Manipulation of central blood volume and implications for respiratory control function

Abstract

The respiratory operating point (ventilatory or arterial PCO 2 response) is determined by the intersection point between the controller and plant subsystem elements within the respiratory control system. However, to what extent changes in central blood volume (CBV) influence these two elements and the corresponding implications for the respiratory operating point remain unclear. To examine this, 17 apparently healthy male participants were exposed to water immersion (WI) or lower body negative pressure (LBNP) challenges to manipulate CBV and determine the corresponding changes. The respiratory controller was characterized by determining the linear relationship between end-tidal PCO 2 (PETCO 2 ) and minute ventilation (V E) [V E ϭ S ϫ (PET CO 2 Ϫ B)], whereas the plant was determined by the hyperbolic relationship between V E and PETCO 2 (PETCO 2 ϭ A/V E ϩ C). Changes in V E at the operating point were not observed under either WI or LBNP conditions despite altered PET CO 2 (P Ͻ 0.01), indicating a moving respiratory operating point. An increase (WI) and a decrease (LBNP) in CBV were shown to reset the controller element (PETCO 2 intercept B) rightward and leftward, respectively (P Ͻ 0.05), without any change in S, whereas the plant curve remained unaltered at the operating point. Collectively, these findings indicate that modification of the controller element rather than the plant element is the major factor that contributes toward an alteration of the respiratory operating point during CBV shifts. system analysis; respiratory control; central blood volume; head-out water immersion; lower body negative pressure THE RESPIRATORY SYSTEM is an important chemoreflex-feedback control system that maintains arterial PCO 2 (Pa CO 2 ), O 2 , and pH remarkably constant via ventilatory regulation. It can be divided into two subsystems (Fig. 1A): a controller (controlling element) and a plant (controlled element) (5,17,18,21,35,41,45,46).Recently, we have characterized these subsystem elements in an open-loop condition and constructed a respiratory equilibrium diagram to illustrate the mechanisms of respiratory control at rest and during exercise in endurance-trained and untrained subjects (46,48,52). Briefly, the controller element approximates a straight line where minute ventilation (V E) increases as a function of Pa CO 2 . The element can be broadly divided into chemoreflex and nonchemoreflex drives to breathe (39). The plant element approximates a hyperbola with a positive asymptote where Pa CO 2 decreases asymptotically as a function of V E (APPENDIX).Since respiration is determined from an intersection point between these two elements on the respiratory equilibrium diagram (Fig. 1B), quantitative analysis of both subsystems can determine how changes in both the controller and plant elements affect V E or Pa CO 2 (5,6,17,18,41,45,46,48); however, to what extent changes in central blood volume (CBV) influence these variables and thus, by consequence, the operating point (V E or Pa CO 2 response) of the respiratory co...

Does respiratory drive modify the cerebral vascular response to changes in end‐tidal carbon dioxide?

“…Therefore, it seems that the change in observed during these experimental conditions is likely to reflect changes in . Robbins, Conway, Cunningham, Khamnei, & Paterson () reported that consistently underestimated , a finding that is consistent with our studies (Miyamoto et al., , ). Jones, Robertson, & Kane () reported that is higher than when is increased, whereas it is lower in normal conditions.…”

“…First, in the methods determining CVR that use , this is based on the notion that is closely related to . Although the estimate of might have limitations in the present study, our previous studies revealed that was tightly correlated with throughout the hypercapnic and hypocapnic range during hypercapnia and hyper‐ and hypoventilation across various experimental conditions (Miyamoto et al., ). Therefore, it seems that the change in observed during these experimental conditions is likely to reflect changes in .…”

Blood flow in internal carotid and vertebral arteries during graded lower body negative pressure in humans

“…One possible explanation is lower CO 2 reactivity in VA compared with that of ICA (Sato et al 2012b). It is well established that orthostatic stress causes hypocapnia with hyperventilation (Ogoh et al 2013a;Miyamoto et al 2014), and both arteries should vasoconstrict during orthostatic stress, although hypoperfusion is not caused solely by a lower arterial partial pressure of CO 2 (Immink et al 2006). In the present study, however, VA blood flow may react only to the lower arterial partial pressure of CO 2 caused by high hyperventilation during high orthostatic stress (−50 mmHg LBNP).…”

System physiology of respiratory control in man

“…The intersection point between the controller and plant curves predicts the closed-loop operating point of respiration (G and H). LBNP moved the operating point of the respiratory equilibrium diagram leftwards, indicating that a decrease in central blood volume (CBV) reduced PETCO2 without changing V ・ E. This finding provides the evidence that these respiratory and cardiovascular responses to CBV shifts are related to alterations in the elements of both controller and plant subsystems in the respiratory chemoreflex system 15) . Importantly, the plant curve was unchanged around the operating point during LBNP despite the downward shift in the modified metabolic hyperbola.…”

“…(Reprinted from Ref. [15]) Fig. 9 Determination of equilibrium (steady-state) values of V ・ E and PaCO2 during light-and heavy-intensity exercise.…”