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J Appl Physiol 86: 1544-1551, 1999;
8750-7587/99 $5.00
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Vol. 86, Issue 5, 1544-1551, May 1999

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

Barry W. Scheuermann1, John M. Kowalchuk1,2, Donald H. Paterson1, and David A. Cunningham1,2

1 Centre for Activity and Ageing, School of Kinesiology, and 2 Department of Physiology, The University of Western Ontario, London, Ontario, Canada N6A 3K7

The effect of carbonic anhydrase inhibition with acetazolamide (Acz, 10 mg/kg) on the ventilatory response to an abrupt switch into hyperoxia (end-tidal PO2 = 450 Torr) and hypoxia (end-tidal PO2 = 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 (VE) was measured breath by breath. Arterial oxyhemoglobin saturation (%SaO2) was determined by ear oximetry. After the switch into hyperoxia, VE remained unchanged from the steady-state exercise prehyperoxic value (60.6 ± 6.5 l/min) during Acz. During control studies (Con), VE decreased from the prehyperoxic value (52.4 ± 5.5 l/min) by ~20% (VE nadir = 42.4 ± 6.3 l/min) within 20 s after the switch into hyperoxia. VE increased during Acz and Con after the switch into hypoxia; the hypoxic ventilatory response was significantly lower after Acz compared with Con [Acz, change (Delta ) in VE/Delta SaO2 = 1.54 ± 0.10 l · min-1 · SaO2-1; Con, Delta VE/Delta SaO2 = 2.22 ± 0.28 l · min-1 · SaO2-1]. 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.

carotid bodies; control of breathing; hypoxia; hyperoxia


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