| Abstract: | We reviewed the response and regulation of alveolar ventilation, chest wall mechanics, and alveolar-to-arterial gas exchange to the demands imposed by increases in tissue metabolic rate. The primary mediator of iso-capnic exercise hyperpnea remains a dilemma--with conflicting evidence presented on both sides of a "CO2 flow" humoral hypothesis versus a "neurogenic" non-humoral hypothesis. The increased expiratory flows and tidal volumes at any given level of hyperpnea are achieved at a "minimum" of increased mechanical work exerted on the lung and chest wall, owing to a control system that has multiple levels of nervous integration (from cortex to spinal motor neuron) readily accessible to a wide variety of sensory information concerning the mechanical status of the lung and respiratory muscles. The maintenance of arterial PO2 in the face of a falling CVO2 during exercise was attributed to a precise regulation over factors that limit diffusion equilibrium and intra- and interregional ventilation: perfusion distributions in the lung. Finally, we noted that the near-optimal nature of these responses and their control during exercise had many exceptions in the real world of physical exercise outside of the laboratory. |
