During steady-state exercise, minute ventilation correlates most closely with CO2 output, suggesting that CO2 released into the alveoli is the primary stimulus for exercise hyperpnea.
Supports CO2 output as ventilatory driver in steady-state exercise; leaves open causal mechanisms and relevance in disease.
In order to know the role of cardiodynamic factors for exercise hyperpnea, ventilation and several cardiorespiratory variables were measured simultaneously in human subjects during exercise. Cardiac output (Q) and mixed venous CO2 content (CVCO2) were determined by a rebreathing method. The correlation coefficients (r) for the relationships between minute expiratory ventilation (VE) and each of end-tidal CO2 tension (PETCO2), Q, CVCO2, CO2 flow into the lung (QCO2, the product of Q and CVCO2), oxygen consumption (VO2), and CO2 output (VCO2) were determined during the steady-state exercise up to 90 W. The correlation was highly significant (r = 0.84-0.99, p less than 0.001) in each case except for PETCO2 (r = 0.13, N.S.). The highest correlation was observed in the VE-VCO2 relationship. It was assume that VCO2 released from the pulmonary capillaries into the alveoli is the most likely stimulus leading to exercise hyperpnea. Arterial CO2 oscillation may be regarded as a potential linkage between VCO2 and VE.
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Miyamoto et al. (1989) studied this question.
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