Contribution of acid-base changes to control of breathing during exercise

The mechanisms mediating the exercise hyperpnea remain controversial; there is no unequivocal evidence that any of numerous proposed mechanisms mediates the hyperpnea. However, a great deal has been learned including the potential role of changes in PCO2, [H+], strong ion differences (SID), weak acids, or any other acid-base component. The contribution of acid-base changes to the hyperpnea during exercise is likely through known or postulated chemoreceptors. Two of these, pulmonary and intracranial chemoreceptors, do not appear critical for the ventilatory adjustments to meet the metabolic demands of exercise. A third, the carotid chemoreceptors, appear to fine-tune alveolar ventilation during exercise to minimize disruptions in arterial blood gases. The role of the fourth chemoreceptors, those within skeletal muscles, is least clear. However, there is evidence that they do contribute to the hyperpnea, and it is quite clear that a muscle chemoreflex contributes to the exercise muscle pressor reflex; thus the contribution of these chemoreceptors to the exercise hyperpnea requires additional study.