Control of breathing during exercise: Who is the leader?

Abstract

Control of breathing during exercise has been discussed widely in the literature. Generally, it is accepted that feedforward central command makes an important contribution to increased breathing, or hyperpnoea, at the onset of exercise. It is also accepted that a variety of peripheral signals are capable of regulating breathing during exercise. However, the exact contributions of multiple concomitant mechanisms to exercise hyperpnoea are contested. This is evident in a recent Exchange of Views on feedback control of ventilation during exercise (Haouzi, 2020; White & Bruce, 2020). Furthermore, although not the focus of the Exchange of Views, another contributor that we think deserves consideration is afferent input originating from pulmonary vascular baroreceptors. Almost 50 years ago, Wasserman, Whipp, and Castagna (1974) suggested a feedforward, cardiodynamic component to exercise hyperpnoea; that is, the increase in breathing during exercise might be linked mechanistically to the increase in cardiac output for efficient ventilation-perfusion matching. However, no signal or receptor capable of coupling ventilation to cardiac output was identified. The pulmonary circulation provides an ideal location for a receptor that couples right ventricular outflow and ventilation. Pulmonary arteries are more compliant than systemic counterparts and distend relatively easily to accommodate increases in right ventricular outflow.