With the addition of external dead space in normoxia, PCO2-ventilation response and CO2 production were determined in 10 healthy male subjects. Overall "gain" (G) of the respiratory control system was calculated from the slope of the CO2-response curve (S) and that of the metabolic hyperbola (SL) at alveolar partial pressure of CO2 (PACO2) of the respective experimental run. We found that 1) despite the depression of ventilation during non-rapid-eye-movement (NREM) sleep, G was generally not changed due to decreased SL, although considerable individual variations were seen; 2) effects of external dead space on PACO2 change during sleep and wakefulness were similar in magnitude; and 3) the above PACO2 changes experimentally induced agreed well with the predicted values estimated from G. Contrary to general opinion, these results demonstrated that overall gain of the respiratory control system is generally not depressed during NREM sleep in normal healthy subjects.
Fifty-four male track-and-field athletes and 18 male non-athletes were examined by isocapnic progressive hypoxia and CO2 rebreathing tests. Ventilatory and heart rate (HR) responses to hypoxia were analysed by a hyperbolic relationship and the ventilatory response to hypercapnia by a linear regression. The results showed that ventilatory sensitivity during hypoxia was significantly attenuated in the long-distance runners and sprinters compared to the non-athletes. Although heart rate sensitivity during hypoxia in none of the athletes showed a significant difference compared to that of the non-athletes, baseline HR in the long-distance runners was significantly lower than that of the non-athletes. None of the athletes showed significant differences in ventilatory sensitivity during hypercapnia compared to the non-athletes.
Cross-sectional studies on hypercapnic and hypoxic ventilatory chemosensitivities were performed in 71 children ranging in age from 7 to 18 yrs. The subjects were classified into 6 successive 2-year age groups. CO2 ventilatory response was measured by rebreathing 5 % CO2 in Oz, a slight modification of the method originally proposed by Read. The results were evaluated when the C02-ventilation feedback control system was supposed to have attained the open-loop condition. Hypoxic ventilatory response was measured by the isocapnic progressive hypoxia test. To obtain good reproducibility in the ventilatory response, end-tidal P~oz was maintained at 5 mmHg higher than the resting condition throughout the test. Normalized ventilatory responses to CO2 by body surface area (S/BSA) progressively decreased from the 7-8 through the 11-12 yr groups, and then tended to decrease further in a more gradual manner with increasing age. This trend was very similar to the normalized CO2 output (V"oz/BSA), but did not parallel so closely the normalized Oz intake (Voz/BSA). When ventilatory and metabolic parameters were normalized by body weight (BW), or the lean body mass (LBM), qualitatively similar relationships between CO2 sensitivities and metabolic parameters were also obtained. Contrary to the hypercapnic response, hypoxic ventilatory chemosensitivities were not significantly different among the 6 different age groups. We concluded that normalized hypercapnic chemosensitivity decreased during growth and corresponded well with decreased CO2 output per unit body mass.Key words : hypercapnic ventialtory response, hypoxic ventilatory response, body weight, body surface area, lean body mass.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.