Comparison of Respiratory and Circulatory Human Responses to Progressive Hypoxia and Hypercapnia

Abstract

The effects of acute, progressive isocapnic hypoxia and hyperoxic hypercapnia on lung ventilation, heart rate, cardiac output and arterial blood pressure were determined simultaneously in 32 normal individuals. All subjects were exposed to hypoxia and hypercapnia in an entire range of individual tolerance. The piecewise linear approximation technique was used for analysis of the ventilatory and circulatory response curves. In all subjects, the changes in hemodynamics in the response to hypoxia paralleled those occurring in ventilation, during both the first phase of slow increase and the second phase of sharp increase. Fracture point coordinates for ventilation and circulation coincided, with the fracture being registered at an end-tidal PO₂ of 79.7 ± 3.8 mm Hg for ventilation and 79.0 ± 4.5 mm Hg (p > 0.1) for cardiac output. This may give evidence of analogous entries from the peripheral O₂-sensitive receptors to the respiratory and vascular motor bulbar centers. By contrast, a more significant rise in ventilation observed during the hypercapnic versus hypoxic drive was not accompanied by any change in the heart rate, cardiac output and arterial blood pressure until the end-tidal PCO₂ (PETCO₂) had reached a critical level. Fracture point coordinates for ventilation and circulation did not coincide, with the fracture being registered at a PETCO₂ of 51.1 ± 1.9 mm Hg for the former and 57.0 ± 2.2 mm Hg (p < 0.01) for the latter. Such differences in the response to hypoxia and hypercapnia were repeatedly observed during 5 test days. The data do not seem to show evidence in favor of an involvement of the hypercapnic challenge in the central regulation of the circulation.

Cardiovascular response to hypoxia after endurance training at altitude and sea level and after detraining

“…Also, there is an interaction between the baroreceptors and the chemoreflex responses to hypoxia (39). Concerning hemodynamic response to progressive isocapnic hypoxia developed in parallel to ventilatory response, Serebrovskaya (37) assumed that parallel reflex reactions of respiration and circulation may be induced by the impulses from the peripheral chemoreceptors sensitive to the hypoxia simultaneously reaching the respiratory and vasomotor centers. From several reports mentioned above, because the mechanism of BP response to hypoxia is complicated and the significant correlations between ␦HVR and ␦⌬SBP/⌬Sa O 2 by endurance training and detraining cannot establish cause and effect, it cannot be proved that the changes in the SBP response in the present study are simply induced by the changes in ventilatory response to hypoxia as proposed by Insalaco et al (15), but it seems reasonable to suppose that there is an interaction between the changes in the SBP and ventilatory responses to isocapnic hypoxia by endurance training and detraining.…”

Intermittent Hypoxia Research in the Former Soviet Union and the Commonwealth of Independent States: History and Review of the Concept and Selected Applications

“…In both studies, 2 weeks of IHT increased the hypoxic ventilatory response, which was taken to indicate an increased hypoxic responsiveness of the carotid body with altitude acclimatization. Examination of the time course has suggested that the enhancement of ventilatory sensitivity begins with the first hypoxic exposure, and approaches a plateau by the third day (Serebrovskaya, 1992;Serebrovskaya and Ivashkevich, 1992). If so, then in normal humans only a few minutes of daily hypoxic exposure rapidly induces detectable increments in hypoxic ventilatory response, a hallmark of altitude acclimatization.…”

Hypercapnic blood pressure response is greater during the luteal phase of the menstrual cycle

“…In men, acute hypercapnia leads to a pressor response in the systemic circulation (14,15,17), which is at least partially mediated via an increased sympathetic tone (17), but this response has not been reported in female subjects. The purpose of this study was to investigate the pressor effect of acute hyperoxic hypercapnia during the normal menstrual cycle.…”