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This Article Full Text Full Text (PDF) All Versions of this Article: 92/1/273    most recent expphysiol.2006.033159v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wood, H. E. Articles by Robbins, P. A. Search for Related Content PubMed PubMed Citation Articles by Wood, H. E. Articles by Robbins, P. A.

¹ University Laboratory of Physiology, University of Oxford, Parks Road, Oxford OX1 3PT, UK

Both exercise and hypoxia increase pulmonary ventilation. However, the combined effects of the two stimuli are more than additive, such that exercise may be considered to potentiate the acute ventilatory response to hypoxia (AHVR), and vice versa. Exposure to sustained hypoxia of 8 h duration or more has been shown to increase the acute chemoreflex responses to hypoxia and hypercapnia. The purpose of this study was to determine whether sustained exposure to hypoxia also changed the stimulus interaction between the effects of exercise and hypoxia on ventilation. Ten subjects undertook two main protocols on two separate days. On one day, subjects were exposed to isocapnic hypoxia (IH) at an end-tidal partial pressure of O₂ of 55 mmHg and on the other day, subjects were exposed to air as a control (C). Before and after each exposure, the sensitivity of AHVR was assessed during both resting conditions and exercise at 35% of the subjects' maximal oxygen uptake capacity. Average values (means ± S.D.) obtained for the sensitivity of AHVR from protocol IH were 0.85 ± 0.35 (rest, prehypoxic exposure), 1.60 ± 0.66 (exercise, prehypoxic exposure), 1.69 ± 0.63 (rest, posthypoxic exposure) and 1.81 ± 0.86 l min^–1 %^–1 (exercise, posthypoxic exposure). A non-dimensional variable, , was used to quantify the interaction present between exercise and hypoxia. The variable fell significantly following the sustained exposure to hypoxia (P < 0.02, ANOVA), indicating that the degree of stimulus interaction between acute hypoxia and exercise had declined. We suggest that the mechanisms by which sustained hypoxia modifies peripheral chemoreflex function may also modify the effects of exercise on the peripheral chemoreflex.

(Received 4 January 2006; accepted after revision 5 September 2006; first published online 11 September 2006)
Corresponding author P. A. Robbins: University Laboratory of Physiology, University of Oxford, Parks Road, Oxford OX1 3PT, UK. Email: peter.robbins{at}physiol.ox.ac.uk