CO₂-H⁺ Stimuli and Neural Muscular Drive to Ventilation during Dynamic Exercise: Comparison of Stimuli at Constant Levels of Ventilation

Abstract

In exercising man, the ventilatory responses to CO₂-H⁺ stimuli and neural muscular drives were compared at constant ventilation (V̇_E. For that purpose, a small increase of the CO₂-H⁺ stimulus in exercise was to be counterbalanced by work load reductions in such a way that the magnitude of ventilation remained unchanged. Control of end-tidal PO₂ and PCO₂ (P_ETO₂. P_ETCO₂) was established to minimize the influence of changed mixed venous gas tensions on the arterial levels.

Only in metabolic acidosis could the additional CO₂ stimulus be compensated by work load reduction. This compensation was due to the concomitant decrease of acidosis.

Below the 2 mmol · l^-1 |La|_a threshold, decrements of work load, V̇O₂, and VCO₂ showed no effect on V̇_E, when P_ETCO₂ and P_ETO₂ were regulated at constant levels. After the termination of end-tidal clamps, the proportional relation of V̇_E to V̇O₂, V̇CO₂, and work load was largely re-established.

The results show that neural muscular drives cannot decrease ventilation against a background of constant arterial feedback stimuli. Transient decreases of the CO₂-H⁺ stimulus seem to be necessary to readjust the ventilation to a decreased CO₂ flow to the lungs. It is suggested that the overall effect of decreasing CO₂ is to inhibit the respiratory centers and that positive ventilatory effects of CO₂ are the result of a disinhibitory influence.

Key words

ventilatory control - neurogenic muscular afferents - CO₂-H⁺ stimulus - isoventilation technique - exercise - man