Our study demonstrates that strenuous exercise induces significant reflux and related symptoms in conditioned athletes.

Aims: To evaluate capsaicin’s effects on heartburn, dyspepsia, gastric acidity and emptying, and gastro‐oesophageal reflux, and to test the hypothesis that capsaicin induces heartburn and exacerbates symptoms by sensitizing the oesophagus. Methods: Eleven heartburn sufferers underwent two separate pH monitoring sessions and assessments of gastric emptying (13C‐octanoic acid breath test), heartburn and dyspepsia (100 mm VAS) after a non‐irritant meal. The meal consisted of a sausage biscuit with egg, cheese and 30 g raw onion, 8 oz chocolate milk and a peppermint patty. Thirty minutes prior to meal consumption, subjects were administered a placebo capsule. On visit 1, subjects consumed the meal containing 100 μl 13C‐octanoic acid cooked in the egg, over 15 min. On visit 2, subjects consumed the meal plus 5 mg capsaicin in gelatin capsules. Results: Oesophageal and gastric pH profiles and gastric emptying were not different between meals. Capsaicin did not alter mean heartburn and dyspepsia scores (P > 0.05), but significantly decreased time to peak heartburn (120 min vs. 247 min; P < 0.003). Time to peak dyspepsia was not altered by capsaicin (P > 0.05). Conclusion: Capsaicin enhances noxious postprandial heartburn, presumably by direct effects on sensory neurons.

Integrated esophageal and gastric acidity provide quantitative measures of GERD pathophysiology and, compared to conventional pH parameters, should enhance evaluation of therapeutic interventions.

Chronic heartburn can reflect a wide range of diagnostic findings, including important underlying pathological features, and may warrant a full medical examination to detect such abnormal conditions and to permit selection of appropriate therapy.

Use of continuous pH recordings has become the cornerstone for assessment of gastro-oesophageal re¯ux disease (GERD) and its treatment with antisecretory agents. 1±9 Despite the fact that pH recordings involve about 900 measurements per hour, these data are frequently collapsed to a single value, such as the percentage of the recording period that pH < 4 or median pH for a particular recording period. It seems likely that fuller use of all available data from pH recordings should provide better de®nition of acidity and the differential effects of speci®c pharmacologic agents.Previously, 10 we calculated values for integrated gastric and oesophageal acidity from 24-h pH recordings performed in the conventional manner. Values that resulted from these calculations fully quanti®ed oesophageal and gastric acidity, in contrast to conventional measurements of the percentage of time that the pH is below a particular value, which only partially quanti®ed oesophageal or gastric acidity. As a result, values for integrated acidity were used to examine quantitative relationships between oesophageal acidity and gastric acidity. In addition, calculating integrated acidity made it possible to assess changes in acidity over time in a SUMMARY Background: Integrated gastric and oesophageal acidity can be calculated from measurements of gastric and oesophageal pH and used to quantify gastric and oesophageal acidity over time. Rabeprazole is a new proton pump inhibitor that is effective in treating gastro-oesophageal re¯ux disease (GERD). Aim: To use measurement of integrated gastric and oesophageal acidity to determine the onset, duration and overall effect of rabeprazole in subjects with GERD. Methods: Subjects with GERD were required to have oesophageal pH £ 4 for at least 10% of a 24-h recording. Effects of 20 mg rabeprazole on 24-h gastric and oesophageal pH were measured on days 1 and 7 of dosing. Integrated gastric and oesophageal acidity were calculated from time-weighted average hydrogen ion concentrations at each second of the 24-h record.

Approximately 30% of individuals chronically using antacids for heartburn had esophageal sensitivity to mechanical or chemical stimuli despite negative endoscopy and pH monitoring. Our findings suggest that a significant subset of typical heartburn sufferers have a lower threshold for esophageal sensation and pain, which may influence options for pharmacological intervention in such subjects.

Patients with nonerosive gastroesophageal reflux disease often have relatively low esophageal acid exposure and respond suboptimally to gastric acid suppression. In these patients, other constituents of gastric contents may induce esophageal symptoms. We have demonstrated that gastric contents can cause heartburn when the gastric pH >4. (Aliment Pharm Ther 14:129-134, 2000). The aim of this study was to determine relative sensitivities to chenodeoxycholic and ursodeoxycholic acids, and 0.1 N HCl, administered as provocative perfusion tests. Patients with functional heartburn and healthy control subjects were evaluated. Patients underwent a modified Bernstein acid infusion test and esophageal Barostat balloon distention. Time and volume to pain were recorded. Barostat balloon distention was performed using our standard protocol. Stepwise distentions were performed and pain was recorded. Sensitivity to chenodeoxycholic acid (Cheno) and Ursodeoxycholic acid (Urso) were assessed similarly to the Bernstein test using 2 mM concentrations of each, followed immediately by 5 mM if no pain was reported with 2 mM. Volume of bile acid infusion and length of time until pain was induced were assessed and compared to the same endpoints for acid sensitivity. "Total" time and "total" volume to induce pain were calculated for Cheno and Urso. Least-squares means were generated and two-tailed t-tests and regression analyses were performed (P < 0.05 level of significance). Ten functional heartburn patients and six healthy controls were evaluated (3 M, 13 F; age range, 19 to 56 years). Since five of six controls had pain with acid infusion (hypersensitive), all subjects were analyzed as one group. Only three subjects (all controls) had no pain with infusion of 2 mM Cheno and received the follow-up infusion of 5 mM. These same three subjects tolerated the maximum infusion (150 ml and 15 min) of 5 mM Cheno. Nine subjects did not have pain with 2 mM Urso and received the follow-up infusion of 5 mM Urso (five functional heartburn, four controls). Significantly more subjects tolerated the maximum bile acid infusion of 2 mM Urso vs 2 mM Cheno (nine vs three; P < 0.05, Chi-square test). The pain threshold (volume and time) for Urso was significantly higher than that for Cheno and acid (P < 0.05), and the pain threshold for Cheno was significantly higher than that for acid (P < 0.05). Conclusions are as follows: (1) Bile acids differ in their ability to induce pain. (2) Changing bile acid composition by treatment with Urso may change symptom presentation and symptom severity in patients with bile acid-induced esophageal pain.

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