• Keisuke Miki, Ryoji Maekura, Mari Miki, Seigo Kitada, Kenji Yoshimura, Yoshitaka Tateishi, and Masahide Mori.
• Department of Internal Medicine, National Hospital Organization Toneyama National Hospital, Toyonaka, Osaka, Japan. mikisuke@toneyama.go.jp
• Respir Physiol Neurobiol. 2013 Feb 1; 185 (3): 653-8.

AbstractTo understand the mechanism of exertional dyspnea, we postulated that, despite hyperoxia during exercise, patients with idiopathic pulmonary fibrosis (IPF) might not regulate exertional acidosis by ventilatory compensation to stop exercise. The exercise responses during 30% O(2) or compressed air (CA) were examined in 13 patients with IPF. The PaO(2), PaCO(2), and HCO(3)(-) levels were higher during exercise with hyperoxia than with CA. At peak exercise, hyperoxia reduced the plasma lactate level. The dyspnea-ratio (%) of the ΔV(O(2)) (peak minus resting oxygen uptake) curve reached a break point that occurred at a similar exercise point with hyperoxia and CA, preceded by a break point in the breathing frequency-ratio of the ΔV(O(2)). Accordingly, the dyspnea score and pH each reached similar levels with hyperoxia and CA to stop exercise. Regardless of breathing CA or 30% O(2), IPF patients did not regulate exertional acidosis by ventilatory compensation to stop exercise, resulting in reaching a specific pH.Copyright © 2012 Elsevier B.V. All rights reserved.

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