Powers S K, Beadle R E
J Sports Sci. 1985 Spring;3(1):51-65. doi: 10.1080/02640418508729732.
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 VE 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.
本综述讨论了关于次最大运动期间通气控制的主要假说。次最大运动开始时的通气反应已得到广泛研究。人们普遍认为，运动开始时呼出通气量（VE）迅速增加，随后VE增加速度减慢，直至达到稳定状态。一般来说，关于运动性呼吸急促的机制有四种观点。其中两种假说将VE的增加与神经调节联系起来。一组认为工作期间VE的增加主要是由于对通气控制中心的传入神经反馈，而另一组则提出传出神经活动可以解释呼吸急促。第三组假说认为体液机制必定积极参与运动期间VE的增加。该领域的主要假说基于一些实验，这些实验表明二氧化碳返回肺部为通气控制提供了一种刺激。最后，第四种假设是运动性呼吸急促可能是由于神经和体液机制共同作用。总之，尽管有确凿证据表明体液和神经因素可能在介导运动性呼吸急促中发挥作用，但该反应是否仅由体液或神经机制引起这一基本问题仍未解决。
