Control of ventilation during submaximal exercise: A brief review

This review discusses the leading hypotheses concerning ventilatory control during submaximal exercise. The ventilatory response at the onset of submaximal exercise has been studied extensively. It is generally agreed that expired ventilation (VE) increases rapidly at the initiation of exercise followed by a slower increase in FE until a steady state is reached. In general, there are four schools of thought concerning the mechanisms that are responsible for the exercise hyperpnoea. Two of the hypotheses relate the increase in VE to neural regulation. One group argues that the increase in VE during work is primarily due to afferent neural feedback to the ventilatory control centre while the other group proposes that efferent neural activity can explain the hyperpnoea. A third group of hypotheses submit that humoral mechanisms must be actively involved in the increase in VE during exercise. The leading hypothesis in this area is based on experiments that suggest that CO2 return to the lung provides a stimulus for ventilatory control. Finally, the fourth supposition is that the exercise hyperpnoea may be due to both neural and humoral mechanisms. In summary, although there is persuasive evidence that both humoral and neural factors may play a role in mediating the exercise hyperpnoea, the basic question of whether the response is due solely to humoral or neural mechanisms remains unresolved.