Abstract
The stability of arterial blood gas tensions and pH during steady-state moderate exercise has suggested an important humoral element of ventilatory control in humans. However, the involvement of central and peripheral chemoreflexes in this humoral control remains controversial. This reflects, in large part, technical and interpretational limitations inherent in currently used estimators of chemoreflex "sensitivity." Evidence suggests that the central chemoreceptors (a) contribute little during moderate exercise, given the relative stability of cerebrospinal pH, (b) constrain the hyperpnea of high-intensity exercise, consequent to the respiratory compensation for the metabolic acidemia, and (c) may play a role in the respiratory compensation during chronic metabolic acidemia. In contrast, the peripheral chemoreceptors appear to (a) exert considerable influence on ventilatory kinetics in moderate exercise, but are less important in the steady state, and (b) induce much of the respiratory compensation of high-intensity exercise.
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