This is a copy and paste from my post on the CEM board, concerning the topic of lactic acid accumulation under metabolic or alakaline conditions.
"It seems to be that in metabolic acidosis the lactate accumulation is less than in the alkaline state, at least in this study:
J Appl Physiol 1983 Jul;55(1 Pt 1):225-9
Effects of pH on maximal power output and fatigue during short-term dynamic exercise.
McCartney N, Heigenhauser GJ, Jones NL.
Six healthy subjects performed four exercise studies in random order on separate days: a control study, metabolic acidosis induced by ammonium chloride, metabolic alkalosis induced by sodium bicarbonate, and respiratory acidosis induced by 5% CO2 inhalation. The subjects exerted maximal force on the pedals of a constant-velocity cycle ergometer at 100 rpm for 30 s; torque was measured and power calculated. Arterialized venous blood was sampled, and plasma lactate concentrations was measured immediately after and at 2-min intervals for 10 min following exercise. Although maximal peak power and total work, for the 30-s test, were lower in the two acidosis conditions, this effect was not statistically significant. Plasma lactate 30-s postexercise was lower in metabolic acidosis (2.8 +/- 1.6 mmol X 1(-1) (mean +/- SD) and respiratory acidosis (1.5 +/- 0.8 mmol X 1(-1) than in placebo conditions (5.9 +/- 3.3 mmol X 1(-1) and metabolic alkalosis 7.8 +/- 4.2 mmol X 1(-1). These differences were maintained but lessened during 10 min of recovery. In contrast to previous studies, which showed a marked reduction in endurance time during sustained heavy exercise, reductions in blood pH are associated with only small reductions in the total work performed in 30 s of maximal exercise. A delayed and smaller accumulation of lactate in plasma was observed following exercise during acidosis.
But in this study, the effects on performance were negligible between acidosis and alkaline state. Same result here but also with no differences in lactate accumulation between the different pH conditions:
Eur J Appl Physiol Occup Physiol 1986;55(5):524-9
The effect of sodium bicarbonate and sodium citrate ingestion on anaerobic power during intermittent exercise.
Parry-Billings M, MacLaren DP.
The effect of sodium bicarbonate and sodium citrate ingestion on cycling performance in three 30 s Wingate Anaerobic Tests separated by 6 min recovery periods has been studied using 6 male subjects. Subjects ingested either sodium bicarbonate (B), sodium bicarbonate plus sodium citrate (BC), sodium citrate © or sodium chloride (P) 2.5 h prior to exercise in a dose of 0.3 g kg-1 body weight. Pre-exercise blood pH was 7.44 +/- 0.06, 7.42 +/- 0.05, 7.41 +/- 0.05 and 7.38 +/- 0.04 in the C, BC, B and P conditions respectively. Mean and peak power output were significantly reduced by successive Wingate tests but not significantly affected by the treatments. Performance in the second and third tests was highest following C, BC and B ingestion. The total work done in the 3 tests was 103%, 102% and 101% of that achieved in the P condition after C, BC and B ingestion respectively. The increased alkali reserve recorded subsequent to bicarbonate and citrate treatment reduced mean post-exercise acidosis, although pH was significantly higher only in the C condition (p less than 0.05) compared to P after each exercise bout. No significant differences in plasma lactate concentration were recorded at any time. Citrate ingestion appears to be most effective in elevating blood pH and [HCO3-], and in enhancing performance in short-term intermittent exercise. This study demonstrates that alkali ingestion results in significant shifts in the acid-base balance of the blood and has a small, but non-significant, effect on anaerobic power and capacity as measured in a series of 3 Wingate Anaerobic Tests.
Same here:
Exp Physiol 1997 Nov;82(6):1041-56
The effect of sodium citrate ingestion on the metabolic response to intense exercise following diet manipulation in man.
Ball D, Maughan RJ.
Feeding a high-carbohydrate (CHO) diet and administration of alkalinizing agents have both been shown to improve performance in high-intensity exercise. The effect of these treatments in combination was investigated in the present study. Six healthy male subjects exercised to exhaustion on an electrically braked cycle ergometer at a power output equivalent to 100% of their maximum oxygen uptake (VO2,max) on four separate occasions. Each subject consumed either a diet with the same composition as his normal diet (termed the experimental normal (N) diet; 54 +/- 7% CHO, 13 +/- 2% protein, 33 +/- 7% fat) or a high-CHO diet (81 +/- 2% CHO, 13 +/- 2% protein, 6 +/- 1% fat) that had the same energy and protein content for the 3 days prior to the exercise tests. Subjects then ingested either a placebo (CaCO3) or trisodium citrate (0.3 g (kg body mass)-1) 3 h before exercise. Time to fatigue was not different between experimental conditions. Consumption of the high-CHO diet had no effect on blood acid-base status, but the ingestion of sodium citrate induced a mild metabolic alkalosis after both the N diet and the high-CHO diet. This alkalinizing effect was also evident after exercise, since blood pH, plasma bicarbonate and blood base excess were higher (P < 0.05) after the ingestion of sodium citrate than under the placebo conditions. The changes in blood lactate, pyruvate and glucose and plasma glycerol after exercise were similar for all experimental conditions. Blood lactate, glucose and pyruvate and plasma glycerol concentrations increased from resting values (P < 0.01) following exercise but this increase was similar under all experimental conditions. These data demonstrate that when the energy and protein content of the diets is the same, exercise capacity and the metabolic response to intense exercise are similar following consumption either of a high-CHO diet or a more normal diet. Acute ingestion of sodium citrate prior to exercise resulted in a reduction in post-exercise acidosis despite a blood lactate concentration that was similar to that observed after the ingestion of a placebo, but did not affect exercise performance under the conditions of this study.
This study confirms the first with a higher lactic acid generation in the alkaline state:
Am J Physiol 1988 Sep;255(3 Pt 2):F479-85
Effect of systemic pH on pHi and lactic acid generation in exhaustive forearm exercise.
Hood VL, Schubert C, Keller U, Muller S.
To investigate whether changes in systemic pH affect intracellular pH (pHi), energy-rich phosphates, and lactic acid generation in muscle, eight normal volunteers performed exhaustive forearm exercise with arterial blood flow occluded for 2 min on three occasions. Subjects ingested 4 mmol/kg NH4Cl (acidosis; A) or NaHCO3 (alkalosis; B) or nothing (control; C) 3 h before the exercise. Muscle pHi and phosphocreatine (PCr) content were measured with 31P-nuclear magnetic resonance (31P-NMR) spectroscopy during exercise and recovery. Lactate output during 0.5-7 min of recovery was calculated as deep venous-arterial concentration differences times forearm blood flow. Before exercise, blood pH and bicarbonate were lower in acidosis (7.303 +/- 0.009, 18.6 +/- 0.5 meq/l) than alkalosis (7.457 +/- 0.010, 32.2 +/- 0.7 meq/l) and intermediate in control (7.389 +/- 0.007, 25.3 +/- 0.6 meq/l). Lactic acid output during recovery was less with A (245 +/- 39 mumol/100 ml) than B (340 +/- 55 mumol/100 ml) (P less than 0.05) and intermediate in C (293 +/- 31 mumol/100 ml). PCr utilization and resynthesis were not affected by extracellular pH changes. pHi did not differ before exercise (A, 7.04 +/- 0.01; B, 7.09 +/- 0.01; C, 7.06 +/- 0.01) or at its end (A, 6.28 +/- 0.07; B, 6.28 +/- 0.11; C, 6.31 +/- 0.09). Hence systemic acidosis inhibited and alkalosis stimulated lactic acid output. These findings suggest that systemic pH regulates cellular acid production, protecting muscle pH, at the expense of energy availability.
So for me the results are equivocal. From personal experience and from my athletes I'd say you can definitely generate more lactic acid under buffering conditions. The burning sensation in the muscles is clearly lower after ingestion of citrates or bicarbonate."
But, I wonder as well, if the stimulation of MAPK erk1/2 will be lower on the 15's with buffering agents. But the whole body acidosis is counteracted with citrates, so this is definitely an advantage.
