INFLUENCE OF BODY POSITION ON PULMONARY VENTILATION DURING ARREST AND RELEASE OF LOWER LIMB CIRCULATION AFTER EXERCISE IN HEALTHY HUMANS

Abstract

Pulmonary ventilation (V̇E) response to exercise is greater when exercise is performed seated versus supine. Maybe this phenomenon is partially attributed to interaction between neural mechanisms involved on the regulation of V̇E. For instance, venous return is reduced during seated exercise, which activates the cardiopulmonary baroreflex. Therefore we sought to investigate if the cardiopulmonary baroreflex interacts with the muscle metaboreflex and the carotid chemoreflex to the regulation of V̇E in healthy humans. Thirteen young healthy subjects participated in the study (7 men). Subjects performed isometric plantar flexion with the dominant limb for 1.5 min in the semi recumbent position. Close to the end of exercise, the circulation of the dominant leg was arrested at the thigh level via cuff inflation. Then, subjects stopped exercising and their position was shifted from semi‐recumbent to either: 1) seated with the non‐dominant limb lowered to inhibit the cardiopulmonary baroreflex; or 2) supine with the non‐dominant limb raised to activate the cardiopulmonary baroreflex. Circulatory arrest took 2 min and aimed to trap metabolites into the exercised muscles to sustain muscle metaboreflex activation. Next, the tight cuff was deflated, releasing metabolites from skeletal muscles to the systemic circulation. Another experiment, under free flow recovery, served as unconcluded control. A subset of the subjects (n = 3) have undergone hyperoxia breathing (100% O2) only during release of circulatory arrest at the seated position to inhibit the carotid chemoreflex. A normoxic experiment served as control. A rebreathing system was used in an attempt to maintain the end‐tidal partial pressure of CO2 constant throughout all experiments. We found that circulatory arrest did not change V̇E versus unconcluded control in the seated (P > 0.05) and supine (P > 0.05) positions throughout the 120‐s period of cuff inflation. V̇E increased above unconcluded control in the seated position after 60 s of circulatory release (mean ± SD: Δ = 20 ± 29%, P = 0.05) and it remained elevated until the end of data recording at 120 s (Δ = 21 ± 31%, P = 0.04). However, release of circulatory arrest did not change V̇E versus unconcluded control in the supine position (P > 0.05). Furthermore, hyperoxia did not change the V̇E increase after circulatory release at the seated position. Collectively, these results suggest that the cardiopulmonary baroreflex did not interact with either the muscle metaboreflex or the carotid chemoreflex. The underling mechanisms of the V̇E increase during release of circulatory arrest at the seated position deserve further investigation.Support or Funding InformationCAPES and CNPq