The use of nutritional ergogenic supplements are commonplace within sport as both recreational and professional athletes aim to improve performance and increase training adaptations (19). Previous research into the benefits of induced metabolic alkalosis on both prolonged continuous and intermittent high-intensity exercise has proved to be equivocal (22). The majority of research has found no significant improvement in endurance performance following induced alkalosis in cycling (1,32,36). The exception to these, however, was McNaughton et al. (21), who reported a 14% increase in work capacity during 60 minutes of high-intensity cycling following the ingestion of sodium bicarbonate (NaHCO3). If the results from such fixed time duration studies could be replicated in a more practical setting such as time trial cycling involving set distance, then NaHCO3 could prove to be an inexpensive ergogenic aid. A negative side effect of NaHCO3, however, is the possibility of gastrointestinal (GI) distress (6,34), which ultimately may offset any possible positive benefits to be gained.
Decreases in intramuscular pH have previously been reported to inhibit the contractile processes by either (a) restricting myofilament function through reducing Ca2+ sensitivity (7,11) or (b) effecting the excitation-contraction process relating to the uptake and release of Ca2+ by the sarcoplasmic reticulum (16,33). By ingesting NaHCO3 before exercise, extracellular bicarbonate (HCO3 −) reserves are supplemented, resulting in an increased plasma pH and an induced state of metabolic alkalosis (30). The extracellular to intracellular pH gradient therefore increases as HCO3 − is impermeable to cellular membranes (22), resulting in a greater efflux of H+ and lactate from active muscles (26). This occurs via either simple diffusion or by the lactate/H+ co-transporters (17) and has been demonstrated by the higher lactate concentrations postexercise following NaHCO3 ingestion (1,28). Increases in plasma HCO3 − have also been reported following the ingestion of lactate with no reported GI distress (24,39), showing potential for it to be used as an alternative exogenous buffer to NaHCO3.
Within exercise metabolism, the role of lactate and, in particular, its production has been a source of much dispute (4,11,15). Debate remains whether the presence of lactate acts as a limiting factor during exercise by inducing acidosis or actually attenuates the onset of fatigue by consuming the excess H+ responsible for acidosis (4). Many of the studies associating lactate with the development of fatigue tend to be based on correlational data (4); therefore a cause and effect relationship cannot be ascertained. Furthermore, lactate has the potential to serve as a source of glucose generated from within the body as a substrate for gluconeogenesis (3). Based on the lactate shuttle theory (2), exogenous lactate supplementation therefore has the potential to increase plasma glucose supplied via gluconeogenesis, thus sparing glycogen stores (20). However, to date, research (3,27,38) has failed to support this theory.
The purpose of this study therefore was to determine whether either NaHCO3 or lactate supplementation had any ergogenic potential to improve 40-km time trial performance. Additionally, it was designed to establish whether any improvement in performance was associated with changes in acid-base status and buffering capacity. It was hypothesized that the use of either NaHCO3 or a lactate supplement would improve the performance of a 40-km cycling time trial. Furthermore, it was hypothesized that lactate supplementation would increase both plasma lactate levels and buffering capacity while causing less GI distress than is associated with NaHCO3 consumption.
Experimental Approach to the Problem
Using a randomized, double placebo-controlled design, subjects were required to complete a total of 5 trials: 1 familiarization trial and 4 experimental trials. Subjects were instructed to arrive for testing in a rested state having refrained from strenuous exercise and alcohol in the 24 hours before testing and had no history of either NaHCO3 or lactate supplementation. Subjects were asked to ingest a minimum of 500 ml of water before arriving at the laboratory to ensure they arrived in a well-hydrated state, avoiding caffeine in the 12 hours before each trial. They were also asked to consume the same standardized breakfast a minimum of 1 hour before arriving for each trial. Subjects performed each of the 5 trials at the same time of day to control for circadian variation in performance (9). Additionally, each trial was separated by a period of 6–9 days to ensure an adequate recovery period was attained while limiting the opportunity for any improvement being the result of training.
The 4 experimental conditions were as follows: (a) 300 mg·kg−1 body mass NaHCO3 (BICARB), (b) 45 mg∣kg–1 body mass sodium chloride (PL-BICARB) as the placebo for the NaHCO3 trial, (c) 1115 mg lactate from a combination of calcium lactate pentahydrate and magnesium lactate dihydrate, equivalent to a mean of 14.1 mg∣kg–1 body mass per participant based on mean body weight (Sport Specifics, Inc., Chagrin Falls, OH, USA) (LACTATE), and (d) plain flour as the placebo for the lactate trial (PL-LACTATE). All supplements were ingested within gelatine capsules with 500 ml of low calorie cordial over a 10-minute period, 60 minutes before exercise. Because of the disparity between the NaHCO3 and lactate trials in terms of capsules required, a double placebo design was chosen to improve validity. The use of 300 mg·kg−1 body mass NaHCO3 has been established as the optimal dose for enhanced buffering capacity (22) and has previously been used in a number of studies into NaHCO3 supplementation (5,25,33). Furthermore, peak HCO3 − levels are typically achieved 60 minutes after ingestion (34). The lactate supplement dosage used was as per the manufacturer's instructions. It was felt that this dosage of the supplement should be chosen as consumers who purchase this supplement are unlikely to exceed the recommended dosage.
In terms of performance, the dependent variables of interest were overall performance time, split performance time, heart rate, and rate of perceived exertion (RPE). For changes in acid-base status, the dependent variables were pH, base excess (BE), HCO3 −, lactate, and H+. Changes in overall performance time represent an accurate comparison between trials while ultimately being the key variable of interest for competitive cyclists. The use of split times allowed for changes during individual stages to also be identified. The use of pH, BE, HCO3 −, and H+ in research looking at changes in buffering capacity following supplementation is well established (5,34,35). Furthermore, as one of the supplements contained exogenous lactate, it was important to establish whether any changes in plasma lactate occurred following its ingestion.
Seven recreationally active nonsmoking male subjects (mean ± SD: age, 22.3 ± 3.3 years; height, 182.5 ± 6.5 cm; body mass, 79.2 ± 6.3 kg) with no previous history of supplementing their diets with ergogenic agents volunteered to participate in this study. The subjects consisted of 4 cyclists, 2 footballers, and 1 long distance runner, all of whom were in a period of regular training at the time of testing. They were all completing a minimum of 4 hours (6.3 ± 3.3 hours) training per week and all were free from any known cardiac or metabolic diseases. All subjects provided written informed consent, and the study was approved by the Departmental Human Ethics Committee and following the principles outlined in the Declaration of Helsinki.
On arrival at the laboratory, the subject had a capillary blood sample taken to establish basal acid-base measurements (pH, BE, HCO3 −, lactate, and H+) before ingesting the relevant supplement. During the 60-minute postingestion period, further capillary blood samples were taken at 10, 20, 30, 45, and 60 minutes postingestion to evaluate any induced changes in the acid-base variables. All blood samples were collected using 100 μL balanced heparin blood capillary tubes (Radiometer, West Sussex, United Kingdom) and immediately analyzed (ABL800; Radiometer, Copenhagen, Denmark).
During the ingestion period, subjects were asked to rate any GI discomfort experienced every 15 minutes using a visual analog scale until the exercise commenced. The potential symptoms listed were nausea, flatulence, stomach cramping, stomach bloating, stomach ache, belching, vomiting, bowel urgency, and diarrhea. The visual analogue scale consisted of 9 separate 100-mm scales, anchored at each end with either “no symptom” or “severe symptom,” and subjects indicated with a vertical mark the severity of each symptom during the ingestion period (5,34). None of the subjects reported any instances of GI disturbance during the 60-minute pre-exercise period as a result of ingesting BICARB, LACTATE, or either placebo.
Following the 60-minute postingestion capillary blood sample, the subject completed a 10-minute warm-up at an intensity of 75 W before beginning the 40-km time trial. The time trial was conducted using a Wattbike cycle ergometer (Wattbike Ltd, Nottingham, United Kingdom) with heart rate (Polar FS1 HRM, Polar Electro OY, Kempele, Finland) and RPE recorded at 5-minute intervals. Rate of perceived exertion was monitored using a modified version of perceived exertion scale by Foster et al. (12). Subjects were permitted to drink water ad libitum. During each trial, subjects were blinded to all performance data except the distance countdown. The purpose for this was to minimize any learning effect to be gained from previous trials. Additional capillary blood samples were collected at 20 and 40 km and at 15 minutes postexercise.
Statistical analyses were completed using IBM PASW statistics 18 (SPSS Inc., Chicago, IL, USA). Central tendency and dispersion of all data are displayed as mean ± SD. Performance time data were compared using a 1-way analysis of variance (ANOVA) with repeated measures, whereas changes in acid-base status, heart rate, and RPE were investigated using 2-way ANOVA with repeated measures. Sidak-adjusted p values were used for subsequent pairwise comparisons to establish the significant paired differences when significant F ratios were found by the respective ANOVA. Statistical significance was accepted as p ≤ 0.05, with effect size reported according to partial eta squared.
The mean times for 10, 20, 30, and 40 km along with the individual split times for each 10-km interval are displayed in Table 1. Although overall performance time for LACTATE was between 1 and 3% faster than the other 3 conditions, the difference was not significant (p > 0.05,
). Furthermore, the individual split times for each 10-km stage of the time trial were not significantly different between the 4 conditions (p > 0.05). Individual responses to the supplements were varied, with 3 subjects performing their fastest trial in the LACTATE condition, while 2 performed fastest in PL-LACTATE, and 1 subject completing the time trial fastest in each of the BICARB and PL-BICARB conditions (Figure 1).
Average heart rate during the LACTATE condition (169 ± 9 b·min−1) was significantly higher than in the other 3 conditions (BICARB: 160 ± 16 b·min−1; PL-BICARB: 158 ± 13 b·min−1; and PL-LACTATE: 160 ± 14 b·min−1 respectively; p < 0.05,
) throughout the duration of the time trials. No significant difference was seen, however, between the other 3 conditions. Both heart rate and RPE (both p < 0.05,
, respectively) were seen to increase progressively with each 10-km stage of the time trial (Table 2). No significant main effect for condition or interaction effect between condition and stage (both p > 0.05,
, respectively) was seen for RPE between the 4 conditions.
Changes in pH, BE, HCO3 −, lactate, and H+ for the 4 conditions across the study are displayed in Table 3. There was no significant difference between pre-ingestion levels for any of the blood variables between the 4 conditions. During the BICARB condition, blood pH was significantly higher at 45 and 60 minutes postingestion than seen at pre-ingestion (p < 0.05,
), whereas H+ levels were significantly lower at the same time points (p < 0.05,
). By 60 minutes post-BICARB ingestion, BE had increased by in excess of 5 mEq·L−1 (p < 0.05,
) and plasma HCO3 − by approximately 4.5 mmol·L−1 compared with the pre-ingestion levels (p < 0.05,
) and significantly increased compared with LACTATE, PL-BICARB, and PL-LACTATE (all p < 0.05) at the same time point. No significant differences were seen within the other 3 experimental conditions during the pre-ingestion to 60 minutes postingestion period. Furthermore, no significant difference was seen for lactate concentration between pre-ingestion and 60 minutes postingestion (p > 0.05,
) for any of the 4 conditions.
After 20 and 40 km, pH, BE, and HCO3 − remained elevated and H+ was lower for the BICARB condition compared with the other 3 conditions (Table 3). All the differences between the BICARB condition and the other 3 conditions were significant except for pH and H+ at 40 km compared with PL-LACTATE (both p > 0.05) and BE at 40 km compared with the LACTATE condition (p > 0.05). Although at the end of the time trial, plasma lactate was between 2 and 3 mmol·L−1 higher for the BICARB condition, the difference was only significant compared with PL-LACTATE (p < 0.05,
). No significant difference was seen for lactate between the LACTATE, PL-LACTATE, and PL-BICARB.
Although mean performance time following the ingestion of the lactate supplement was over 30 seconds faster than the next nearest condition (Table 1), the performance effect was not significant. This mean difference was influenced by subject 2 whose individual time during the LACTATE trial was around 3 minutes faster than the other 3 conditions (Figure 1). Additionally, ingestion of NaHCO3 did not provide any significant ergogenic effect on 40-km time trial performance. Using the same lactate supplement, Peveler and Palmer (27) also found no significant effect on performance of 20-km time trial cycling, heart rate, or mean power with the lactate condition actually marginally slower than placebo by ∼17.4 seconds on average. They did, however, fail to show the individual performance times for each condition, making it difficult to establish if there was an individual specific response from any of their subjects. Additionally, other forms of lactate supplementation focusing on lactate as a gluconeogenic precursor for endurance exercise have also been previously used unsuccessfully. Both Bryner et al. (3) and Swensen et al. (38) combined lactate and carbohydrate to examine its effect on time to exhaustion (TTE). Bryner et al. (3) found no significant effect on either TTE or peak power using a protocol that involved cycling at 10 beats below target heart rate and ended with a Wingate power test during the last 30 seconds of the trial. Swensen et al. (38) also found no effect on TTE when cycling at 70% V[Combining Dot Above]O2max until exhaustion.
Although the current study also supports the majority of research in finding that NaHCO3 did not improve prolonged exercise performance (1,28,36), one exception remains (21). McNaughton et al. (21) reported an increase in both overall work (in kilojoules) and average power following the ingestion of NaHCO3 over a 60-minute period of maximal cycling. In this study, the 40-km time trial was chosen as it represented a similar duration to that seen in McNaughton et al. (21); however, the use of a set distance as opposed to set time duration provided a greater reflection of competitive cycling.
The increase in buffering capacity achieved by ingesting NaHCO3 before exercise has previously been well documented (6,22,35), although the benefits are typically associated with events lasting between 30 seconds and 3 minutes (22,30,34). Lactate levels during the current study were higher following NaHCO3 ingestion than that of the other 3 conditions at both 20 and 40 km although only to a significant level at 40 km over PL-LACTATE (Table 3). It has been suggested that by increasing extracellular levels of HCO3 −, the efflux of lactate and H+ from within the muscle is facilitated (13,21) with similar results having previously been found by Price et al. (28). In theory, this could have improved performance by maintaining pH closer to the homeostatic levels (21). McNaughton et al. (21) attributed their significant increase in work during their 60-minute cycling study to the maintenance of pH nearer to resting levels, allowing greater contractile performance. Interestingly though, McNaughton et al. (21) also reported plasma lactate levels lower than those of their control (no supplement) and placebo (sodium chloride) trials. Although conflicting with the expected higher lactate levels seen in the current study, a difference in protocol may account for the disparity between studies.
Despite the improved acid-base status before and during exercise following NaHCO3 ingestion in the current study, the lack of improvement in performance would seem to indicate an alternative factor separate from acidosis was the predominant cause of fatigue. Although using an alternative buffer in the form of sodium citrate, Schabort et al. (32) supported this as during the trial with the highest pH, lactate concentrations were not the highest, showing other factors contributed to the fatigue. Although allowing the subjects to consume the same standardized breakfast before each trial was intended to attenuate the effect of glycogen depletion on fatigue, its effects cannot be ruled out. Furthermore, the accumulation of inorganic phosphate rather than H+ has also been associated with restricting the contractile processes (40) however, as these were not measured in the current study, its role cannot be determined.
Lactate supplementation has also been suggested as an alternative acid-base buffer to NaHCO3 (24); however, the results from this study fail to support this. Previous research has reported increases in plasma HCO3 − following lactate ingestion (10,24,39); however, a lack of reported pre-ingestion HCO3 − levels mean that the level of increase is difficult to quantify (10,39). Morris et al. (24) reported increases in plasma HCO3 − levels of approximately 3 mmol·L−1 between pre-ingestion levels and 80 minutes postingestion. In the present study, 4 of the 7 subjects experienced an increase in HCO3 − following ingestion of the lactate supplement although the largest increase seen was just 1 mmol·L−1 between pre-ingestion and 60 minutes postingestion compared with an average increase of 4.6 mmol·L−1 for the NaHCO3 condition. However, the concentration of lactate supplement in this study was considerably less than the 120 mg·kg−1 body mass of lactate used by Morris et al. (24) or the 320 mg·kg−1 body mass of lactate used by Van Montfoort et al. (39). The reduced dosage in the current study was used as it followed the manufacturers' guidelines and is similar to that previously used by Peveler and Palmer (27).
In the current study, the expected increase in plasma lactate failed to be observed following the ingestion of the lactate supplement. The lactate shuttle theory by which exogenous lactate supplementation is thought to increase gluconeogenesis and improve performance, however, is highly disputed (27). An increase in plasma lactate is thought to promote increased plasma lactate oxidation while inhibiting intramuscular lactate production (14). Miller et al. (23) regulated lactate plasma levels to 4 mmol·L−1 during exercise of moderate intensity via intravenous infusion. As a result of this, the contribution of glycogenolysis in supplying plasma glucose decreased as increased lactate oxidation compensated potentially sparing glycogen stores. However, in the current study, an increase in plasma lactate levels was not observed following ingestion. Neither Morris et al. (24) nor Van Montfoort et al. (39) reported significant increases in plasma lactate despite using considerably larger quantities of lactate. Although a change in the rate of lactate oxidation potentially may account for a rise in plasma lactate not being shown, other explanations may exist. It is possible that the oral consumption of lactate was either too small to elicit a change or it failed to increase lactate availability because of either degradation by stomach acid or through a lack of absorption, unlike the direct intravenous method used by Miller et al. (23).
Given athletes are likely to follow manufacturers' recommendations when using supplements because of safety and overall cost issues (27), both the small change in acid-base status and the absence of an increase in plasma lactate following lactate supplementation suggest that the dosage used does not represent a viable alternative to NaHCO3 for increasing buffering capacity. The use of a chronic dosing of lactate over a number of days may be an option in the future as it has been previously shown to increase acid-base status when using NaHCO3 (8,20). However, given the negligible increases in acid-base status in this current study, each individual dose would possibly need to be increased from the current study for any effect to be seen. Future investigations into alternative dosing strategies are therefore warranted.
An increase in RPE over time was observed but this was not different between conditions (Table 2). However, average heart rate was higher during the LACTATE condition compared with the other 3 conditions. Although performance differences were not significant overall in this group, the increased heart rate during the LACTATE condition may therefore have contributed for the faster performance time, although heart rate measurements were only recorded every 5 minutes, meaning heart rate for each 10-km stage is based on a total of 2 or 3 measurements, which may have affected the results gained. Although the increased heart rate in the LACTATE condition occurred without altering perceived exertion, the subjective nature of RPE measures makes it difficult to conclude if the difference was related to the supplement. In a similar study, Peveler and Palmer (27) reported reduced RPE following the ingestion of a lactate supplement, although this may have been accounted for by the slower performance time compared with the placebo condition. The effect of induced alkalosis upon the RPE following NaHCO3 and lactate ingestion has been equivocal to date with both positive (18,31,37) and negative (13) effects reported. This variety in results, however, can probably be accounted for by the variety of different exercise protocols, ingestion strategies, and subject training statuses used throughout the previous literature (10,13,18,31,37).
The pursuit of legal ergogenic aids continues at both a recreational and a professional level (21). Although the majority of NaHCO3 supplementation research has focused on either single or multiple bouts of short duration maximal intensity exercise (22,30,34), the research conducted into prolonged continuous and intermittent exercise has proved equivocal (1,21,28). The current study has demonstrated that there is little ergogenic benefit to be gained by inducing metabolic alkalosis via NaHCO3 supplementation before prolonged cycling. Although not significant, the lactate condition was fastest for 3 of the 7 subjects and was on average approximately 30 seconds faster than the nearest condition. Although this figure was influenced by an individual performance of around 3 minutes faster during the LACTATE condition than the other 3 conditions, it raises the possibility that the ergogenic effect is individual specific. Considering the tight winning margins typically associated with time trial competition, any legal supplement that could provide such performance gains obviously would prove beneficial.
Using the dosages seen in the current study, lactate supplementation did not offer a viable alternative to NaHCO3 in terms of improving blood buffering capacity. However, given NaHCO3 ingestion is associated with GI distress (5,6,34), which may reduce any ergogenic benefits that may be achieved (34), research into alternative buffering agents is warranted. In this study, no GI distress for either supplement was reported, suggesting that lactate supplementation is not associated with GI distress at this concentration and that the response to NaHCO3 is individual specific, as recently alluded to by Price and Simons (29). Future work on lactate supplementation should therefore focus of dosing strategies to maximize the potential for an ergogenic effect to be seen on performance. Given any ergogenic effect of lactate supplementation seems to be individual specific, experimentation of the supplement before prolonged use is essential to assess the cost-benefit analysis to the individual.
The authors thank all the volunteers who participated in this study. The authors also like thank SportLegs; Sports Specifics, Inc., Chagrin Falls, OH, USA, for providing the product. The authors have no undisclosed professional relationships with any companies or manufacturers that would benefit them from the results of this study and therefore no conflicts of interest. There was no grant support for this study. The results of this investigation do not constitute endorsement of the product by the authors or the National Strength and Conditioning Association.
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Keywords:Copyright © 2014 by the National Strength & Conditioning Association.
buffering; alkalosis; ergogenic aid; NaHCO3; acid-base