title: Breathing during exercise: demands, regulation, limitations.
abstract: In humans alveolar ventilation (VA) is adjusted almost perfectly to the metabolic demands of mild and moderate exercise. For example, in exercise transitions and in the steady state, PaCO2 rarely deviates by more than 1 to 3 mmHg from the value at rest. This near-homeostasis contrasts to most other mammalian species; equines for example, demonstrate a progressive hypocapnia and alkalosis as exercise intensity is increased to moderate levels. In equines, the control systems seem programmed for a specific hyperventilation that contributes to maintenance of PaO2 homeostasis. Generally, during heavy exercise all species hyperventilate creating hypocapnia, increased PAO2, widened A-a O2 gradient, and PaO2 homeostasis. The origin of the metabolic ventilatory stimulus remains controversial. Evidence exists for: a) "neural" mediation, either central command or peripheral afferent in nature; and b) "humoral" mediation with an intra-thoracic metabolite receptor being a possibility. The mechanism of the species differences in hyperventilation during exercise does not appear to be due to species variation in chemoreceptor "fine tuning". Contrary to traditional thinking, recent findings suggest that the hyperventilation during heavy exercise might not be mediated by lactacidosis stimulation of chemoreceptors. The increase in VA during exercise is achieved efficiently in that airway diameter is modulated and the pattern of breathing and the recruitment of respiratory muscles are set to minimize the O2 cost of breathing. It has been postulated that mechanoreceptors in airways, lung parenchyma and the chest wall are important to efficient breathing. Their role and contribution to the exercise hyperpnea has been shown by reductions in respiratory neural output within breath when respiratory impedance is reduced via helium breathing. Hilar nerve afferents do not appear to be critical to this response. However, carotid chemoreceptors appear essential for "fine tuning" of VA when respiratory impedance is reduced. In most healthy exercising mammals, the efficiency component of the exercise stimulus does not compromise VA. There are two known major exceptions. One is the extremely fit human athlete during very high workloads when atypically there is minimal or no hyperventilation resulting in arterial hypoxemia. That indeed the high O2 cost of breathing compromises VA is indicated by hyperventilation and alleviation of hypoxemia with resistance unloading through helium breathing. A second example of a compromise of VA is that of a galloping racehorse at very high workloads.(ABSTRACT TRUNCATED AT 400 WORDS)
authors.affiliation: Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
authors.forename: H V
authors.initials: HV
authors.lastname: Forster
authors.forename: L G
authors.initials: LG
authors.lastname: Pan
mesh_terms: D000818:Animals; D006801:Humans; D005082:Physical Exertion; D012119:Respiration