Effect of acute sodium bicarbonate ingestion on excess CO2 output during incremental exercise

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Deutscher übersetzter Titel:Auswirkung von akuter Natriumbikarbonateinnahme auf die überschießende Kohlendioxydabgabe während körperlicher Belastung von ansteigender Intensität
Autor:Hirakoba, Kohji; Maruyama, Atsuo; Misaka, Kouji
Erschienen in:European journal of applied physiology
Veröffentlicht:66 (1993), 6, S. 536-541, Lit.
Format: Literatur (SPOLIT)
Publikationstyp: Zeitschriftenartikel
Medienart: Gedruckte Ressource Elektronische Ressource (online)
Sprache:Englisch
ISSN:1439-6319, 0301-5548
DOI:10.1007/BF00634306
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Erfassungsnummer:PU199307066257
Quelle:BISp

Abstract des Autors

The effect of bicarbonate ingestion on total excess volume of CO2 output (CO2 excess), due to bicarbonate buffering of lactic acid in exercise, was studied in eight healthy male volunteers during incremental exercise on a cycle ergometer performed after ingestion (0.3 g/kg body mass) of CaCO3 (control) and NaHCO3 (alkalosis). The resting arterialized venous blood pH and bicarbonate concentration (<HCO3>b) were significantly higher in acute metabolic alkalosis than in the control. The blood lactate concentrations (<la->b) during exercise below the anaerobic threshold (AT) were not affected by AMA, while significantly higher <la->b at exhaustion and at 3 min after exercise were found in AMA compared with the control. The CO2 excess increased significantly from the control to AMA. The CO2 excess per body mass was found to be significantly correlated with both the increase of <la->b from rest to 3 min after exercise and with the decrease of <HCO3-> from rest to 3 min after exercise, indicating that CO2 excess per body mass increased linearly with both delta <la->b and delta <HCO3->b. As a consequence, CO2 excess per body mass per unit increase of <la->b (CO2 excess/mass/delta <la->b) was similar for the two conditions. The present results would suggest that the relationship between CO2 excess and blood lactate accumulation was unaffected by acute metabolic alkalosis, because the relative contribution of bicarbonate buffering of lactic acid was the same as in the control.