Effect of acute sodium bicarbonate ingestion on excess C02 output during incremental exercise

Summary The effect of bicarbonate ingestion on total excess volume of CO₂ Output (CO₂ excess), due to bicaronate 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^–1 body mass) of CaCO₃ (control) and NaHCO₃ (alkalosis). The resting arterialized venous blood pH (P<0.05) and bicarbonate concentration (HCO₃ ^–]_b;P<0.01) were significantly higher in acute metabolic alkalosis AMA; pH, 7.44 (SD 0.03); HCO₃ ^–]_b; 29.4 (SD 1.5) mmol·1^-1] than in the control pH, 7.39 (SD 0.03); HCO₃ ^–]_b, 25.5 (SD 1.0) mmol·1^–1]. 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 12.29 (SD 1.87) vs 9.57 (SD 2.14) mmol·1^–1,P < 0.05] and at 3 min after exercise 14.41 (SD 1.75) vs 12.26 (SD 1.40) mmol · l^–1,P < 0.05] were found in AMA compared with the control. The CO₂ excess increased significantly from the control 3177 (SD 506) ml] to AMA 3897 (SD 381) ml;P < 0.05]. 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 ( la^–]_b;r=0.926,P < 0.001) and with the decrease of HCO₃ ^–]_b from rest to 3 min after exercise ( HCO₃ ^–]_b;_r=0.872,P<0.001), indicating that CO₂ excess per body mass increased linearly with both la^– _b and HCO₃ ^–]_b. As a consequence, CO₂ excess per body mass per unit increase of la^–]_b (CO₂ excess·mass^–1· 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.