This article is based on a lecture presented in the Symposium on Ventilatory Control During Exercise at the 24th Annual Meeting of the American College of Sports Medicine, May 25-28, 1977, Chicago, Illinois.
WHIPP, BRIAN J. and JAMES A. DAVIS. Peripheral chemore-ceptors and exercise hyperpnea. Med. Sci. Sports. Vol. 11, No. 2, pp. 204-212, 1979. The carotid bodies appear to be the only peripheral chemoreceptors mediating ventilatory control during exercise in man. While little is known about the mechanism of stimulation, much is known about the effects of carotid body stimulation upon pulmonary ventilation (VE). These effects have been produced by hypercapnia, hypoxia, metabolic acidosis, arterial blood pressure, temperature, and catecholamines. A signal from CO2 flow is attractive because of the strong correlation between CO2 output and VE during exercise. The carotid body's role in the hyperpnea depends on the intensity of exercise. During heavy exercise, pH falls and hyperventilation ensues. The carotid bodies appear to be the exclusive mediators of the ventilatory compensation for the acidosis at this exercise intensity. For moderate exercise, mean arterial Pco2 does not change. There-fore, how is the CO2 signal transmitted to the respiratory center? Two current theories are: (1) since arterial Pco2 and pH oscillate with each breath, the amplitude and period of these oscillations may change during exercise and may be of sufficient magnitude to stimulate the carotid bodies, and (2) there exists a disequilibrium between hydrogen ion activity within the red blood cell and in the plasma because carbonic anhydrase is found in the former but not the latter. This theory assumes that the enzyme is not accessible to the plasma.