Role of metabolic CO2 production in ventilatory response to steady-state exercise.

Abstract

A B S T R A C T We examined the role of metabolic CO2 production in the hyperpnea of muscular exercise by comparing the response of alveolar ventilation to moderate levels ofexercise with the response to venous infusion of CO2 at rest. Studies were performed in four awake sheep that were trained to run on a treadmill. The sheep had been cannulated for veno-venous extracorporeal perfusion so that CO2 could be infused into the peripheral venous blood through membrane lungs in the perfusion circuit. The sheep breathed room air through an endo-tracheal tube inserted through a tracheostomy, and samples of expired gas were collected for measurement of the rates of CO2 production and 02 consumption. All measurements were made in the steady state. In each of the four sheep, the relationship between alveolar ventilation and the rate of CO2 production could be described by a single linear function (r > 0.99; P < 0.001), regardless of whether CO2 production was increased by exercise, venous CO2 infusion, or combinations of both procedures. This relationship applied for values of CO2 production up to 350% of control. In contrast, no unique relationship was found between the rate of alveolar ventilation and either the rate of 02 consumption, cardiac output, or mixed venous blood gas pressures. The findings indicate that the hyperpnea of mild to moderate steady-state exercise can be attributed to the associated increase in the rate of CO2 production. Therefore, there is no need to invoke obligatory nonmetabolic stimuli to account for the ventilatory response to steady-state exercise.

Ventilation and Respiratory Mechanics

“…Thus, under resting conditions, both loading and unloading venous CO 2 produce hypercapnic hyperpnea and hypocapnic hypopnea, respectively. Other studies have shown that the relationship of alveolar ventilation toV co 2 was the same in exercising sheep as during venous CO 2 loading, implying that the increase inV co 2 elicited by exercise can solely account for the ventilatory response, at least under these specific experimental conditions (419); this is consistent with the idea that nonmetabolic stimuli are not obligatory for the hyperpnea of mild-to-moderate levels of exercise.…”

Variability in End‐Tidal PCO2 and Blood Gas Values in Humans

“…Thus, the subjects were starved for at least 3 h before any measurements were made. Finally, there is some debate as to whether or not alterations in CO 2 elimination are accompanied by any change in arterial P CO 2 (Fordyce & Grodins, 1980;Phillipson et al 1981). Thus it seems quite unlikely that any residual differences in metabolic rate on different days could really explain the variations in P ET,CO 2 on different days in our subjects.…”

Control of Breathing During Exercise

“…These studies used an extracorporeal gas exchanger to increase or decrease venous and thus delivered CO 2 . In several studies on anesthetized animals, it was claimed thatV E changed in proportion to the change in CO 2 delivery to maintain homeostasis of PaCO 2 (206,214,274,314,338). In contrast, in an equal number of studies, there was a change in PaCO 2 sufficient to account for the hyperpnea or hypopnea during CO 2 loading and unloading (39,118,138,171,209,277,284,300).…”