Aerobically generated CO2 stored during early exercise

Department of Medicine, Division of Respiratory and Critical Care Physiology and Medicine, Harbor-University of California Los Angeles Medical Center, Torrance, California 90509 Previous studies have shown that a metabolic alkalosis develops in the muscle during early exercise. This has been linked...

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Bibliographic Details
Published in:Journal of applied physiology (1985) 1999-09, Vol.87 (3), p.1048-1058
Main Authors: Chuang, Ming-Lung, Ting, Hua, Otsuka, Toshihiro, Sun, Xing-Guo, Chiu, Frank Y. L, Beaver, William L, Hansen, James E, Lewis, David A, Wasserman, Karlman
Format: Article
Language:English
Subjects:
Biological and medical sciences
Blood gas. Hemoglobin. Myoglobin. Hemotissulary gas exchange. Acid-base balance
Carbon dioxide
Exercise
Fundamental and applied biological sciences. Psychology
Kinetics
Vertebrates: respiratory system
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Summary:Department of Medicine, Division of Respiratory and Critical Care Physiology and Medicine, Harbor-University of California Los Angeles Medical Center, Torrance, California 90509 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 + and HCO 3 concentrations increase without an increase in P CO 2 . Thus CO 2 from aerobic metabolism is converted to HCO 3 rather than being eliminated by the lungs. The purpose of this study was to quantify the increase in early CO 2 stores and the component due to the exercise-induced metabolic alkalosis (E-I Alk). To avoid masking the increase in CO 2 stores by CO 2 released as HCO 3 buffers lactic acid, the transient increase in CO 2 stores was measured only for work rates (WRs) below the lactic acidosis threshold (LAT). The increase in CO 2 stores was evident at the airway starting at ~15 s; the increase reached a peak at ~60 s and was complete by ~3 min of exercise. The increase in CO 2 stores was greater, but the kinetics were unaffected at the higher WR. Three components of the change in aerobically generated CO 2 stores were considered relevant: the carbamate component of the Haldane effect, the increase in CO 2 stores due to increase in tissue P CO 2 , and the E-I Alk. The Haldane effect was calculated to be ~5%. Physically dissolved CO 2 in the tissues was ~30% of the store increase. The remaining E-I Alk CO 2 stores averaged 61 and 68% for 60 and 80% LAT WRs, respectively. The kinetics of O 2 uptake correlated with the time course of the increase in CO 2 stores; the size of the O 2 deficit correlated with the size of the E-I Alk component of the CO 2 stores. We conclude that a major component of the aerobically generated increase in CO 2 stores is the new HCO 3 generated as phosphocreatine is converted to creatine. carbon dioxide stores; gas-exchange kinetics; near-infrared spectroscopy; lactic acidosis threshold; phosphocreatine hydrolysis; oxygen deficit
ISSN:8750-7587
1522-1601
DOI:10.1152/jappl.1999.87.3.1048