Abstract

BackgroundFood intake augments CO2 production; however, minute ventilation is not augmented during exercise after food intake. Respiratory chemoreceptors respond to CO2 and influence respiration. We examined the effect of food intake on respiratory chemosensitivity to CO2 in young adults.MethodsThe hypercapnic ventilatory response was measured in eleven healthy individuals before and after food intake. To evaluate the respiratory chemoreflex response to CO2, minute ventilation was plotted against end-tidal PCO2 using data obtained with the rebreathing method.ResultsSublingual temperature, CO2 output, minute ventilation, and end-tidal PCO2 were all significantly higher at baseline in the session after food intake than in the session before food intake. On the other hand, there was no significant difference in chemosensitivity to CO2 between the sessions before and after food intake (1.60 ± 0.62 vs. 1.53 ± 0.62 l min−1 mmHg−1).ConclusionsFood intake does not influence respiratory chemosensitivity to CO2 in young adults, which is different from infants. This suggests that control of respiration differs between young adults and infants and that the elevated minute ventilation after food intake in young adults is not caused by a change in respiratory chemosensitivity.

Highlights

  • Food intake augments CO2 production; minute ventilation is not augmented during exercise after food intake

  • We speculated that this elevation in VE was caused by an elevation in the H+ ion concentration related to increases in CO2 output (VCO2) and the plasma noradrenaline concentration [4], which can be induced by an increase in sympathetic nervous system activity [5]

  • The present study showed that food intake leads to increases in Sublingual temperature (Tsl), Oxygen uptakeVTTidal volume (VO2), VCO2, VE, and End-tidal PCO2 (PETCO2), which is consistent with earlier studies [1,2,3]

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Summary

Introduction

Food intake augments CO2 production; minute ventilation is not augmented during exercise after food intake. We examined the effect of food intake on respiratory chemosensitivity to CO2 in young adults. Food intake increases metabolism and body temperature [1,2,3]. This is the so-called postprandial thermogenesis or thermic effect of food. We recently reported that food intake influences the respiratory response at rest [1]— i.e., food intake increases minute ventilation (VE) in resting young individuals. Young adults in that study exercised at 50% of peak oxygen uptake 90 min after food intake, and the increase in metabolism elicited by the food intake was

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