For many years, the production and metabolism of lactate have been scrutinized by exercise physiologists. In the early days of study, lactate was considered to be a waste product formed when glucose-6-phosphate was catabolized by glycolysis under hypoxic conditions. Lactate production was also thought to release hydrogen ions, which promoted skeletal muscle fatigue by contributing to acidosis. Others suggested that high levels of lactate in the muscle cell could promote reductions in work capacity (7). Thus, no viable reason could be seen for using orally consumed lactate as an ergogenic aid.
Viewpoints on lactate started to change in the 1980s, when researchers began providing evidence that it was not a harmful waste product but an energy intermediate that could be further metabolized to provide substrate for the tricarboxylic acid cycle or gluconeogenesis (11). In either case, lactate could enhance energy substrate status during exercise by sparing muscle glycogen or by fortifying blood glucose stores. More recent studies of lactate have called into question its role in promoting muscle fatigue either directly (5,9) or through contributing to metabolic acidosis (14). Close examination of glycolysis reveals that complete metabolism of glucose to lactate results in no net release of protons and, thus, does not contribute to acidosis. In fact, during the production of lactate from pyruvate, protons are consumed and acidosis is inhibited (14). Furthermore, lactate oxidation and lactate consumption via gluconeogenesis consume hydrogen ions and are alkalinizing processes.
Lactate’s role as an energy substrate and mediator of pH balance has sparked interest into the metabolic and exercise performance effects of orally consumed lactate. This article aimed to review published studies on the metabolic and ergogenic effects of lactate consumption. The review will first address the studies that have focused on lactate consumption as an energy supplement and then will present works that have investigated its use as a buffering agent.
Oral Lactate as an Energy Substrate
The initial investigations of lactate consumption as an energy supplement evolved from previous works that studied the metabolic fates of intravenously infused lactate in exercising subjects (8,11). These studies of lactate metabolism demonstrated that substantial amounts of infused lactate were oxidized in exercising skeletal muscle and led some investigators to ponder the effects of oral lactate consumption on endurance exercise performance. Early attempts of lactate ingestion were unsuccessful because oral consumption of large boluses was found to result in extreme gastric distress. However, Fahey et al. (6) eventually identified tolerable oral doses of lactate and compared the effects of consuming beverages containing 7% lactate, 7% maltodextrin, or aspartame on various metabolic responses during 3 h of cycle ergometry at 50% of V˙O2max. The beverages were provided in 250-mL doses 5 min before and every 20 min during exercise. Treatments were applied in a randomized, double-blind, crossover design. Blood was drawn before and during exercise and analyzed for glucose, lactate, pH, and bicarbonate. In each of the three treatments, blood glucose remained at basal levels through 100 min of exercise. During the final 60 min of exercise, blood glucose dropped significantly from preexercise levels, when subjects consumed the placebo, but was maintained at basal levels in the lactate and maltodextrin trials. No difference in blood glucose was observed between the lactate and maltodextrin trials. Blood pH and bicarbonate increased significantly over basal levels during the final 60 min of the lactate trial, while no differences in these variables were observed in the placebo and maltodextrin trials.
While these results demonstrated positive metabolic responses to lactate ingestion, the investigation lacked key evidence to support the use of oral lactate consumption as an ergogenic aid. The exercise intensity was low and not reflective of intensities typically found in competitive endurance events. More importantly, a performance trial was not included in the assessment of the supplements.
Swensen et al. (15) compared the effects of a combined 7% carbohydrate-lactate beverage to a 7% beverage containing only carbohydrate on various metabolic variables and time to exhaustion in trained cyclists during cycle ergometry at 70% of V˙O2max. The original intent of this study was to compare a 7% carbohydrate beverage to a 7% lactate beverage identical to that used by Fahey et al. (6). However, during pilot trials, the subjects of Swensen et al. (15) developed severe gastric distress after consuming the 7% lactate beverage. Ultimately, these investigators used a 7% carbohydrate-lactate beverage containing 6.25 g of glucose polymer and 0.75 g of lactate per 100 mL of water. This combined beverage was similar to a commercially available carbohydrate-lactate beverage (CytoMax®) but with a higher concentration of lactate. Consumption of each beverage commenced at the beginning of exercise and was repeated every 20 min during exercise. At each feeding, the subjects consumed enough of each drink to provide 0.3 g of carbohydrate per kilogram of body mass. The treatments were applied in a randomized, double-blind, crossover fashion, and both solutions were flavored with an artificial sweetener to help blind the subjects to the treatments. Blood glucose levels were maintained at resting levels during the first 3 h of exercise in both trials, and no significant differences were observed between treatments. Carbohydrate oxidation rates also were similar for both treatments. Finally, no significant difference in time to exhaustion between the two treatments was observed (214.7 ± 17 min for the carbohydrate trial vs 214.4 ± 22 min for the carbohydrate-lactate trial).
Bryner et al. (3) measured the effects of beverages containing only water, 2% lactate, 8% carbohydrate, and a combination of 8% carbohydrate and 2% lactate on exercise performance and physiological responses in trained cyclists during cycle ergometry. These investigators also used a randomly assigned, double-blind, crossover design. The exercise challenge combined a moderate-intensity exercise test to exhaustion followed by a 30-s Wingate test in an attempt to mimic a competitive situation in which athletes would have to indulge in a long, exhaustive competition and sprint against competitors at the end of the race. Work rates for the endurance portion of the exercise challenge were designed to elicit approximately 86% of maximum heart rate and were maintained at a cadence of 80 rpm. When the subjects indicated that they could no longer maintain 80 rpm they immediately performed a 30-s Wingate test against a resistance of 0.09 kg·kg−1 body mass. The subjects consumed the beverages at the start of exercise and every 20 min thereafter until exhaustion. Identical volumes of each beverage were given at each consumption period for all treatments, and these volumes were equal to the amount that would provide 0.3 g of carbohydrate per kilogram of body mass from the 8% carbohydrate beverage. The authors measured time to exhaustion during the submaximal ride and perceived exertion, RER, blood bicarbonate, blood pH, and blood glucose levels before and at 30-min intervals during exercise. Blood bicarbonate, pH, and glucose levels also were measured following the Wingate test. During the 30-s Wingate test, peak power, and fatigue rate were measured and were expressed in absolute terms and in relation to the same values obtained during an initial 30-s Wingate test that was performed several days before the advent of the experimental trials.
Bryner et al. (3) found no difference in time to exhaustion between treatments. During the 30-s Wingate test, no significant differences were observed between treatments with respect to absolute peak power or peak power relative to the initial peak power output obtained in the days before the experimental trials. Inexplicably, the absolute fatigue rate was lower in the placebo trial compared with the carbohydrate and carbohydrate-plus-lactate trials. Perceived exertion did not differ between the treatments at any point during the exercise test to exhaustion. RER was significantly lower in the lactate trial when compared with placebo and the carbohydrate-lactate trial during the second hour of the exercise test to exhaustion. No significant drops in blood glucose levels from baseline were observed in the carbohydrate or carbohydrate-lactate trials at any time point during or following exercise. Blood glucose levels were significantly lower than preexercise levels following the Wingate test in both the lactate-only and placebo trials and at 30 and 60 min of the exercise to exhaustion test during the lactate-only trial. These blood glucose levels were not, however, significantly different from those observed at the same time points in the carbohydrate or carbohydrate-lactate trials.
In measurements of pH, Bryner et al. (3) found significant elevations compared with baseline after 30 min of exercise in the placebo and lactate-only trials. This elevation was extended to the 60-min measurement in the lactate-only trial. No other differences due to time or treatment were observed. Blood bicarbonate was significantly lower compared with baseline after 30 min of exercise in the placebo treatment and after 60 min of exercise in the lactate treatment. Following the Wingate test, blood bicarbonate levels were significantly lower compared with baseline in all but the carbohydrate trial.
The results of Bryner et al. (3) can be difficult to interpret because of the variability in many of the measures and the statistical approached used to analyze the data. While means and standard deviations were not presented for all of the dependent variables, those that were generally had high standard deviations resulting in coefficients of variation that ranged from approximately 0.30 to greater than 0.50. Unfortunately, no tests of statistical power were performed. The authors also used a series of paired t-tests to compare baseline measurements to those recorded during exercise and at fatigue. This practice is known to cause alpha inflation and increase the likelihood of a type 1 error. Thus, the statistical approach and low statistical power could have contributed to the seemingly random observations of statistical significance.
Azevedo et al. (1) also used a two-stage exercise test to investigate the metabolic and performance effects of orally consumed lactate. Trained cyclists performed 90 min of cycle ergometry at a work rate that elicited 62% of V˙O2max followed by an exercise test to exhaustion at a work rate that elicited 86% of V˙O2max. Subjects consumed 6% w/v beverages containing either carbohydrate (glucose + fructose) or a combination of carbohydrate and lactate. Drinks were provided in isocaloric 250-mL doses 2 min before the advent of exercise and every 15 min during the 3-h exercise period. Both drinks were enriched with 13C-labeled glucose, fructose, or lactate (carbohydrate + lactate beverage only). Blood and expired air were collected during the initial exercise period and analyzed for the carbon isotope to assess substrate utilization. The subjects performed three trials of the carbohydrate-lactate treatment and two trials of the carbohydrate-only treatment to assess substrate utilization of all of the components of each drink. The treatments were applied in a randomized crossover fashion, but only the subjects were blinded to the composition of the drinks.
The metabolic results revealed a high rate of lactate oxidation during the carbohydrate-lactate trials. Subjects increased their time to exhaustion in the 86% V˙O2max portion of the exercise trial by 25% from 5.2 ± 1.0 min in the carbohydrate trial to 6.5 ± 0.8 min in the carbohydrate-lactate trial (P < 0.05). Interclass correlation coefficients were high for both treatments (r = 0.89, P < 0.03 for carbohydrate only; r = 0.957, P < 0.04 for carbohydrate-lactate), indicating a high degree of reliability for this type of performance test.
The mechanism for the increase in performance observed during the carbohydrate-lactate trial is not clear entirely. The subjects received isocaloric amounts of each beverage, so it is doubtful that energy balance contributed to the difference in performance. A possible explanation for the increase in performance is an increase in the blood bicarbonate and pH levels following the ingestion of lactate. Significant evidence suggests that acidosis contributes to development of muscle fatigue and high-intensity exercise performance has been shown to be enhanced when the blood is alkalinized by consumption of sodium bicarbonate (10). Lactate consumption also has been shown to increase blood pH and bicarbonate levels in previous investigations (2,6,15). Although Azevedo et al. (1) did not measure bicarbonate or pH levels, prolonged exercise at intensities similar to those used in their performance test has been shown to elicit acidosis (12). Thus, if acidosis was a major contributing factor to fatigue in their protocol, the consumption of lactate could have provided an ergogenic effect by acting as a buffering agent.
Oral Lactate as a Buffering Agent
Numerous investigations have monitored the metabolic fates of infused or ingested lactate (1,8,11). During rest, approximately half of exogenous lactate has is oxidized while the remainder is used as substrate for numerous metabolic processes, most notably gluconeogenesis (11). Disposal of lactate by oxidation (C3H5O3 + 3O2 + H+ → 3CO2 + 3H2O) or gluconeogenesis (2C3H5O3 + 2H+ → C6H12O6) consumes protons and thus has the potential to affect blood bicarbonate and pH levels.
Van Montfoort et al. (16) were the first to investigate the use of oral lactate consumption as a buffering agent. In their investigation, 15 trained distance runners completed a single, high-intensity run to exhaustion following consumption of 400 mg·kg−1 body mass of sodium lactate, 525 mg·kg−1 body mass of sodium citrate, 300 mg·kg−1 body mass of sodium bicarbonate, or 209 mg·kg−1 body mass of sodium chloride given in a randomized, double-blind, crossover fashion. Ninety minutes following the ingestion of the supplements, the subjects began a 15-min warm-up and then proceeded to the exercise test to exhaustion. Compared to placebo (NaCl), lactate consumption resulted in a 4% improvement in performance by increasing time to exhaustion from 77 to 80 s.
While these results are promising, there are several concerns about this investigation. High-intensity exercise tests to exhaustion typically have intrasubject variation in performance of approximately 5% to 10% (2,4), which is greater than the performance improvement that was observed by Van Montfoort et al. (16). The limitations of treadmill running as an exercise test also must be recognized. Work performed on a treadmill is very difficult to measure and is affected by the body mass of the subject. No mention was made about monitoring the body mass of the subjects before each exercise trial and, thus, some fluctuation in performance could have been due to changes in body mass. Yet another possible shortcoming in this investigation is the time span between ingestion of the lactate and the performance of the exercise trial. The subjects were given 60 min to consume their supplements followed by a 90-min rest period before starting their warm-up. The performance trial began approximately 15 min after the commencement of the warm-up, or about 105 min following the consumption of the last capsule of sodium lactate and 165 min after consumption began. Subsequent data have suggested that the optimum time for performance enhancement following lactate ingestion may be closer to 80 min after ingestion (13).
In a pilot work for the study of lactate ingestion, we measured blood bicarbonate responses for 120 min following the ingestion of 20, 120, and 220 mg·kg−1 body mass of lactate. In contrast to Van Montfoort et al. (16), our subjects consumed their supplements in a bolus within a 5-min period. Blood samples were taken and analyzed for blood bicarbonate levels before, and every 20 min for 120 min following the ingestion of the supplements. These trials revealed that blood bicarbonate levels peaked at 80 min following the ingestion of the lactate supplements followed by a steady decline through the 120-min measurement point. This response pattern was seen in each of the three doses. Furthermore, while the 120- and 220-mg·kg−1 body mass doses resulted in substantially higher blood bicarbonate levels compared with the 20-mg·kg−1 dose, no differences were noted between the 120- and 220-mg·kg−1 doses with respect to the magnitude of increase in blood bicarbonate levels. Finally, while Van Montfoort et al. (16) reported that postingestion blood pH and bicarbonate were significantly higher after lactate ingestion when compared with NaCl consumption, they did not compare the postingestion to preingestion levels of these variables in any of the treatments. Thus, the effects of lactate ingestion on blood pH and bicarbonate were not entirely clear.
In a subsequent investigation by Morris et al. (13), 11 trained cyclists consumed 120 mg·kg−1 body mass of lactate in a single bolus 80 min before performing high-intensity cycle ergometry to exhaustion. The exercise protocol consisted of four 1-min work intervals at 100% of V˙O2max work rate each followed by 1-min recovery periods performed at 25% of V˙O2max work rate. Immediately following the final rest period, the subjects performed a final work bout to exhaustion at 100% of V˙O2max work rate. Each subject repeated the protocol under three conditions: following consumption of lactate, an equal volume of placebo, and no treatment. The lactate and placebo were provided in a double-blinded manner and a randomized crossover approach was used for the application of the treatments. Time to exhaustion in the lactate trial (168 ± 31 s) was significantly greater than in the no-treatment (143 ± 29 s) and placebo (137 ± 41 s) trials. This represented an increase in performance of 18% compared with the no-treatment trial and 17% compared with the placebo trial, which is much greater than the variability typically seen in repeated applications of high-intensity exercise tests to exhaustion. Furthermore, blood bicarbonate levels were significantly elevated following consumption of lactate when compared with preconsumption levels and when compared with preconsumption and postconsumption levels of the placebo and no-treatment protocols. No changes due to any of the treatments were observed in blood pH.
The study of exogenous lactate as an ergogenic has focused on its use as an energy substrate and as an alkalinizing agent. Investigations have shown that orally consumed lactate is oxidized readily by working muscle and can maintain blood glucose levels during extended exercise bouts. However, lactate is not well tolerated by the gastrointestinal track and can be consumed only in relatively dilute solutions (∼2% w/v solution vs 6% to 9% w/v solution in carbohydrate beverages). Thus, the total caloric load that can be provided by oral lactate consumption is limited and relatively low. Two studies have investigated the effects of lactate, consumed alone or with carbohydrate, on time to exhaustion during low- to moderate-intensity exercise and neither demonstrated ergogenic effects. However, lactate consumption may be effective as a buffering agent. Numerous investigations have demonstrated that oral consumption of lactate can increase blood pH and/or bicarbonate levels. Three studies of the effects of lactate consumption on performance of high-intensity exercise revealed increases in exercise time to exhaustions ranging from 4% to 25%. Although each of these three studies supported the use of lactate as a buffering agent, continued research in this area is encouraged. Dozens of similar studies using sodium bicarbonate as a buffer have provided conflicting results and revealed the importance of proper dosing and timing of the ingestion of buffering agents in relation to the exercise task. The intensity, duration, and type of exercise challenge, i.e., time to exhaustion versus time trials, single exercise bouts versus repeated efforts, may influence the efficacy of buffering agents as ergogenics and should be explored in relation to lactate consumption.
The author declares no conflict of interest and does not have any financial disclosures.
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