{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T09:41:27Z","timestamp":1769161287402,"version":"3.49.0"},"reference-count":54,"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>Below the lactate threshold (\u03b8<jats:sub>L<\/jats:sub>), ventilation \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_356_mu1.gif\" xlink:title=\"inline image\"\/> responds in close proportion to CO<jats:sub>2<\/jats:sub> output \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_356_mu2.gif\" xlink:title=\"inline image\"\/> to regulate arterial partial pressure of CO<jats:sub>2<\/jats:sub>\n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_356_mu3.gif\" xlink:title=\"inline image\"\/>. While ventilatory control models have traditionally included proportional feedback (central and carotid chemosensory) and feedforward (central and peripheral neurogenic) elements, the mechanisms involved remain unclear. Regardless, putative control schemes have to accommodate the close dynamic \u2018coupling\u2019 between \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_356_mu4.gif\" xlink:title=\"inline image\"\/> and \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_356_mu5.gif\" xlink:title=\"inline image\"\/>. Above \u03b8<jats:sub>L<\/jats:sub>, \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_356_mu6.gif\" xlink:title=\"inline image\"\/> is driven down to constrain the fall of arterial pH by a compensatory hyperventilation, probably of carotid body origin. When \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_356_mu7.gif\" xlink:title=\"inline image\"\/> requirements are high (as in highly fit endurance athletes), \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_356_mu8.gif\" xlink:title=\"inline image\"\/> can attain limiting proportions. Not only does this impair gas exchange at these work rates, but there may be an associated high metabolic cost for generation of respiratory muscle power, which may be sufficient to divert a fraction of the cardiac output away from the muscles of locomotion to the respiratory muscles, further compromising exercise tolerance.<\/jats:p>","DOI":"10.1113\/expphysiol.2006.034371","type":"journal-article","created":{"date-parts":[[2007,1,19]],"date-time":"2007-01-19T01:34:55Z","timestamp":1169170495000},"page":"357-366","source":"Crossref","is-referenced-by-count":40,"title":["Ventilatory control in humans: constraints and limitations"],"prefix":"10.1113","volume":"92","author":[{"given":"Susan 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