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

The effect of carbonic anhydrase inhibition with acetazolamide (Acz, 10 mg/ kg) on the ventilatory response to an abrupt switch into hyperoxia (end-tid al PO2 = 450 Torr) and hypoxia (end-tidal PO2 = 50 Torr) was examined in fi ve male subjects [30 +/- 3 (SE) yr]. Subjects exercised at a work rate chos en to elicit an O-2 uptake equivalent to 80% of the ventilatory threshold. Ventilation ((V)over dotE) was measured breath by breath. Arterial oxyhemog lobin saturation (%Sa(O2)) was determined by ear oximetry. After the switch into hyperoxia, (V)over dotE remained unchanged from the steady-state exer cise prehyperoxic value (60.6 +/- 6.5 1/min) during Act. During control stu dies (Con), (V)over dotE decreased from the prehyperoxic value (52.4 +/- 5. 5 1/min) by similar to 20% ((V)over dotE nadir = 42.4 +/- 6.3 1/min) within 20 s after the switch into hyperoxia. (V)over dotE increased during Act an d Con after the switch into hypoxia; the hypoxic ventilatory response was s ignificantly lower after Act compared with Con [Act, change (Delta) in (V)o ver dotE/Delta Sa(O2) = 1.54 +/- 0.101.min(-1).Sa(O2)(-1); Con, Delta(V)ove r dotE/Delta Sa(O2) = 2.22 +/- 0.28 1.min(-1) Sa(O2)(-1)]. The peripheral c hemoreceptor contribution to the ventilatory drive after acute Acz-induced carbonic anhydrase inhibition is not apparent in the steady state of modera te-intensity exercise. However, Act administration did not completely atten uate the peripheral chemoreceptor response to hypoxia.