Respiratory Compensation, as Evidenced by a Declining Arterial and End-Tidal PCO₂,Is Attenuated During Fast Ramp Exercise Functions

Abstract

During low to moderate intensity exercise below the ventilatory threshold (T_vent), ventilation $({\dot V_E})$ increases in proportion to CO₂ production ($\dot V$CO₂), resulting in arterial PCO₂(P_aCO₂) remaining at, or increasing slightly above, resting levels. As the exercise intensity increases beyond the T_vent, ${\dot V_E}$ increases at a faster rate than $\dot V$CO₂ (i.e. hyperventilation with respect to $\dot V$CO₂) when the work rate (WR) is incremented slowly (i.e. a steady-or quasi-steady-state is reached during each step) (7,8). However, when the WR is increased rapidly (i.e. using step increments of min or ramp exercise functions), ${\dot V_E}$ continues to increase in proportion to $\dot V$CO₂ as the end-tidal (P_ETCO₂) and arterial PCO₂remain relatively constant (i.e. isocapnic buffering) (8,9). This isocapnic buffering phase reflects a specific ventilatory response to exercise above the T_vent where a combination of increased breathing frequency (f) and decreased time of expiration (T_E) effectively curtail the systematic increase in P_ETCO₂ and P_aCO₂ associated with exercise below T_vent(8). In this exercise paradigm respiratory compensation for the developing acidosis is delayed relative to the T_vent and follows the period of isocapnic buffering.