{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T05:39:11Z","timestamp":1790314751068,"version":"4.1.0"},"reference-count":28,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[1999,9,1]]},"abstract":"<jats:p> Previous studies have shown that a metabolic alkalosis develops in the muscle during early exercise. This has been linked to phosphocreatine hydrolysis. Over a similar time frame, the femoral vein blood pH and plasma K<jats:sup>+<\/jats:sup> and[Formula: see text] concentrations increase without an increase in [Formula: see text]. Thus CO<jats:sub>2<\/jats:sub> from aerobic metabolism is converted to [Formula: see text] rather than being eliminated by the lungs. The purpose of this study was to quantify the increase in early CO<jats:sub>2<\/jats:sub> stores and the component due to the exercise-induced metabolic alkalosis (E-I Alk). To avoid masking the increase in CO<jats:sub>2<\/jats:sub> stores by CO<jats:sub>2<\/jats:sub> released as[Formula: see text] buffers lactic acid, the transient increase in CO<jats:sub>2<\/jats:sub> stores was measured only for work rates (WRs) below the lactic acidosis threshold (LAT). The increase in CO<jats:sub>2<\/jats:sub> stores was evident at the airway starting at \u223c15 s; the increase reached a peak at \u223c60 s and was complete by \u223c3 min of exercise. The increase in CO<jats:sub>2<\/jats:sub> stores was greater, but the kinetics were unaffected at the higher WR. Three components of the change in aerobically generated CO<jats:sub>2<\/jats:sub> stores were considered relevant: the carbamate component of the Haldane effect, the increase in CO<jats:sub>2<\/jats:sub> stores due to increase in tissue [Formula: see text], and the E-I Alk. The Haldane effect was calculated to be \u223c5%. Physically dissolved CO<jats:sub>2<\/jats:sub> in the tissues was \u223c30% of the store increase. The remaining E-I Alk CO<jats:sub>2<\/jats:sub> stores averaged 61 and 68% for 60 and 80% LAT WRs, respectively. The kinetics of O<jats:sub>2<\/jats:sub> uptake correlated with the time course of the increase in CO<jats:sub>2<\/jats:sub>stores; the size of the O<jats:sub>2<\/jats:sub> deficit correlated with the size of the E-I Alk component of the CO<jats:sub>2<\/jats:sub> stores. We conclude that a major component of the aerobically generated increase in CO<jats:sub>2<\/jats:sub> stores is the new[Formula: see text] generated as phosphocreatine is converted to creatine. <\/jats:p>","DOI":"10.1152\/jappl.1999.87.3.1048","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:18:18Z","timestamp":1513955898000},"page":"1048-1058","source":"Crossref","is-referenced-by-count":25,"title":["Aerobically generated CO<sub>2<\/sub>stored during early exercise"],"prefix":"10.1152","volume":"87","author":[{"given":"Ming-Lung","family":"Chuang","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Respiratory and Critical Care Physiology and Medicine, Harbor-University of California Los Angeles Medical Center, Torrance, California 90509"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hua","family":"Ting","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Respiratory and Critical Care Physiology and Medicine, Harbor-University of California Los Angeles Medical Center, Torrance, California 90509"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshihiro","family":"Otsuka","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Respiratory and Critical Care Physiology and Medicine, Harbor-University of California Los Angeles Medical Center, Torrance, California 90509"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xing-Guo","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Respiratory and Critical Care Physiology and Medicine, Harbor-University of California Los Angeles Medical Center, Torrance, California 90509"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank Y. 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