Peripheral chemoreceptor function after carbonic anhydrase inhibition during moderate-intensity exercise

Abstract

The effect of carbonic anhydrase inhibition with acetazolamide (Acz, 10 mg/kg) on the ventilatory response to an abrupt switch into hyperoxia (end-tidal [Formula: see text]= 450 Torr) and hypoxia (end-tidal[Formula: see text] = 50 Torr) was examined in five male subjects [30 ± 3 (SE) yr]. Subjects exercised at a work rate chosen to elicit an O2 uptake equivalent to 80% of the ventilatory threshold. Ventilation (V˙e) was measured breath by breath. Arterial oxyhemoglobin saturation (%[Formula: see text]) was determined by ear oximetry. After the switch into hyperoxia, V˙eremained unchanged from the steady-state exercise prehyperoxic value (60.6 ± 6.5 l/min) during Acz. During control studies (Con),V˙e decreased from the prehyperoxic value (52.4 ± 5.5 l/min) by ∼20% (V˙enadir = 42.4 ± 6.3 l/min) within 20 s after the switch into hyperoxia. V˙e increased during Acz and Con after the switch into hypoxia; the hypoxic ventilatory response was significantly lower after Acz compared with Con [Acz, change (Δ) inV˙e/[Formula: see text]= 1.54 ± 0.10 l ⋅ min−1 ⋅ [Formula: see text] −1; Con, ΔV˙e/[Formula: see text]= 2.22 ± 0.28 l ⋅ min−1 ⋅ [Formula: see text] −1]. The peripheral chemoreceptor contribution to the ventilatory drive after acute Acz-induced carbonic anhydrase inhibition is not apparent in the steady state of moderate-intensity exercise. However, Acz administration did not completely attenuate the peripheral chemoreceptor response to hypoxia.