Short-duration high-intensity bouts of exercise require a greater reliance on adenosine triphosphate generation from glycolysis and the phosphagen system. The adenosine triphosphate that is derived from these pathways is used to fuel muscle contraction and liberates proton release, which is thought to be one of the causes of muscular acidosis during intense exercise (30). Both intra- and extracellular buffer systems act to reduce the buildup of H+ and therefore aid in the regulation of intracellular pH. Carnosine has been identified as an important physiochemical buffer (1), and extracellular HCO3− is also thought to play an important role in the maintenance of intramuscular pH (7).
Carnosine (β-alanyl-L-histidine) is a naturally occurring dipeptide found in high concentrations in skeletal muscle and nervous tissue. Carnosine has been hypothesized to play a vital role in delaying the onset of muscular fatigue by acting as an intracellular buffer (14), neutralizing free radicals (8), regulating enzymes (20), and increasing calcium sensitivity of the contractile apparatus (4).
Previous literature has shown that β-alanine supplementation is capable of significantly elevating skeletal muscle carnosine content in both trained and untrained participants after 4 to 10 wk of β-alanine supplementation (4.0–6.4 g·d−1) (2,3,11,15). The induced elevation in skeletal muscle carnosine content has been associated with improvements in short-term intense bouts of exercise performance in untrained participants (∼2.5 min) (15). Several studies have suggested that carnosine may also play an important role in delaying the onset of muscular fatigue in trained athletes such as sprinters (11) and rowers (2); however, these studies were unable to demonstrate a significant performance improvement after β-alanine supplementation. A recent study found a significant performance improvement in trained cyclists after 8 wk of β-alanine supplementation (2–4 g·d−1) in average (5.0%) and peak (11.4%) power output in a maximal 30-s cycling sprint after a 110-min exhaustive endurance ride at varied intensities (35). From the available literature investigating β-alanine supplementation performance improvements have been demonstrated in intense bouts of short-duration exercise performance (1–7 min), which seems to be the ideal duration of exercise in which carnosine exhibits its role as an intramuscular pH buffer.
In addition to the intracellular buffering capacity, the extracellular buffering system, primarily the bicarbonate ion (HCO3−), also plays an important role in the maintenance of intracellular pH, although the sarcolemma has been shown to be relatively impermeable to HCO3− (23). Several studies (21,34) have been able to demonstrate that increased extracellular pH and augmented HCO3− content enhance the H+/La− efflux from the exercising muscle. This is largely due to the increase in activity of the H+/La− cotransporter, which becomes more active when the intracellular/extracellular H+ gradient is increased during intense exercise (31). This is thought to allow more work to be completed from the exercising muscles during bouts of intense anaerobic exercise. In light of this, numerous studies have examined the exogenous administration of sodium bicarbonate (NaHCO3) in an attempt to enhance performance in highly trained athletes (7).
Many studies have shown significant improvements in exercise performance after supplementation with either β-alanine or NaHCO3 alone. To our knowledge, only one study has examined the combined effect of β-alanine and NaHCO3 supplementation on exercise performance (33). Although Sale et al. (33) reported a significant improvement in cycling time to fatigue after supplementation with β-alanine, there was no further improvement in exercise performance with the addition of acute NaHCO3 supplementation in recreationally active males (33).
Chronic β-alanine supplementation has been shown to elevate skeletal muscle carnosine content and improve short-term exercise performance, predominantly in the untrained population (2,3,11,15). It remains to be determined whether β-alanine supplementation can improve exercise performance in trained athletes using sport-specific performance measures such as a time trial, which have a lower coefficient of variation than time-to-fatigue tests (9). Furthermore, it remains to be determined whether β-alanine and NaHCO3 supplementation can provide an additional ergogenic benefit in highly trained athletes. Therefore, the first aim of the present study was to investigate the effects of 28 d of β-alanine supplementation on a maximal cycling performance trial lasting 4 min. The second aim was to determine whether there was an additive effect of β-alanine and acute NaHCO3 supplementation on high-intensity cycling performance in highly trained cyclists.
METHODS
Participants.
Fourteen highly trained male cyclists (mean ± SD: age = 25.4 ± 7.2 yr, mass = 71.1 ± 7.1 kg, V˙O2max = 66.6 ± 5.7 mL·kg−1·min−1) were recruited for the current study. All participants were informed verbally and in writing as to the requirements of the study and any possible adverse effects that could be experienced, and all gave their written informed consent. Participants had not taken any supplement in the 3 months before the study. The study was conducted in the University of Tasmania Exercise Science Laboratory and was approved by the Institutional Human Research Ethics Committee Network.
Experimental design.
Participants attended the laboratory on five separate occasions (Fig. 1). The two initial visits to the laboratory consisted of a graded exercise test to determine the V˙O2max and familiarization of the maximal 4-min cycling performance trial. The remaining three visits to the laboratory were for the completion of the performance trials. The first performance trial was a baseline trial that preceded a 28-d double-blind β-alanine or placebo supplementation regimen. Participants were supplemented with either 65 mg·kg−1 body mass of β-alanine capsules each day (100% pure β-alanine; Vitaco Health, Auckland, New Zealand) or an equivalent amount of placebo capsules (dextrose monohydrate). This particular dosage of β-alanine is similar to that used by Hill et al. (15), whose participants consumed, on average, between 50 and 80 mg·kg−1 body mass of β-alanine and exhibited significant increases in skeletal muscle carnosine of 59%. Participants were asked to consume the capsules in four even daily doses in conjunction with meals. Participants were asked to report any adverse effects experienced and to bring in the supplement packaging on completion of the 28-d supplementation period to monitor compliance.
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FIGURE 1: The study design required participants to attend the laboratory on five separate occasions. The two initial visits consisted of a graded exercise test to determine the V˙O2max and to ensure familiarization of the maximal 4-min cycling performance trial. The remaining three visits to the laboratory were for the completion of the performance trials.
The two postsupplementation performance trials required participants to ingest either NaHCO3 or a placebo in a randomized crossover design (Fig. 1). The amount of NaHCO3 ingested by each participant before the performance trial was 0.3 g·kg−1 body mass. This particular dosage has previously been associated with exercise performance improvements (7). The same number of capsules was consumed in the acute placebo condition. Each dose of capsules was ingested with 10 mL·kg−1 body mass of plain water. Participants were supervised during the ingestion of NaHCO3 to ensure compliance with the supplementation protocol. Two days elapsed between the postsupplementation performance trials for the purpose of a NaHCO3 washout period (28). The study was therefore composed of four experimental conditions (n = 7 in each group): placebo + placebo (PP), β-alanine + placebo (BAP), placebo + NaHCO3 (PSB), and β-alanine + NaHCO3 (BASB).
Preliminary testing.
Each participant first underwent an incremental test to exhaustion on an electronically braked cycle ergometer (Lode Excalibur Sport; Quinton, WA) modified with clip-in pedals and low-profile racing handlebars to determine V˙O2max, maximum HR, and maximum aerobic power output. The saddle and handlebar position of the cycle ergometer were adjusted to accurately match the dimensions of each of the participants’ road bicycle measurements, and each participant warmed up at a self-selected pace for 5 min. The test consisted of an initial workload of 100 W, followed by a ramped protocol in which power output was increased by 15 W per 30 s until volitional fatigue (22). HR was continuously measured (S610; Polar Electro Oy, Kempele, Finland), and respiratory variables were measured and recorded every 30 s (ParvoMedics TrueOne 2400, Salt Lake City, UT).
On a separate day, each participant underwent a familiarization of the performance trial to minimize any learning effect for subsequent trials (17). The performance trial consisted of a single maximal bout of cycling lasting 4 min. Participants performed each trial on an air-braked front access cycle ergometer (Repco Cycle Company, Canberra, Australia). The ergometer was connected to a custom-made Power Evaluation System (PES Version 2.0; School of Human Life Sciences, University of Tasmania, Launceston, Australia), which measured the peak and average power (W) and total work done (kJ). Before the study, the cycle ergometer was dynamically calibrated using a protocol that has been described elsewhere (25). Participants were given a standardized warm-up consisting of three 3-min workloads (2, 2.5, and 3 W·kg−1 body mass) on a friction-braked cycle ergometer (Ergomedic 828E; Monark Crescent, Varberg, Sweden). HR was continuously measured, and respiratory variables were measured and recorded every 30 s.
Performance trials.
Before reporting to the laboratory for the performance trials, each participant was asked to abstain from caffeine and alcohol and avoid strenuous exercise for the 24 h preceding each performance trial. Each participant was also required to record a 24-h diet diary leading up to the baseline performance trial, which was then replicated in the 24 h preceding each subsequent performance trial. When the participants reported to the laboratory on the day of each performance trial, they were weighed and then had a finger prick blood sample collected into a preheparinized capillary tube. Blood samples were analyzed for pH and HCO3− using the i-STAT® blood gas analyzer (i-STAT®, Princeton, NJ). During the performance trial, participants were verbally encouraged and were instructed to attempt each performance trial with a maximal effort.
Before each postsupplementation performance trial, each participant ingested an acute dose of either NaHCO3 or placebo 90 min before exercise. The capsules were consumed in six equal doses during a 1-h period. Each participant then rested for a further 30 min before a second blood sample was collected. The standardized warm-up was then completed followed by the performance trial. Upon cessation of the exercise bout, a final blood sample was taken for analysis of pH and HCO3−.
Training diary.
To standardize training intensity and volume across groups, participants were instructed to complete two high-intensity interval training (HIT) sessions per week during the 28-d supplementation period and were asked to record the HIT sessions in a training diary. Each HIT session consisted of eight 2.5-min bouts aimed to achieve an HR corresponding to 90% V˙O2max at the completion of the interval, interspersed with 3-min recovery intervals aimed to achieve an HR corresponding to 40% V˙O2max, which was determined from the graded exercise test.
Participants were instructed to continue their normal dietary and training regimen throughout the duration of the study and were also asked to keep an accurate record of training sessions (including their HIT sessions) and intensities during the 28-d supplementation period. Furthermore, participants recorded all types of training (e.g., cycling, running, resistance training) and the duration of each training session in the training diaries for all sessions completed. Participants also gave an intensity rating after each training session using the CR10 Borg Scale (6) for RPE. To quantify the training that was completed during the supplementation period, the current study used the session RPE method (12).
Statistical analysis.
Sample size determination for the study was determined using a statistical spreadsheet previously described (16). The spreadsheet estimates sample size requirements for magnitude-based inferences when the typical error and the smallest worthwhile change for the primary performance measure (4-min cycling test) are entered. Data used for these values were obtained through previous unpublished laboratory results measuring the variation in 4-min cycling test performance in similar athletes. These values were 4.0 W (0.98%) and 7.3 W (1.8%) for the typical error and smallest worthwhile change, respectively. Sample size calculation using these values indicated the need for five participants in each group. We also allowed for an attrition rate of ∼30% based on experience from our previous studies when dealing with highly trained athletes (ensuring a minimum of five participants in each group).
All data are presented as mean ± SD for the seven participants in each group. An independent t-test was used to determine any difference between the β-alanine and placebo groups at baseline. A two-way repeated-measures ANOVA was used to evaluate the performance data (average power and total work done) with group (placebo, β-alanine, NaHCO3) as the between-participants factor and trial (pre- vs postsupplementation trials) as the within-participants factor. A three-way ANOVA (group × trial × time) was used to analyze the blood variables (GraphPad statistical software, GraphPad version 5.0; San Diego, CA). When appropriate, Bonferroni post hoc comparisons were used to examine differences between groups. Statistical significance was accepted at the P < 0.05 level.
In addition to the use of statistical significance, magnitude-based inferences were used to determine the practical significance of PP, BAP, PSB, and BASB on 4-min time trial performance. Using a Microsoft Excel spreadsheet designed for sports science research (18), mean effects and the 90% confidence limits were estimated to establish the percent likelihood of each experimental condition having a positive/trivial/negative effect on performance. The smallest worthwhile improvement in total work done was considered to be 0.2 of the between-participant SD established from baseline performance, which was 2.31 kJ (2.37%) (19).
The training intensity and volume of the two groups during the 28-d supplementation/training period were compared using an independent-samples t-test to identify any differences between the two groups throughout this period. To determine whether there was any order effect during the postsupplementation performance trials, the performance achieved in the first postsupplementation performance trial was compared with the performance achieved during the second postsupplementation performance trial using a paired-sample t-test.
RESULTS
Performance trial.
Before the 28-d supplementation period, there was no difference in 4-min cycling average power (P = 0.308, placebo = 420.6 ± 49.1 W and β-alanine = 392.4 ± 42.3 W) and total work done (P = 0.308, placebo = 101 ± 11.8 kJ and β-alanine = 94.17 ± 11.8 kJ) between the placebo and β-alanine groups.
There was a significant effect of trial (P < 0.001) with no significant group × time interaction (P = 0.076). Compared with the baseline 4-min cycling performance trial, there was no significant change in average power and total work done after PP (average power = +0.3% ± 2.2%, P = 0.77 and total work done = +0.3% ± 2.2%, P = 0.77) or BAP (average power = +1.6% ± 1.7%, P = 0.20 and total work done = +1.45% ± 1.8%, P = 0.28). For PSB, there was a significant increase in average power (+3.1% ± 1.8%, P = 0.04) and total work done (+3.0% ± 2.2%, P = 0.04). BASB resulted in a significant increase in average power (+3.3% ± 3.0%, P = 0.035) and total work done (+3.2% ± 3.1%, P = 0.044). In the β-alanine group, six of the seven participants showed a further increase in average power with the addition of NaHCO3 (BAP compared with BASB); however, the results did not reach statistical significance (average power, P = 0.22; total work done, P = 0.13). Table 1 provides the performance improvements in comparison with the PP experimental condition and the percent likelihood that each condition was beneficial/trivial/negative when compared with the PP condition.
TABLE 1: The change in average power output and total work done in each loading condition from the baseline trial relative to the change in PP from baseline.
The percentage change from baseline performance is shown in Figure 2. In comparison with baseline performance, BAP was associated with a 37% likelihood of producing a performance benefit and 63% likelihood of a trivial effect. Compared with baseline performance, PSB and BASB were associated with a ≥89% likelihood of producing a performance benefit (Fig. 2).
FIGURE 2: Improvement in average power output in the maximal 4-min cycling performance trial in each treatment group. The likelihood of a practically substantial difference of the supplementation condition relative to the baseline performance trial for each group (β-alanine or placebo) were provided as percent positive/percent trivial/percent negative above each bar. *Significantly different from baseline (P < 0.05).
Analysis of the completed training diaries showed that there was no significant difference in the total amount of training performed (P = 0.29) between the β-alanine and placebo supplementation groups during the 28-d supplementation period, as identified by the session RPE method (β-alanine = 19,703 ± 4067 arbitrary units (AU), placebo = 21,208 ± 4895 AU). There was no order effect for average power for the postsupplementation performance trials (trial 1 = 415.7 ± 50.2 W, trial 2 = 414.9 ± 53.5 W, P = 0.86).
Blood pH and HCO3−.
Blood pH and HCO3− were elevated from before loading to pretest after acute NaHCO3 supplementation (PSB and BASB) (P < 0.001) (Table 2) compared with acute placebo supplementation (PP and BAP). There was a significant decrease in blood pH and HCO3− from pretest to posttest in all 4-min cycling performance trials (P < 0.001) (Table 2). The magnitude of the change in HCO3− from pretest to posttest in the acute NaHCO3 loading trials (BASB and PSB) was significantly greater compared with the acute placebo loading trial (P < 0.001).
Of the participants, two cyclists who took β-alanine as a supplement reported mild symptoms of paresthesia. After the acute NaHCO3 supplementation trials, 3 of the 14 participants reported mild gastrointestinal symptoms.
TABLE 2: pH and HCO3 − values before loading (90 min before exercise in postsupplementation trials) and at pretest (0 min before exercise) and posttest (immediately after exercise) in the placebo and β-alanine groups during the baseline trial, acute placebo loading trial, and acute NaHCO3 trial.
DISCUSSION
The main findings from the present study were that 28 d of β-alanine supplementation did not significantly improve high-intensity cycling performance; however, magnitude-based inferences demonstrated that in highly trained cyclists, β-alanine supplementation was 37% likely to improve performance with 0% likelihood of a negative effect. Furthermore, acute NaHCO3 supplementation significantly improved average power and total work done in a 4-min cycling trial. There seemed to be a minimal additive effect after the combined supplementation of β-alanine and NaHCO3 with similar improvements in high-intensity cycling performance under the BASB condition and the PSB condition.
β-alanine supplementation alone did not significantly improve performance during the 4-min cycling performance trial. The absence of a significant performance improvement in the current study is consistent with previous literature investigating the effects of β-alanine supplementation on maximal exercise efforts in trained populations (2,11). Derave et al. (11) found no improvement in 400-m running time in trained sprinters after a similar 4-wk β-alanine supplementation period (4.8 g·d−1), despite a significant increase in skeletal muscle carnosine in the soleus (47%) and gastrocnemius (37%). Furthermore, Baguet et al. (2) found no significant improvement in performance of elite rowers after 7 wk of β-alanine supplementation (5 g·d−1) despite a significant increase in muscle carnosine content in the soleus (45%) and gastrocnemius (28%). This may suggest that despite significant increases in the skeletal muscle carnosine content of highly trained athletes, the already highly developed buffering capacity may not allow for further improvements in exercise performance to be attained in sport-specific competitive events (32). In the current study, muscle carnosine was not measured; however, previous research has demonstrated that a similar 4-wk β-alanine supplementation regimen (4.8 g·d−1) can significantly increase muscle carnosine content in trained athletes (2). However, the participants in the current study ingested the capsules in four equal daily doses, in contrast to six equal daily doses (2), which may have had an effect on the magnitude of increase in skeletal muscle carnosine.
Acute supplementation of NaHCO3 before the 4-min cycling performance trial significantly increased average power by 3.1% (PSB) and 3.3% (BASB) compared with baseline performance. This finding is similar to previous studies that have reported exercise performance improvements after NaHCO3 ingestion before sport-specific performance in highly trained athletes (5,26,27). For example, NaHCO3 supplementation has been associated with ∼3% improvements in 400-m (13), 800-m (36), and 1500-m (5) running times in middle- and long-distance runners. McNaughton and Cedaro (26) also reported a ∼3% improvement in a maximal 6-min rowing ergometer test after a similar dose of NaHCO3 in highly trained rowers. For trained cyclists, previous research has indicated that acute NaHCO3 supplementation can significantly improve total work done (+6.6%) in a 1-min maximal cycling effort (27). The likely mechanism for the improved exercise performance in the current study may have been due to the increased buffering capacity. In the current study, NaHCO3 supplementation significantly elevated blood pH and HCO3− levels before the cycling performance trials compared with the placebo. Many studies have confirmed that an increased extracellular pH and HCO3− concentration can raise the La− and H+ efflux from active muscles (21,34) and increase the activity of the La−/H+ cotransporter. It has been suggested that this mechanism can cause a decrease in muscular fatigue and assist in maintaining intracellular pH allowing higher work intensities to be maintained for a longer period and more work to be completed (24). Therefore, in the current study, it can be speculated that the augmented extracellular reserve of HCO3− may have been the mechanism responsible for the performance improvement.
There seemed to be a minimal additive effect of β-alanine and NaHCO3 (BASB) when compared with β-alanine alone (BAP). Sale et al. (33) reported a significant increase in cycling performance after β-alanine supplementation; however, there was no additional ergogenic benefit after the combined supplementation of β-alanine and NaHCO3. The lack of a significant performance improvement after β-alanine supplementation in the current study may relate to the already highly developed buffering capacity of the trained athletes not allowing for further improvements in exercise capacity. Despite a 4.1% improvement in time to exhaustion compared with β-alanine alone, Sale et al. (33) found no additional ergogenic benefit after the combined supplementation of β-alanine and NaHCO3. The nonsignificant improvement in time to exhaustion in the cycling capacity test may reflect the variability in cycling performance or potential for improvement of the untrained participants of the study by Sale et al. (33) compared with the highly trained cyclists in the current study (19). Furthermore, the current study used a constant-duration performance test, which provides a more appropriate physiological simulation of actual performance and correlates well with sport-specific competitive events when compared with time-to-fatigue tests (9).
In the current study, there was no significant change in 4-min time trial performance in PP compared with baseline after the 4-wk supplementation period that included two high-intensity interval sessions per week. A comprehensive review on chronic HIT interventions (29) has shown performance improvements of between 3.0% and 8.3% after interval training at maximal and supramaximal intensities. In the current study, the absence of a significant improvement in cycling performance is a testament to the training status of the participants who took part in the current study because the inclusion of two high-intensity interval sessions per week was not sufficient to significantly improve maximal 4-min cycling performance.
A limitation of the current study was that two participants reported mild symptoms of paresthesia after β-alanine supplementation, which may have compromised the blinding of the two participants to the supplementation condition. This adverse effect is thought to be triggered by a high acute dose of β-alanine (larger than 800 mg) (14) and can be avoided by increasing the frequency of daily doses, which limits the amount consumed per dose or by ingesting a slow-release β-alanine formula as opposed to a pure solution, which has been shown to have slower absorption kinetics, improved whole-body retention, and sensory adverse effects that cannot be differentiated from a placebo (10).
The present study has shown that 28 d of β-alanine supplementation does not significantly improve 4-min cycling performance in highly trained cyclists. Although the effects of β-alanine on performance were mostly trivial, the beneficial effects on performance provide some support for the use of β-alanine supplementation in trained cyclists. Furthermore, acute NaHCO3 supplementation significantly improved 4-min cycling performance; however, there seemed to be a minimal additive effect after the combined supplementation of β-alanine and NaHCO3, which was associated with similar improvements in high-intensity cycling performance compared with acute NaHCO3 supplementation alone.
There were no external funding sources for this work.
The authors have no conflict of interest.
The results of the current study do not constitute endorsement by the American College of Sports Medicine.
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