Ventilatory effects of hypercapnic end-tidal PCO2 clamps during aerobic exercise of varying intensity.
Nine subjects performed a sequence of sustained and randomised changes between 40 W and 100 W on a cycle ergometer while the end-tidal PO2 was kept close to 17.3 kPa (130 mm Hg) by means of a dynamic forcing technique (reference experiment). In a second series inspiratory CO2 was additionally manipulated so as to hold end-tidal PCO2 (PETCO2) near 6.5 kPa (49 mm Hg; 'CO2-clamp' experiment). By this forcing PETCO2 oscillations were attenuated and more evenly distributed over the frequency range. Ventilation (VT) responded to this manoeuvre with an upward trend that could not be ascribed to a slow CO2-response component, changes in metabolic rate or a dissociation of end-tidal and arterial PCO2. VT differences between reference and CO2-clamp experiments were abolished within a 3-min period following the termination of the external CO2 control. The present results suggest that the CO2-H+ stimulus plays a major role in adjusting ventilation when exercise intensity is decreased. The underlying CO2 effect appears to be neither additive nor bi-directionally symmetrical.
Essfeld
D
D
Physiologisches Institut, Deutschen Sporthochschule Köln, Cologne, Federal Republic of Germany.
Hoffmann
U
U
Stegemann
J
J
D001158:Arteries; D002245:Carbon Dioxide / Q000097:blood; D003250:Constriction; D015444:Exercise; D006801:Humans; D006935:Hypercapnia / Q000097:blood / Q000503:physiopathology*; D010313:Partial Pressure; D012119:Respiration; D013990:Tidal Volume
D002245:Carbon Dioxide