WHIPP, B. J. Peripheral chemoreceptor control of exercise hyperpnea in humans. Med. Sci. Sports Exerc., Vol. 26, No. 3, pp. 337–347, 1994. Estimates of the proportional contribution of the peripheral chemoreceptors (i.e., the carotid bodies) to human ventilatory control during moderate exercise (i.e., below the lactate threshold, ·1) suggest that they: (a) exert no discernible influence on the initial (usually rapid) phase I component; (b) provide significant modulation of the slower, exponential phase II dynamics, therefore contributing to the tightness of arterial PCO2 regulation and the magnitude of the transient hypoxemia in this phase; and (c) account for ∼20% of the steady-state phase III drive, which can rise to over 50% in hypoxia (PaO2 ∼50 mm Hg). Above θ1, the carotid bodies constrain the transient fall in arterial pH by mediating much (but not all) of the compensatory hyperventilation for the metabolic acidemia. The carotid body contribution above θ1, estimated by Dejours O2 testing, is not appreciably different from subthreshold estimates, suggesting that: (a) the respiratory alkalosis in blood and cerebrospinal fluid resulting from the hyperventilation may suppress carotid chemonsitivity; (b) an artifact resulting from secondary hyperoxia-induced stimulation of central chemoreceptors may lead to underestimation of the carotid body contribution; or (c) the carotid bodies may not be entirely “silenced” by hyperoxia during a metabolic acidemia.
©1994The American College of Sports Medicine