ABSTRACT
PURPOSE: This study was done to test the hypothesis that hypercapnia has a direct, inhibitory effect on swallowing. METHODS: We investigated changes in the frequency and timing of repeated swallows induced by continuous infusion of water into the pharynx before, during, and after transient airway occlusion at normocapnia and hypercapnia in 12 healthy volunteers. Hypercapnia was induced by adding a dead space. Ventilation was monitored using a pneumotachograph, and swallowing was identified by submental electromyogram. RESULTS: We found that hypercapnia decreased the frequency of swallows (8.2 +/- 3.7 vs 11.4 +/- 5.3 swallows.min-1 [mean +/- SD]: hypercapnia vs normocapnia; P < 0.05), together with a loss of the preponderant coupling of swallows with expiratory phase observed at normocapnia. We also found that the withdrawal of phasic lung inflation produced by airway occlusion at end-expiration suddenly increased the swallowing frequency, both at normocapnia (from 11.4 +/- 5.3 to 16.7 +/- 3.7 swallows.min-1; P < 0.01) and at hypercapnia (from 8.2 +/- 3.7 to 22.0 +/- 6.7 swallows.min-1; P < 0.01). Although the degree of increased swallowing frequency during airway occlusion was more prominent at hypercapnia than at normocapnia ( P < 0.05), the distribution of the timing of swallows in relation to the phase of the respiratory cycle during airway occlusion at hypercapnia was similar to that during airway occlusion at normocapnia. CONCLUSION: The results of our study strongly suggest that the attenuation of the swallowing reflex during hypercapnia is not due to the direct, inhibitory effect of CO2 on the swallowing center, but, rather, is due to the increased inhibitory influence of a lung-volume-related reflex.
