Reducing Ventilatory Response to Carbon Dioxide by Breathing Cold Air

The effect of nasal breathing of 8% CO2 in oxygen at the cold temperature was to reduce nasal inspiratory resistance at 1 L/s, and the effect of topical nasal anesthesia increased the response to CO2 at the warm temperature.

Abstract

Abstract To study the effect of cooling of nasal receptors on breathing we had 10 normal male volunteers rebreathe through their noses 8% CO2 in oxygen at “warm” (23 to 30° C) and at “cold” (−4 to 10° C) temperatures. In order to further examine the effect of nasal receptors on the control of breathing, 11 subjects had their nasal response to CO2 measured at the warm temperature before and after topical nasal anesthesia. To exclude an increase in nasal resistance as the cause of the reduced response to CO2, 10 subjects had their nasal resistance measured before and after nasal rebreathing of cold 8% CO2 in oxygen. To also exclude increased bronchial resistance, forced expiratory volume in one second (FEV1) was measured in 12 subjects before and after nasal breathing of cold oxygen for 3 min. The mean ventilatory response to CO2 was reduced from 3.0 ± 1.6 L/min/mmHg to 2.5 ± 1.1 L/min/mmHg (p < 0.05) by the cold air. Topical nasal anesthesia increased the response to CO2 at the warm temperature from 2.4 ± 0.7 to 2.7 ± 0.9 L/min/mmHg. The effect of nasal breathing of 8% CO2 in oxygen at the cold temperature was to reduce nasal inspiratory resistance at 1 L/s from 4.3 ± 3.0 cm H2O L/s to 2.6 ± 1.0 cm H2O L/s (p < 0.05). Expiratory resistance at 1 L/s fell from 3.7 ± 1.5 cm H2O L/s to 2.4 ± 0.7 cm H2O L/s (p < 0.02). The FEV1 was unchanged by nasal breathing of cold oxygen. We feel that the reduction in the response to CO2 during nasal breathing of cold air was due to inhibition of respiratory output by nasal receptors and not to changes in nasal or bronchial resistance. The receptors have a minor influence on the control of breathing at warm temperatures and at resting levels of ventilation.