High-intensity exercise results in the accumulation of metabolites such as ADP, Pi, and H+ in the skeletal muscle, which can have deleterious effects on skeletal muscle function and force generation, contributing to fatigue. In particular, a major cause of fatigue during anaerobic exercise is related to the high concentrations of H+, which can limit the ability of the contractile machinery to operate effectively (11,14). Under normal resting conditions, intramuscular pH is around 7.0, with arterial and venous blood pH being slightly higher at 7.4 and 7.3. However, during high-intensity exercise, muscle pH may fall to as low as 6.0 (31). At the same time, arterial and venous blood pH both decline to ∼7.0. These changes present a challenge to sport and exercise performance, and as such, any intervention capable of reducing the negative effect of intracellular H+ accumulation would be of use to athletes and athletic individuals.
Carnosine (β-alanyl-l-histidine) is a cytoplasmic dipeptide found in high concentrations in the skeletal muscle of both vertebrates and nonvertebrates, as well as in the central nervous system. Although several potential roles have been ascribed to carnosine in skeletal muscle, the one undisputable role is that of pH buffering because studies have demonstrated that carnosine has a side chain pK a of 6.83, making it a suitable buffer over the physiological pH range (3,16). Carnosine, in muscle and other tissues, is formed in situ by bonding histidine and β-alanine in a reaction catalyzed by carnosine synthetase, although it is the availability of β-alanine, rather than histidine, which seems to be the limitation to carnosine synthesis in skeletal muscle (17). Previous research has consistently shown increases in muscle carnosine concentration after supplementation with β-alanine for 4 wk or longer, which has also been shown to result in an increase in high-intensity exercise capacity and performance (for reviews, see Derave et al. (9) and Sale et al. (34)). Hill et al. (18) reported an increase in muscle carnosine concentrations after 4 and 10 wk of β-alanine supplementation, which resulted in a significant improvement in cycling capacity at 110% of maximum power output. Baguet et al. (1) reported that β-alanine supplementation attenuated the reduction in blood pH during high-intensity cycling exercise, which might explain some of the exercise performance and capacity increases previously reported. However, not all studies have shown a significant effect of β-alanine supplementation on exercise capacity and performance (for reviews, see Derave et al. (9) and Sale et al. (34)).
In addition to the first line of defense against H+ accumulation provided by several intracellular buffers, including carnosine, protons produced by the working muscle under anaerobic conditions are rapidly transported out of the muscle cell and are buffered by circulating buffers, such as bicarbonate. As such, supplementation with sodium bicarbonate has been recommended as a buffering agent against the development of metabolic acidosis (for review, see McNaughton et al. (30)). A primary role of extracellular bicarbonate during exercise is the regulation of H+ accumulation in the blood. An increase in the extracellular concentration of bicarbonate increases the pH gradient between the intracellular and extracellular compartments promoting the transmembrane transport of H+. Results of studies on the effect of sodium bicarbonate supplementation on cycling capacity are somewhat equivocal, with some showing no effect (22,33,35), despite reporting elevated pH before exercise. However, others have reported that preexercise alkalosis, induced through supplementation with sodium bicarbonate, significantly improves high-intensity exercise performance and capacity (for reviews, see Linderman and Gosselink (24) and McNaughton et al. (30)). Inconsistencies in the performance outcomes of sodium bicarbonate supplementation studies are most likely explained by the different dosing regimens, by the exercise tests used, and by the gastrointestinal discomfort suffered in some, but not all, participants. In particular, sodium bicarbonate supplementation (in doses between 200 and 300 mg·kg−1 body mass (BM)) has been shown to increase work output (28) and delay fatigue (8,21,37) in high-intensity cycling.
Although studies have shown significant improvements in exercise capacity and performance after supplementation with β-alanine and sodium bicarbonate separately, no study has yet examined the effects of cosupplementation on high-intensity exercise capacity. Therefore, the aim of this investigation was to examine the effect of β-alanine supplementation, with and without sodium bicarbonate supplementation, on high-intensity cycling capacity. We hypothesized that the intracellular pH-buffering action of carnosine and the extracellular buffering action of bicarbonate would be additive, resulting in an increased protection against the acidosis produced during high-intensity cycling, thus contributing to a further improvement in high-intensity cycling capacity above that shown after either sodium bicarbonate supplementation or β-alanine supplementation alone.
Twenty physically active males, who regularly participate in high-intensity exercise, volunteered for the study and were split into a β-alanine group and a placebo group (Table 1), matched for maximum cycling power output (W max). Participants were fully informed of any risks and discomforts associated with the study before completing a health screen and providing informed consent. The health screening procedure was repeated before each laboratory visit to ensure the health status of the participants had not changed. Participants had not taken any supplement in the 3 months before the study and had not taken β-alanine for at least 6 months before the study because of the long washout period for muscle carnosine (2). Participants were also requested to maintain similar levels of physical activity and dietary intake for the duration of the study, and compliance with this request was verbally confirmed with subjects before commencement of the study. None of the subjects were vegetarian and therefore would have encountered small amounts of β-alanine in their diet from the hydrolysis of carnosine and methyl derivatives of this in meat, typically 50-400 mg·d−1. The study was approved by the institution's ethical advisory committee.
Participants attended the laboratory on five separate occasions. The first two visits were for the determination of each participant's W max and habituation. The remaining visits were for the completion of the main trials. One main trial was completed before and two main trials after a 4-wk double-blind supplementation period of either β-alanine or placebo (Fig. 1). Participants were supplemented with either 6.4 g·d−1 β-alanine tablets (CarnoSyn™; National Alternatives International, San Marcos, CA) or an equivalent amount of placebo tablets (maltodextrin; NAI). The β-alanine dosing regimen consisted of the consumption of two 800-mg tablets four times per day at 3- to 4-h intervals or the same regimen for placebo tablets. Participants completed a supplementation log to verify compliance, with the degree of compliance being reported at 95% in the β-alanine group and 98% in the placebo group. Supplementation with β-alanine at this level has consistently been shown to increase muscle carnosine concentrations by around 60% (17,18), with others reporting no nonresponders to β-alanine supplementation (2,10,18). Overall increases have been shown to be between 40% and 80% depending on dose (between 3.2 and 6.4 g·d−1) and duration of administration (between 4 and 10 wk).
For the presupplementation trial, participants ingested maltodextrin, and after the 4-wk supplementation period, participants ingested either sodium bicarbonate or maltodextrin in a crossover design (Fig. 1). Two days of recovery elapsed between the postsupplementation trials during which time β-alanine supplementation was continued at 0.5 of the dose (i.e., one 800-mg tablet four times per day) to prevent any decline in carnosine levels during this period. As such, the study comprised four experimental conditions: placebo + maltodextrin (PMD), placebo + sodium bicarbonate (PSB), β-alanine + maltodextrin (BAMD), and β-alanine + sodium bicarbonate (BASB). β-alanine tablets were tested by the manufacturer before release for the study and conformed to the label claim for β-alanine content. All supplements were tested by HFL Sports Science (Cambridge, UK) before use to ensure no contamination with steroids or stimulants according to ISO 17025-accredited tests.
In total, participants consumed 0.3 g·kg−1 BM of sodium bicarbonate in gelatine capsules made up individually for each subject. This total dose was based on that used in numerous other studies (29,39). The total dose of the maltodextrin placebo was ingested in the same number of opaque gelatine capsules. The total dose of sodium bicarbonate was split, with participants ingesting 0.2 g·kg−1 BM of sodium bicarbonate (SIS, Blackburn, UK) or maltodextrin (SIS) with a standardized breakfast (three slices of toast with jam) taken at 9:00 a.m. The remaining sodium bicarbonate (0.1 g·kg−1 BM) was ingested at 11:00 a.m., with the CCT110% commencing at 1:00 p.m. Each dose of sodium bicarbonate or maltodextrin was ingested with 500 mL of plain water. Participants were supervised during the ingestion of sodium bicarbonate and maltodextrin supplements to ensure 100% compliance. A split-dose strategy for sodium bicarbonate ingestion was used to minimize the gastrointestinal discomfort often associated with supplementation at this level. Of the participants, 15 subjects reported no gastrointestinal discomfort after sodium bicarbonate ingestion. However, two participants did report mild gastrointestinal or other symptoms (one had a light headache and the other experienced bloating) and three subjects reported severe symptoms (including stomach cramps, headaches, and diarrhea) with the ingestion of sodium bicarbonate only.
Height (Seca, Birmingham, UK) and BM (Seca) were recorded on arrival at the laboratory. W max was determined by completing a graded cycling exercise test to exhaustion (Lode Excalibur, Groningen, Netherlands). Exercise intensity was increased by 6 W every 15 s (ramp rate of 24 W·min−1) from a starting power output of between 100 and 150 W depending on the perception of the participants' fitness. Participants maintained a constant pedal cadence throughout (mean ± SD = 87 ± 8 rpm, median = 90 rpm, range = 75-100 rpm), until volitional exhaustion. W max was defined as the maximum power output averaged during the final two stages.
The habituation and main trials comprised a 5-min warm-up at 100 W, which was followed by 2 min of self-selected stretching. Participants then completed the cycling capacity test at 110% W max (CCT110%), a test completed at a fixed work rate determined as 110% of the previously determined maximal power output (17). The position on the cycle ergometer (Lode Excalibur Sport) was determined before the habituation session and was recorded and maintained for all subsequent trials. The participants' feet were securely attached to the pedals using toe clips and straps. As the intensity of the test was high and participants were not highly trained cyclists, the first 30 s was incremented at power outputs corresponding to 80% W max for the first 15 s, 95% W max for the second 15 s, and 110% W max until volitional exhaustion. The test was designed to ensure that all subjects would reach volitional exhaustion between 120 and 240 s.
During the test, subjects were verbally encouraged to cycle at, or as close to, a comfortable pedal cadence, which was maintained for all subsequent trials. Volitional exhaustion was quantified as the point when subjects' power and cadence dropped 20 rpm−1 below the required cadence; this would usually happen within a period of 10-15 s, at this point subjects were instructed to stop pedaling. Time to exhaustion (TTE, s) and total work done (TWD, kJ) were recorded as the outcome measures for all tests.
Before the main trials, participants abstained from alcohol and caffeine and completed a food record for the 24-h period before the initial trial. They adopted the same diet and abstained from strenuous exercise for 24 h before each subsequent trial. Participants arrived at the laboratory, in a fasted state, 4 h before the commencement of the CCT110%. A resting finger-prick arterialized blood sample was taken, and the participants consumed the standardized breakfast and commenced maltodextrin or sodium bicarbonate supplementation, as described above.
To determine the reliability of the CCT110% test, we conducted a further test-retest study on 27 participants (age = 23 ± 4 yr, height = 1.79 ± 0.07 m, BM = 77.7 ± 9.1 kg, W max = 294.9 ± 50.1 W) who completed the CCT110% test on two occasions separated by 2 d. Both tests were completed in a fasted state (12 h), with no caffeine or alcohol having been consumed for the previous 24 h. There was no significant difference in TTE or TWD between tests 1 and 2 (P ≥ 0.05). The intraclass correlation for between tests 1 and 2 was r = 0.94 for TTE and r = 0.97 for TWD, with a coefficient of variation being 4.43% for TTE and 4.94% for TWD.
Arterialized finger-prick blood samples were taken immediately before, immediately after, and 5 min after the CCT110%. Finger-prick blood samples were collected into lithium-heparin-coated collection tubes (Radiometer, Crawley, UK). Blood samples were analyzed for lactate (Lactate Pro; Arkray, Kyoto, Japan), blood gases, hemoglobin (Hb), and pH (ABL 400; Radiometer). In addition, bicarbonate and base excess were calculated. Bicarbonate was calculated from PCO2 and pH values according to the Henderson-Hasselbalch equation, and base excess was calculated according to the following equation: (1 − 0.014[Hb]) × ([HCO3 −] − 24 + (1.43[Hb] + 7.7) (pH − 7.4)).
All data are presented as mean ± SD for 10 participants in each group, with the exception of the blood data, which are presented for 9 participants in each group because of blood analyzer malfunction. An independent-samples t-test was used to compare performance of the two groups before the supplementation period and subjects characteristics between groups. Performance data (TWD and TTE) were analyzed using a two-factor ANOVA (group × trial), and blood responses were analyzed using a three-factor ANOVA (group × trial × time; Statistica 8; Statsoft, Tulsa, OK). Tukey tests were used for post hoc analyses, and effect sizes were calculated using Cohen d (7). Statistical significance was accepted at the P ≤ 0.05 level.
There was no significant difference in TTE (P = 0.54; placebo: 137.8 ± 23.2 and β-alanine: 143.1 ± 13.4 s, d = 0.29) and TWD (P = 0.69; placebo: 45.5 ± 9.8 and β-alanine: 44.0 ± 7.1 kJ, d = 0.18) between the placebo and β-alanine groups before the supplementation period. There was no significant improvement compared with before supplementation in TTE and TWD after PMD (TTE: post hoc, P = 0.99; TWD: post hoc, P = 0.99; d = 0.1) or PSB (TTE: post hoc, P = 0.48; TWD: post hoc, P = 0.46; d = 0.4). After BAMD, TTE (Fig. 2) (+17.2 ± 14.0 s; group × trial interaction, P = 0.03; post hoc, P ≤ 0.01; d = 1.1) and TWD (+5.8 ± 5.0 kJ; group × trial interaction, P = 0.03; post hoc, P ≤ 0.01; d = 0.9) were greater than before supplementation. BASB supplementation resulted in a significantly increased TTE (Fig. 2) (+23.3 ± 18.2 s; post hoc, P ≤ 0.001; d = 1.2) and TWD (+8.1 ± 6.2 kJ; post hoc, P ≤ 0.01; d = 1.0) compared with the presupplementation trial. With coingestion of β-alanine and sodium bicarbonate (BASB), 6 of 10 showed a further increase in TTE and TWD (with the seventh unchanged) compared with BAMD. However, in neither case did the results reach significance (TTE: post hoc, P = 0.74; TWD: post hoc, P = 0.70).
Baseline blood pH, bicarbonate, and base excess were similar between all trials (Table 2). There were significant increases in blood pH, bicarbonate, and base excess between baseline and before exercise in both trials where sodium bicarbonate was consumed (PSB and BASB) (trial × time interaction, P ≤ 0.001; post hoc, P ≤ 0.001). Increases were shown in all subjects with sodium bicarbonate ingestion. In the two conditions where sodium bicarbonate was not consumed (PMD and BAMD), there were no significant alterations to blood pH, bicarbonate, or base excess from baseline to before exercise (Table 2).
In all trials, pH, bicarbonate, and base excess were significantly reduced from baseline immediately after exercise and after 5 min of recovery (P ≤ 0.001). In trials where sodium bicarbonate was ingested (PSB and BASB), blood pH, bicarbonate, and base excess were significantly higher than in the trials where maltodextrin was ingested (PMD and BAMD) (trial effects, P ≤ 0.001).
Blood lactate was not significantly different between trials at baseline or before exercise (Table 2). Blood lactate was significantly increased from baseline immediately after exercise and after 5 min of recovery in all trials (P ≤ 0.001) and was significantly higher after sodium bicarbonate ingestion (interaction trial × time, P ≤ 0.001; Table 2). There was no difference in lactate response between the β-alanine and placebo groups (P = 0.4).
This is the first study to our knowledge to examine the effect of coingestion of β-alanine and sodium bicarbonate on high-intensity exercise capacity. The main findings from this study were that there was a significant increase in cycling capacity after β-alanine supplementation but, in the 10 subjects studied, cosupplementation with β-alanine and sodium bicarbonate did not confer any further significant benefit.
Four weeks of supplementation with β-alanine alone significantly increased TWD during high-intensity cycling exercise by 14.6%. This compares favorably with the data reported by Hill et al. (18), which showed a 13.0% increase in TWD after 4 wk of supplementation and a 16.2% increase after 10 wk of supplementation with β-alanine, using the same CCT110% test. The CCT110% test was originally designed (18) to provide a high-intensity cycling test that lasts between 120 and 240 s. Presupplementation cycling times in the present study were 137.8 ± 23.2 s in the placebo group and 143.1 ± 13.4 s in the β-alanine group, which also compares favorably with the 156.5 ± 4.3 s reported by Hill et al. (18) and lies within the expected time frame for the test.
The two possible explanations for the improvement in high-intensity cycling capacity with β-alanine supplementation are increased calcium sensitivity in muscle fibers that could augment force production and TWD (4,12,23) and an increase in intracellular buffering capacity. We believe that the latter is the most likely explanation of the exercise capacity improvements seen in the present investigation, with a seventh increased skeletal muscle carnosine content resulting in an attenuation of the reduction in intracellular pH during high-intensity exercise. In this regard, the present study concurs with the findings of Hill et al. (18) and Baguet et al. (1).
Previous studies have indicated that intracellular H+ accumulation with high-intensity exercise can affect metabolism, contributing to fatigue (36). In particular, the accumulation of H+ in the skeletal muscle might disrupt the resynthesis of phosphorylcreatine (15), inhibit glycolysis (38), or interfere with the contractile machinery directly (11,14). In addition, there is some evidence to suggest that accumulation of H+ in the blood results in an increased perception of effort during high-intensity intermittent exercise (32), which might also contribute to the early cessation of exercise. In support of an effect of H+ accumulation on the development of fatigue, numerous studies have shown an association between an increase in muscle buffering capacity and an improvement in high-intensity exercise performance and capacity (6,13,41), although not all agree (40). However, as reported by Hill et al. (18), we cannot exclude the possibility that the increase in high-intensity cycling capacity observed with β-alanine supplementation was caused by some of the other purported physiological effects of elevated muscle carnosine concentrations (for a review, see Sale et al. (34)).
Contrary to the effect of β-alanine on high-intensity cycling capacity, sodium bicarbonate ingestion alone did not significantly increase TTE or TWD during the CCT110%. From our data, power analysis was completed using G*Power based on effect size and showed that 90 subjects would be required to see a difference in cycling capacity with sodium bicarbonate supplementation. Blood analyses confirmed that sodium bicarbonate ingestion was successful in significantly increasing pH, bicarbonate, and base excess in line with previous studies of sodium bicarbonate ingestion (22,33,35). Previous studies have also reported no significant effect of sodium bicarbonate supplementation on TWD or delayed fatigue during cycling of around 2 min (20) or longer (25). However, these studies both supplemented participants with relatively low doses of sodium bicarbonate (between 100 and 200 mg·kg−1 BM) compared to the total dose given in the present study. Those studies using a higher dose of sodium bicarbonate (300 mg·kg−1 BM) have tended to report significant delays to the onset of fatigue in cycling tasks lasting between 3 and 7 min (21,37). These results are in contrast to the results of the present study, although it should be noted that the duration of the exercise in the present study (around 2-2.5 min) was slightly lower than in these previous investigations, and the intensity of exercise was slightly higher (110% of maximal intensity vs 95% of maximal intensity), which might explain some of the differences in the findings. Lactate concentrations were significantly elevated during and after exercise when ingesting sodium bicarbonate compared with the ingestion of maltodextrin. This finding is consistent with an increased lactate efflux from the skeletal muscle as a result of increased pH and bicarbonate in the extracellular fluid (19,26,27).
This study was based on the premise that coingestion of β-alanine with sodium bicarbonate would result in an increased skeletal muscle carnosine concentration (not determined directly here, as mentioned above) and increased circulating bicarbonate concentration. As such, the intracellular pH-buffering action of carnosine and the extracellular buffering action of bicarbonate were hypothesized to be additive, resulting in an increased protection against the acidosis produced during high-intensity cycling, as suggested by Hill et al. (18). We hypothesized that this would result in a further improvement in high-intensity cycling capacity above that shown after either sodium bicarbonate supplementation or β-alanine supplementation alone. The results of this investigation provide support for an increased exercise capacity after coingestion of β-alanine and sodium bicarbonate above that of bicarbonate alone but not compared with β-alanine alone (TTE: P = 0.74; TWD: P = 0.70). Although no significant differences were shown in high-intensity cycling capacity between β-alanine alone and β-alanine in combination with sodium bicarbonate, it is possible that, in performance terms, a further increase of 6 s in TTE might be important. Calculation of the magnitude-based inferences (5) shows that there was a 69% and 71% probability that the magnitude of the difference in TTE and TWD between β-alanine and β-alanine plus sodium bicarbonate was meaningful. This suggests a potentially meaningful increase in high-intensity cycling capacity when combining β-alanine and sodium bicarbonate supplementation over the ingestion of β-alanine alone.
There was a degree of individual variability in the exercise capacities of participants after β-alanine and β-alanine plus sodium bicarbonate ingestion, which might explain the lack of a significant finding. Indeed, three subjects improved more on β-alanine alone than on the combination of β-alanine plus sodium bicarbonate. Each of these participants responded to sodium bicarbonate ingestion with an increase in both blood pH and bicarbonate concentrations. Furthermore, although some subjects experienced mild (n = 2) and severe (n = 3) gastrointestinal symptoms, these did not occur in those subjects who showed the greatest improvement with just β-alanine.
In conclusion, the ingestion of 6.4 g·d−1 β-alanine for 4 wk resulted in an increase in high-intensity cycling capacity, confirming the previous findings of Hill et al. (18). However, coingestion of β-alanine and sodium bicarbonate did not confer any further significant benefit to exercise capacity despite a further 6-s (∼4%) increase in TTE, although magnitude-based inferences suggested a ∼70% probability of a meaningful positive difference.
No funding was received for this work.
The authors thank National Alternatives International, San Marcos, CA, for providing the β-alanine (CarnoSyn™) and maltodextrin supplements.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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