Medical College of Wisconsin, Department of Physiology, Milwaukee, Wisconsin, USA.
Compr Physiol. 2012 Jan;2(1):743-77. doi: 10.1002/cphy.c100045.
During exercise by healthy mammals, alveolar ventilation and alveolar-capillary diffusion increase in proportion to the increase in metabolic rate to prevent PaCO2 from increasing and PaO2 from decreasing. There is no known mechanism capable of directly sensing the rate of gas exchange in the muscles or the lungs; thus, for over a century there has been intense interest in elucidating how respiratory neurons adjust their output to variables which can not be directly monitored. Several hypotheses have been tested and supportive data were obtained, but for each hypothesis, there are contradictory data or reasons to question the validity of each hypothesis. Herein, we report a critique of the major hypotheses which has led to the following conclusions. First, a single stimulus or combination of stimuli that convincingly and entirely explains the hyperpnea has not been identified. Second, the coupling of the hyperpnea to metabolic rate is not causal but is due to of these variables each resulting from a common factor which link the circulatory and ventilatory responses to exercise. Third, stimuli postulated to act at pulmonary or cardiac receptors or carotid and intracranial chemoreceptors are not primary mediators of the hyperpnea. Fourth, stimuli originating in exercising limbs and conveyed to the brain by spinal afferents contribute to the exercise hyperpnea. Fifth, the hyperventilation during heavy exercise is not primarily due to lactacidosis stimulation of carotid chemoreceptors. Finally, since volitional exercise requires activation of the CNS, neural feed-forward (central command) mediation of the exercise hyperpnea seems intuitive and is supported by data from several studies. However, there is no compelling evidence to accept this concept as an indisputable fact.
在健康哺乳动物运动期间，肺泡通气和肺泡毛细血管扩散会与代谢率的增加成比例增加，以防止 PaCO2 增加和 PaO2 降低。目前还没有已知的机制能够直接感知肌肉或肺部的气体交换速率；因此，一个多世纪以来，人们一直强烈关注阐明呼吸神经元如何调整其输出以适应无法直接监测的变量。已经测试了几个假设并获得了支持性数据，但对于每个假设，都有矛盾的数据或理由质疑每个假设的有效性。在此，我们报告了对主要假设的批判，得出以下结论。首先，还没有发现一个令人信服且完全解释过度通气的单一刺激或刺激组合。其次，过度通气与代谢率的耦合不是因果关系，而是由于这些变量中的每一个都来自一个共同的因素，该因素将循环和通气反应与运动联系起来。第三，假定作用于肺或心脏受体或颈动脉和颅内化学感受器的刺激物不是过度通气的主要介质。第四，源自运动肢体并通过脊髓传入纤维传递到大脑的刺激物有助于运动性过度通气。第五，在剧烈运动期间的过度通气主要不是由于乳酸酸中毒刺激颈动脉化学感受器引起的。最后，由于自主运动需要中枢神经系统的激活，因此中枢神经前馈（中枢命令）介导运动性过度通气似乎是直观的，并且得到了来自几项研究的数据的支持。然而，没有令人信服的证据可以接受这个概念作为无可争议的事实。
