Ventilatory response to helium-oxygen breathing during exercise: effect of airway anesthesia.

The substitution of a normoxic helium mixture (HeO2) for room air (Air) during exercise results in a sustained hyperventilation, which is present even in the first breath. We hypothesized that this response is dependent on intact airway afferents; if so, airway anesthesia (Anesthesia) should affect this response. Anesthesia was administered to the upper airways by topical application and to lower central airways by aerosol inhalation and was confirmed to be effective for over 15 min. Subjects performed constant work-rate exercise (CWE) at 69 +/- 2 (SE) % maximal work rate on a cycle ergometer on three separate days: twice after saline inhalation (days 1 and 3) and once after Anesthesia (day 2). CWE commenced after a brief warm-up, with subjects breathing Air for the first 5 min (Air-1), HeO2 for the next 3 min, and Air again until the end of CWE (Air-2). The resistance of the breathing circuit was matched for Air and HeO2. Breathing HeO2 resulted in a small but significant increase in minute ventilation (VI) and decrease in alveolar PCO2 in both the Saline (average of 2 saline tests; not significant) and Anesthesia tests. Although Anesthesia had no effect on the sustained hyperventilatory response to HeO2 breathing, the VI transients within the first six breaths of HeO2 were significantly attenuated with Anesthesia. We conclude that the VI response to HeO2 is not simply due to a reduction in external tubing resistance and that, in humans, airway afferents mediate the transient but not the sustained hyperventilatory response to HeO2 breathing during exercise.

Airway anesthesia and respiratory adaptations to dead space loading and exercise.

In exercising humans, added external dead space (VD) increases minute ventilation (VI) and causes a slower and deeper breathing pattern (J. Appl. Physiol. 1991; 70:55-62). Recent studies suggest that airway receptors sensitive to topical anesthesia influence VI and breathing pattern responses to exercise and to added VD. We tested these hypotheses with a technique of airway anesthesia (Anesthesia) that has been shown to reliably attenuate airway reflexes. Anesthesia was administered by local laryngopharyngeal application and aerosolized lidocaine inhalation, and was confirmed by citric acid aerosol inhalation challenges. Twelve normal males performed maximal incremental cycle ergometer exercise on 4 d (randomized) after Anesthesia with (Anesthesia VD) and without added VD (Anesthesia Control) and after normal saline inhalation (Saline) with (Saline VD) and without added VD (Saline Control). There were no differences in the VI and breathing pattern responses during exercise between the Saline Control and the Anesthesia Control tests. After both Saline and Anesthesia inhalation, added VD resulted in an increase in VI both at rest and during exercise. At matched VI (98 L/min), the differences in tidal volume (VT) between the Saline Control and Saline VD tests (delta = 0.23 +/- 0.24 L, mean +/- SD) and the Anesthesia Control and Anesthesia VD tests (delta = 0.20 +/- 0.28 L) were not significantly different. Our study had a power of greater than 95% to detect significant differences in VI or breathing pattern due to Anesthesia. We conclude that in normal humans, airway receptors do not play a major role in ventilation and breathing pattern control during exercise, and that the respiratory adaptations to added VD during exercise are not mediated by airway afferent reflexes.