Pulmonary control systems in exercise: update.

We examined recent ideas and findings concerned with the regulation of ventilation and gas transport in moderate and heavy exercise. The primary mediation of exercise hyperpnea remains unknown and highly controversial, but two unique approaches to the problem have advanced our understanding of this neurohumoral regulatory scheme. On the one hand, experimental separation of the pulmonary and systemic circulations was used to reveal a vagally mediated ventilatory response that is clearly attributable to CO2 flow to the lung. This mechanism seems to be most effective as a homeostatic regulator of ventilatory control near resting levels of metabolic rate. On the other hand, a descending neurogenic drive to hyperpnea from the locomotor regions of the central nervous system was also demonstrated experimentally. The importance of regulatory feedback by conventional chemoreceptors in determining the precision of the hyperpneic response was emphasized in explaining the wide spectrum of arterial acid-base regulation during exercise in humans and non-human species. Two commonly accepted homeostatic regulators believed to be operative during heavy exercise were questioned, i.e., the compensatory hyperventilatory response and the maintenance of arterial oxygenation. For example, the hyperventilatory response was shown not to require metabolic acidosis; hyperventilation was not always observed at high work rates despite an abundance of chemical stimuli; and arterial hypoxemia occurred at very high metabolic rates in a significant number of highly fit athletes. These data implied that the capabilities of some aspects of even the healthy pulmonary system may be approached-or even exceeded-during heavy exercise.