This review highlights that the primary mechanism (humoral vs. neural) driving hyperventilation during incremental exercise remains unresolved.
Leaves open the dominant mechanism of exercise hyperventilation; no immediate change to testing protocols or interpretations warranted.
The ventilatory response to incremental exercise in man has been well described. It is generally agreed that [Vdot]E increases as a linear function of [Vdot] 2 up to 50–75% [Vdot]O 2 max, after which [Vdot]E begins to rise expotentially. Recently, the term “ventilatory threshold” (Tvent) has been proposed to describe this [Vdot]E “inflection point” during graded work. In general, two major schools of thought exist concerning the mechanism(s) that are responsible for the Tvent. One group proposes that the Tvent occurs due to a humoral stimulus whereas the second camp argues that nonhumoral (neural) stimuli account for the hyperventilation seen in incremental work. The most publicized humoral hypothesis to explain the Tvent has been proposed by Wasserman, Whipp, Koyal, and Beaver (1973). These authors suggest that the Tvent occurs during incremental exercise due to augmented ventilatory drive resulting from increased CO 2 return to the lungs, followed by an additional stimulation to breath via lactate induced metabolic acidosis. In addition, Asmussen (1983) has recently proposed a “hypoxic drive” hypothesis which argues that the hyperventilation of heavy exercise results from an exercise potentiation of hypoxemia. Much of the support for nonhumoral explanations for the Tvent center around inconsistencies in the humoral control hypothesis. Although existence of both afferent and efferent neural input to the respiratory center during exercise has been demonstrated, direct evidence for the Tvent being exclusively mediated via neural mechanisms does not appear to exist. Secondary factors such as rising plasma catecholamines, and temperature increases, may also contribute to hyperventilation during heavy work. In summary, although there is persuasive evidence that humoral factors may play an important role in mediation of the Tvent, the basic question of whether humoral or neural mechanisms provide the primary stimulus to hyperventilate during incremental exercise remains unresolved.
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Powers et al. (1985) studied this question.
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