Summary
Nine subjects performed a sequence of sustained and randomised changes between 40 W and 100 W on a cycle ergometer while the end-tidal\(P_{O_2 } \) 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\(P_{CO_2 } \) (P ETCO2) near 6.5 kPa (49 mm Hg; ‘CO2-clamp’ experiment). By this forcingP ETCO2 oscillations were attenuated and more evenly distributed over the frequency range. Ventilation (\(\dot V_T \)) 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\(P_{CO_2 } \).\(\dot V_T \) 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.
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Eβfeld, D., Hoffmann, U. & Stegemann, J. Ventilatory effects of hypercapnic end-tidalPCO2 clamps during aerobic exercise of varying intensity. Europ. J. Appl. Physiol. 60, 412–417 (1990). https://doi.org/10.1007/BF00705029
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DOI: https://doi.org/10.1007/BF00705029