{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T14:13:34Z","timestamp":1791036814177,"version":"4.1.0"},"reference-count":34,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2007,3,7]],"date-time":"2007-03-07T00:00:00Z","timestamp":1173225600000},"content-version":"vor","delay-in-days":6,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2007,3]]},"abstract":"<jats:p>During moderate exercise (below the lactate threshold, \u03b8<jats:sub>L<\/jats:sub>), muscle CO<jats:sub>2<\/jats:sub> production (\n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_346_mu1.gif\" xlink:title=\"inline image\"\/>) kinetics are monoexponential, with a time constant (\u03c4) similar to that of O<jats:sub>2<\/jats:sub> consumption. Following a delay incorporating the muscle\u2013lung vascular transit time, \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_346_mu2.gif\" xlink:title=\"inline image\"\/> is expressed at the lungs (\n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_346_mu3.gif\" xlink:title=\"inline image\"\/>) with an appreciably longer \u03c4, reflecting the influence of intervening high\u2010capacitance CO<jats:sub>2<\/jats:sub> stores. Above \u03b8<jats:sub>L<\/jats:sub>, \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_346_mu4.gif\" xlink:title=\"inline image\"\/> kinetics become complex, resulting from the conflation of the differing rates of HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> breakdown and degrees of compensatory hyperventilation with that of the underlying aerobic component. During incremental exercise, the increased rate of \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_346_mu5.gif\" xlink:title=\"inline image\"\/> relative to pulmonary O<jats:sub>2<\/jats:sub> uptake (\n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_346_mu6.gif\" xlink:title=\"inline image\"\/>) can be used to quantify \u03b8<jats:sub>L<\/jats:sub> validly if aerobic and hyperventilatory sources can be ruled out, i.e. \u03b8<jats:sub>L<\/jats:sub> is then attributable to the decrease in muscle and blood [HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>]. In many cases, however, very rapid incrementation of work rate and\/or prior depletion of CO<jats:sub>2<\/jats:sub> stores (by volitional or anticipatory hyperventilation) can yield a \u2018false positive\u2019 non\u2010invasive estimation of \u03b8<jats:sub>L<\/jats:sub> (\u2018pseudo\u2010threshold\u2019) resulting from a slowing of the rate of wash\u2010in of transient CO<jats:sub>2<\/jats:sub> stores.<\/jats:p>","DOI":"10.1113\/expphysiol.2006.034363","type":"journal-article","created":{"date-parts":[[2006,12,22]],"date-time":"2006-12-22T01:28:53Z","timestamp":1166750933000},"page":"347-355","source":"Crossref","is-referenced-by-count":81,"title":["Physiological mechanisms dissociating pulmonary CO<sub>2<\/sub> and O<sub>2<\/sub> exchange dynamics during exercise in humans"],"prefix":"10.1113","volume":"92","author":[{"given":"Brian 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