EFFECT OF ASTHMA AND VENTILATORY LOADING ON ARTERIAL PCO2 OF HUMANS DURING SUBMAXIMAL EXERCISE

In humans, attenuating carotid chemoreceptor activity by hyperoxia doe s not alter arterial Pco2 (Pa(CO2)) during submaximal exercise, yet a transient hypercapnia occurs in carotid chemoreceptor-resected (CBR) a sthmatic subjects during submaximal exercise. We hypothesized that thi s difference was due to asthma and not CBR causing the abnormal respon se. Accordingly, we determined the temporal pattern of Pa(CO2) during mild and moderate exercise in chemoreceptor-intact asthmatic (n = 10) and nonasthmatic subjects (n = 10). We also hypothesized that hyperoxi a alters Pa(CO2) during exercise if exercise already has disrupted Pa( CO2) homeostasis. Accordingly, we studied, during exercise, asthmatic subjects while hyperoxic; nonasthmatic subjects during loaded breathin g of room air, which increased Pa(CO2); and nonasthmatic subjects duri ng loaded breathing while hyperoxic. While breathing room air, neither asthmatic nor nonasthmatic subjects maintained arterial isocapnia dur ing exercise. An increase in Pa(CO2) between rest and exercise and bet ween mild exercise and 1st min of moderate exercise was greater in ast hmatic than in nonasthmatic subjects (P < 0.05). In six asthmatic subj ects that were hypercapnic breathing room air during exercise, hyperca pnia was accentuated by hyperoxia. The ventilatory load in nonasthmati c subjects resulted in a work load-dependent hypercapnia (P < 0.01) ac centuated (P < 0.01) by hyperoxia. We conclude that normally in humans the carotid chemoreceptors contribute minimally to the hyperpnea of s ubmaximal exercise. However, when Pa(CO2) is increased from resting va lues during exercise, then the chemoreceptors serve to augment ventila tion and thereby minimize the hypercapnia.