Effect of endurance training on excessive CO2 expiration due to lactate production in exercise

We attempted to determine the change in total excess volume of CO2 Output (CO2 excess) due to bicarbonate buffering of lactic acid produced in exercise due to endurance training for approximately 2 months and to assess the relationship between the changes of CO2 excess and distance-running performance. Six male endurance runners, aged 19–22 years, were subjects. Maximal oxygen uptake (VO2max), oxygen uptake (VO2) at anaerobic threshold (AT), CO2 excess and blood lactate concentration were measured during incremental exercise on a cycle ergometer and 12-min exhausting running performance (12-min ERP) was also measured on the track before and after endurance training. The absolute magnitudes in the improvement due to training for C02 excess per unit of body mass per unit of blood lactate accumulation (Ala−) in exercise (CO2 excess·mass−1·Δla−), 12-min ERP, VO2 at AT (AT-VO2) and VO2max on average were 0.8 ml·kg−1·l−1·mmol−1, 97.8m, 4.4 ml·kg−1· min−1 and 7.3 ml·kg−1·min−1, respectively. The percentage change in CO2 excess·mass−1·Δla− (15.7%) was almost same as those of VO2max (13.7%) and AT-VO2 (13.2%). It was found to be a high correlation between the absolute amount of change in CO2 excess·mass−1·Δla− and the absolute amount of change in AT-VO2 (r=0.94, P<0.01). Furthermore, the absolute amount of change in C02 excess·mass−1·Δla−, as well as that in AT-VO2 (r=0.92, P<0.01), was significantly related to the absolute amount of change in 12-min ERP (r=0.81, P<0.05). It was concluded that a large CO2excess·mass−1·Δla−1 of endurance runners could be an important factor for success in performance related to comparatively intense endurance exercise such as 3000–4000 m races

Effect of endurance training on excessive CO2 expiration due to lactate production in exercise

We attempted to determine the change in total excess volume of CO2 Output (CO2 excess) due to bicarbonate buffering of lactic acid produced in exercise due to endurance training for approximately 2 months and to assess the relationship between the changes of CO2 excess and distance-running performance. Six male endurance runners, aged 19–22 years, were subjects. Maximal oxygen uptake (VO2max), oxygen uptake (VO2) at anaerobic threshold (AT), CO2 excess and blood lactate concentration were measured during incremental exercise on a cycle ergometer and 12-min exhausting running performance (12-min ERP) was also measured on the track before and after endurance training. The absolute magnitudes in the improvement due to training for C02 excess per unit of body mass per unit of blood lactate accumulation (Ala−) in exercise (CO2 excess·mass−1·Δla−), 12-min ERP, VO2 at AT (AT-VO2) and VO2max on average were 0.8 ml·kg−1·l−1·mmol−1, 97.8m, 4.4 ml·kg−1· min−1 and 7.3 ml·kg−1·min−1, respectively. The percentage change in CO2 excess·mass−1·Δla− (15.7%) was almost same as those of VO2max (13.7%) and AT-VO2 (13.2%). It was found to be a high correlation between the absolute amount of change in CO2 excess·mass−1·Δla− and the absolute amount of change in AT-VO2 (r=0.94, P<0.01). Furthermore, the absolute amount of change in C02 excess·mass−1·Δla−, as well as that in AT-VO2 (r=0.92, P<0.01), was significantly related to the absolute amount of change in 12-min ERP (r=0.81, P<0.05). It was concluded that a large CO2excess·mass−1·Δla−1 of endurance runners could be an important factor for success in performance related to comparatively intense endurance exercise such as 3000–4000 m races

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

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 (Δ [la−]b;r=0.926,P < 0.001) and with the decrease of [HCO3−]b from rest to 3 min after exercise (Δ [HCO3−]b;r=0.872,P<0.001), indicating that CO2 excess per body mass increased linearly with both Δ [la−b and Δ [HCO3−]b. As a consequence, CO2 excess per body mass per unit increase of [la−]b (CO2 excess·mass−1·Δ [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

Validity in Noninvasive Prediction of Blood Lactate Accumulation from Excess CO2 Output During Exercise

This study was designed to theoretically reexamine the validity in noninvasive prediction of blood lactate (La) accumulation from excess CO2 output (CO2 excess) generated during exercise based on the data obtained in a previous study of Hirakoba et al. (12). Several assumptions were made; 1) total body water (TBW) corresponds to 60% of body mass, 2) La and hydrogen ion (H+) are uniformly distributed in a whole TBW, 3) CO2 excess derives from bicarbonate buffering of H+ dissociated from lactic acid, and is equicalent to La accumulated in the body. From these assumptions, prediction of blood La accumulation (ΔLa,predicted) and distribution volume of La (VLa) were calculated from CO2 excess, TBW and actually measured blood La accumulation (ΔLa,measured) during a three stages of constant work rate exercise test. The ΔLa,predicted was found to be significantly lower than ΔLa,measured was 21.4±5.3 l, which means that an average percent of VLa to TBW (%VLa) was 61.9±11.6%. Namely, it was found that the VLa obtained in this study was not equal to the TBW and %VLa was different among subjects. Therefore, the data indicate that noninvasive prediction error of blood La accumulation from CO2 excess during exercise would be accounted in part for by individuals\u27 VLa during exercise test used in this study

Blood Lactate Changes during Isocapnic Buffering in Sprinters and Long Distance Runners

This study was carried out to compare blood lactate changes in isocapnic buffering phase in an incremental exercise test between sprinters and long distance runners, and to seek the possibility for predicting aerobic or anaerobic potential from blood lactate changes in isocapnic buffering phase. Gas exchange variables and blood lactate concentration ([lactate]) in six sprinters (SPR) and nine long distance runners (LDR) were measured during an incremental exercise test (30 W.min-1) up to subject's voluntary exhaustion on a cycle ergometer. Using a difference between [lactate] at lactate threshold (LT) and [lactate] at the onset of respiratory compensation phase (RCP) and the peak value of [lactate] obtained during a recovery period from the end of the exercise test, the relative increase in [lactate] during the isocapnic buffering phase ([lactate]ICBP) was assessed. The [lactate] at LT (mean +/- SD) was similar in both groups (1.36 +/- 0.27 for SPR vs. 1.24 +/- 0.24 mmol.l-1 for LDR), while the [lactate] at RCP and the peak value of [lactate] were found to be significantly higher in SPR than in LDR (3.61 +/- 0.33 vs. 2.36 +/- 0.45 mmol.l-1 for RCP, P < 0.001, 10.18 +/- 1.53 vs. 8.10 +/- 1.61 mmol.l-1 for peak, P < 0.05). The [lactate]ICBP showed a significantly higher value in SPR (22.5 +/- 5.9%, P < 0.05) compared to that in LDR (14.2 +/- 5.0%) as a result of a twofold greater increase of [lactate] from LT to RCP (2.25 +/- 0.49 for SPR vs. 1.12 +/- 0.39 mmol.l-1 for LDR). In addition, the [lactate]ICBP inversely correlated with oxygen uptake at LT (VO2LT, r = -0.582, P < 0.05) and maximal oxygen uptake (VO2max, r = -0.644, P < 0.01). The results indicate that the [lactate]ICBP is likely to give an index for the integrated metabolic, respiratory and buffering responses at the initial stage of metabolic acidosis derived from lactate accumulation