Control of arterial P_CO2 by somatic afferents in sheep

The ventilatory response (V̇_E) to electrically induced rhythmic muscle contractions (ERCs) was studied in six urethane-chloralose-anaesthetized sheep, while arterial oxygen and carbon dioxide pressure (P_a,_O2, and P_a,_CO2) and perfusion pressure were maintained constant at the known chemoreception sites. With cephalic P_a,_CO2, held constant, the response to inhaled C0₂ was virtually abolished (0.03 ± 0.04 l min^-1 Torr^-1). During low-current ERC, which doubled the metabolic rate (V̇_CO2 increased from 192 ± 23 to 317 ± 84 ml min^-1, P < 0.0 1), V̇_E followed the change in V̇_CO2 closely (from 5.24 ± 1.81 to -9.27 ± 3.601 min^-1, P < 0.01) in the absence of any chemical error signal occurring at carotid and central chemoreceptor level (Δ cephalic P_a,_CO2 = -0.75 ± 1 Torr). Systemic P_a,_CO2, decreased by -2.47 ± 1.9 Torr (P < 0.01). Both heart rate and systemic blood pressure increased significantly by 18.6 ± 5.5 beats min^-1, and 7.0 ± 9.3 mmHg, respectively. When the CO₂ flow to the central circulation was reduced during ERC by blocking venous return (V̇_CO2 decreased by 102 ± 45 1 min^-1, P < 0.01), ventilation was stimulated (from 11.99 ± 4.11 to 13.01 ± 4.63 1 min^-1, P < 0.05). The opposite effect was observed when the arterial supply was blocked. Finally, raising the CO₂ content and flow in the systemic blood did not significantly stimulate ventilation provided that the peripheral and central chemoreceptors were unaware of the changes in blood CO₂/H⁺ composition. Our results support the existence of a system capable of controlling blood P_a,_CO2, homeostasis when the metabolism increases independently of peripheral and central respiratory chemoreceptors. Information from the skeletal muscles related to the local vascular response provides the central nervous system with a respiratory stimulus proportional to the rate at which gases are exchanged in the muscles, thereby coupling ventilation to the metabolic rate.