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¹ Laboratoire de Physiologie, E.A. 3450, Faculté de Médecine de Nancy, Université Henry Poincaré, France

The ventilatory response 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 CO₂ was virtually abolished (0.03 ± 0.04 l min^–1 Torr^–1). During low-current ERC, which doubled the metabolic rate ( increased from 192 ± 23 to 317 ± 84 ml min^–1, P < 0.01), followed the change in closely (from 5.24 ± 1.81 to –9.27 ± 3.60 l min^–1, P < 0.01) in the absence of any chemical error signal occurring at carotid and central chemoreceptor level (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 ( decreased by 102 ± 45 l min^–1, P < 0.01), ventilation was stimulated (from 11.99 ± 4.11 to 13.01 ± 4.63 l 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.

(Received 30 April 2005; accepted after revision 11 October 2005; first published online 13 October 2005)
Corresponding author P. Haouzi: Laboratoire de Physiologie, Faculté de Médecine de Nancy, Avenue de la Forêt de Haye, B.P. 184, 54505 Vandoeuvre-lès-Nancy Cedex, France. Email: p.haouzi{at}chu-nancy.fr

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