Tansley, J. G., C. Clar, M. E. F. Pedersen, and P. A. Robbins. Human ventilatory response to acute hyperoxia during and after 8 h of both isocapnic and poikilocapnic hypoxia. J. Appl. Physiol. 82(2): 513–519, 1997.—During 8 h of either isocapnic or poikilocapnic hypoxia, there may be a rise in ventilation (V˙e) that cannot be rapidly reversed with a return to higher[Formula: see text] (L. S. G. E. Howard and P. A. Robbins. J. Appl. Physiol. 78: 1098–1107, 1995). To investigate this further, three protocols were compared: 1) 8-h isocapnic hypoxia [end-tidal[Formula: see text]([Formula: see text] ) held at prestudy value, end-tidal [Formula: see text]([Formula: see text]) = 55 Torr], followed by 8-h isocapnic euoxia[Formula: see text] = 100 Torr); 2) 8-h poikilocapnic hypoxia followed by 8-h poikilocapnic euoxia; and 3) 16-h air-breathing control. Before and at intervals throughout each protocol, theV˙e response to eucapnic hyperoxia [Formula: see text] held 1–2 Torr above prestudy value,[Formula: see text] = 300 Torr) was determined. There was a significant rise in hyperoxicV˙e over 8 h during both forms of hypoxia ( P < 0.05, analysis of variance) that persisted during the subsequent 8-h euoxic period ( P < 0.05, analysis of variance). These results support the notion that an 8-h period of hypoxia increases subsequent hyperoxic V˙e, even if acid-base changes have been minimized through maintenance of isocapnia during the hypoxic period.
No takes yet. Share an insight, caveat, or question.
Tansley et al. (1997) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: