Phase-Coupling of Arterial Blood Gas Oscillations and Ventilatory Kinetics during Exercise in Humans

Abstract

The carotid bodies (CBs) have been implicated in the kinetic control of ventilation (V_E) during moderate exercise (reviewed in Refs. 10 & 11). That is, augmenting CB responsiveness (eg. by hypoxia or dietary-induced metabolic acidaemia) shortens the time constant of the V_E response (τV_E) to square-wave exercise forcings, while CB suppression (induced by hyperoxia, metabolic alkalaemia or intravenous dopamine infusion) or surgical CB resection is associated with a prolonged τV_E.The present investigation considers the possibility that intra-breath oscillations of arterial PO₂ (PaO₂), PCO₂ (PaCO₂) and pH (pHa) may be involved in this CB modulation. Yamamoto (12) proposed that these oscillations, which have been measured in humans at rest and during exercise (1), could provide a component of respiratory control independent of their mean levels, mediated possibly via the rate of change of pHa in the falling phase of the oscillation (dpHa/dt↓) (3). The reflex efficacy of this humoral oscillation can be modulated by the “phase-coupling” (9) between the ensuing oscillation of CB discharge and the on-going respiratory cycle: stimuli presented to the CBs during inspiration evoke stimulation, while respiration is relatively unaffected (or may even be depressed) by stimuli arriving at the CBs during expiration (2–6). We therefore tested the following hypothesis: if, at exercise onset, the peaks of the oscillating CB discharge were to arrive at the brainstem respiratory integrating areas at a more optimal phase of the respiratory cycle than at rest (e.g., during inspiration, rather than expiration), then the kinetics of the exercise hyperpnoea would be faster compared to a situation where the phase coupling at exercise onset was unchanged or even became “pessimal” (4).