EFFECT OF ACUTE SODIUM-BICARBONATE INGESTION ON EXCESS CO2 OUTPUT DURING INCREMENTAL EXERCISE

Citation
K. Hirakoba et al., EFFECT OF ACUTE SODIUM-BICARBONATE INGESTION ON EXCESS CO2 OUTPUT DURING INCREMENTAL EXERCISE, European journal of applied physiology and occupational physiology, 66(6), 1993, pp. 536-541
Citations number
30
Categorie Soggetti
Physiology
ISSN journal
03015548
Volume
66
Issue
6
Year of publication
1993
Pages
536 - 541
Database
ISI
SICI code
0301-5548(1993)66:6<536:EOASIO>2.0.ZU;2-H
Abstract
The effect of bicarbonate ingestion on total excess volume Of CO2 outp ut (CO2 excess), due to bicaronate buffering of lactic acid in exercis e, was studied in eight healthy male volunteers during incremental exe rcise on a cycle ergometer performed after ingestion (0.3 g . kg-1 bod y mass) of CaCO3 (control) and NaHCO3 (alkalosis). The resting arteria lized 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 . l-1] than in t he control [pH, 7.39 (SD 0.03); [HCO3-]b, 25.5 (SD 1.0) mmol . l-1]. T he blood lactate concentrations ([la-]b) during exercise below the ana erobic threshold (AT) were not affected by AMA, while significantly hi gher [la-]b at exhaustion [12.29 (SD 1.87) vs 9.57 (SD 2.14) mmol . l- 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 contr ol. 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 o f [la-]b from rest to 3 min after exercise (DELTA[la-]b; r = 0.926, P < 0.001) and with the decrease of [HCO3-]b from rest to 3 min after ex ercise (DELTA [HCO3-]b; r = 0.872, P < 0.001), indicating that CO2 exc ess per body mass increased linearly with both DELTA[la-]b and DELTA[H CO3-]b. As a consequence, CO2 excess per body mass per unit increase o f [la-]b (CO2 excess . mass-1 . DELTA[la-]b) was similar for the two c onditions. The present results would suggest that the relationship bet ween 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.