Exercise and Chemoreception ^1, ²

Abstract

1. Does Chemoreception Contribute to the Ventilatory Response to Exercise? The commonly held concept here is depicted in figure 1, i.e., that the steady-state of moderate exercise in healthy persons at sea level is accompanied by arterial isocapnia secondary to increments in alveolar ventilation (VA), which are in direct proportion to those in Vco2 (1). A similar constancy of arterial Po2 and [H + ] occurs with no changes of significance in other potential stimuli such as cerebrospinal fluid [H + ], circulating adrenergic amines, or vascular temperature. It is only when exercise is heavy that this proportionality is disturbed and hyperventilation occurs, presumably as a result of systemic metabolic acidosis acting via peripheral chemoreception. In general, these concepts are well supported both by documentation of arterial blood gases during moderate exercise and by carotid body denervation studies in both humans and animals (1). On the other hand, there are several considerations that limit unqualified application of these principles to both moderate and heavy exercise.