laboratory has been involved in studying these mechanisms. Our overall hypothesis has been that reflux-related upper gastrointestinal or respiratory events trigger a number of reflexes that prevent entry of refluxate into the aerodigestive tract and the lung. Examples of these mechanisms include upper esophageal sphincter (UES) contractile reflexes (14,18,22,28,30,34,36,37), secondary esophageal peristalsis (3,5,7,8,10,16,19,26), vocal cord closure reflexes (6,21,29,(31)(32)(33), and pharyngeal reflexive swallow (35) in response to esophageal or pharyngeal stimulation. The activation of airway-protective mechanisms in response to respiratory events with potential for causing reflux events such as phonation and cough has not been systematically studied.Phonation requires rapid opening and closing of the vocal folds to interrupt the air stream (25), accompanied by an increase in subglottal tracheal pressure that is believed to be generated by contraction of the diaphragm, simultaneously causing an increase in intra-abdominal pressure. This minimal su...