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Original Research

The Effect of β-Alanine Supplementation on Power Performance During Repeated Sprint Activity

Sweeney, Kaitlin M1; Wright, Glenn A1; Glenn Brice, A2; Doberstein, Scott T1

Author Information
Journal of Strength and Conditioning Research: January 2010 - Volume 24 - Issue 1 - p 79-87
doi: 10.1519/JSC.0b013e3181c63bd5
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The activity pattern of many field-based sports consists of intermittent bouts of maximal or near-maximal sprinting followed by short-, moderate- to light-intensity recovery periods. The ability to maintain this pattern of activity throughout an entire game or match requires the rapid resynthesis of adenosine triphosphate (ATP). Rapid ATP resynthesis is primarily accomplished by the limited stores of phosphocreatine (PCr) and fast glycolysis (27). Gaitanos et al. (11) suggested that complete PCr resynthesis cannot occur within short recovery periods, resulting in a progressive depletion of PCr and an increased reliance on fast glycolysis during repeat sprint exercise. The increased dependence on fast glycolysis also implies an increase in hydrogen ion (H+) concentration within the muscle, which decreases pH, slows ATP production, and inevitably causes fatigue. In addition, increased H+ may interfere with muscle contraction and may potentially decrease power production (20). As a result, field-based athletes in sports such as American football, soccer, and field hockey may look for nutritional supplements to aid in improving muscle buffer capacity to improve performance during competition.

The intramuscular dipeptide carnosine is thought to contribute between 7 and 10% to the total buffering capacity in skeletal muscle of untrained subjects (18,23). Carnosine is made up of 2 amino acids, β-alanine (BA), and histidine. Histidine is found in plentiful amounts in muscle, which leads many to suggest that the BA may be the rate-limiting substrate for carnosine production in muscle (2). Studies where subjects supplemented with doses of 3-6 g BA per day for at least 4 weeks have shown to be an effective means of increasing skeletal muscle carnosine levels (9,16,18). Increasing skeletal muscle carnosine levels through BA supplementation delays fatigue and increases anaerobic exercise performance (9,15,17,29), presumably by improving buffer capacity.

Previous investigators observed that BA supplementation improved anaerobic exercise performance (15,17,28); however, not all anaerobic exercises are limited by the same metabolic factors. For example, it is suggested that fatigue during repeat sprint exercise is caused by the rapid depletion of PCr stores in the muscle (12). At the same time, repeat sprint exercise is known to produce moderate to high muscle and blood lactate levels and a resulting decrease in muscle pH (4,8,11), indicating the heavy use of fast glycolysis to resynthesize ATP. Bishop et al. (5) found that there was a strong relationship between power decrement and change in plasma [H+] during a repeat sprint protocol consisting of 5 × 6-second sprints with a 24-second recovery. As a result of this finding and the relationship between blood and muscle pH (1), Bishop et al. (5) suggested that the ability for the muscle to buffer H+ may be important for maintaining repeat sprint performance. It is possible that repeat sprint exercise performance may be improved by BA supplementation because muscle buffer capacity seems to be important for such performance (3); however, no studies have been performed to investigate this hypothesis. Therefore, the purpose of this study was to determine the efficacy of 5 weeks of BA supplementation on repeated brief sprint performance.


Experimental Approach to the Problem

This study was conducted over a 6-week period using a 2-group, matched, double-blind design that was placebo controlled. After 2 familiarization sessions of the repeated sprint protocol used in the study, the participants were assigned to 1 of 2 groups of 10 subjects: BA or placebo (C) matched to their mean power performance during the second familiarization of the sprint protocol. The C group was used rather than a crossover design because the washout time for BA is not at present known. Subjects performed a repeated sprint protocol before and after 5 weeks of supplementation with either a BA or a placebo similar in appearance, taste, and texture. It was hypothesized that BA supplementation would allow sprint performance (horizontal power production, HP; power decrement, % fatigue) to be maintained through a greater number of sprints than without BA.


Twenty, physically active, college-aged men were recruited as subjects in this investigation (descriptive characteristics found in Table 1). Twelve subjects were National Collegiate Athletic Association Division III football players involved in the early phases of their off-season training program, which included 3-4 days of resistance training and 2 days of sprint training. The remaining 8 subjects were involved with a recreational strength training program where the focus was on muscle hypertrophy and were regularly trained 3-4 days per week for at least 6 months before beginning the study. One subject in the BA group dropped out of the study during the week of post-testing because of illness unrelated to the study. Therefore, pre- and post-supplementation data for this subject were not included in data analysis, leaving the BA group with only 9 subjects. The research protocol was approved by the university's Institutional Review Board before its implementation. Subjects were informed of the experimental risks and signed an informed consent document before participation in the study. The subjects were not permitted to use any additional nutritional or performance enhancement supplementation in the previous 8 weeks. We asked our subjects to maintain their normal diet and eat a normal meal within 2-3 hours before each exercise testing session. No other nutritional guidelines were given.

Table 1
Table 1:
Participant characteristics (mean ±SD).*



After pretesting, subjects ingested 2 capsules of the BA supplement (Intra X cell; Athletics Edge Nutrition, Miami, FL, USA) or placebo (rice flour) 3 times per day during the first week. Daily intake of the experimental supplement at this dosage supplied 4 g of BA, 402 mg proprietary blend of N-acetylcysteine/g-lipoic acid, and 15 mg of vitamin E. During the following 4 weeks, participants increased the dose to 6 g of BA or placebo per day by ingesting 3 capsules, 3 times per day. Subjects were asked to take the capsules with meals and record the exact day and time of dose in a dosing journal. Supplements were disbursed at the beginning of weeks 1 and 3.

Sprint Treadmill Testing

The testing protocol consisted of 2 familiarization sessions performed on nonconsecutive days. The second of these sessions was performed 1 week before the first of 2 experimental sessions. Experimental sessions were separated by the 5-week supplementation period. The 2 experimental sessions consisted of a standardized warm-up of 5 minutes on a motorized treadmill at a self-selected fast walk or slow jog followed by 3 short 2- to 3-second bursts on a non-motorized treadmill (Force Treadmill; Woodway USA, Waukesha, WI, USA) against a resistance load equal to 15% of the subject's body weight. This resistance was established through pilot work to find the highest load that would ensure reaching peak power within the first 3 seconds of a 5-second sprint. After the warm-up, subjects rested for 5 minutes before starting the sprint protocol.

The non-motorized treadmill consisted of a hard rubber belt that was user driven. The load was produced by an electromagnetic braking system that provided up to 68 kg of resistance to the treadmill belt. The subject was attached to a vertical strut by a belted tether system that contained a load cell to measure horizontal force. Information from the load cell and the velocity of the treadmill belt were interfaced with a computer and software that determined horizontal force, velocity, power, work, and distance of each sprint at 50 Hz. These data were accumulated on a Microsoft Excel spreadsheet and averaged to 0.5-second intervals. Performance decrement (% fatigue) during the repeat sprint protocol was calculated using recommendations made by Glaister et al. (13) and the performance decrement score devised by Fitzsimons et al. (10): % fatigue = 100 − ([total power output/ideal power output] × 100), where total power output = the sum of the power output values for all sprints and ideal power output = the number of sprints × highest power output of all sprints.

The repeat sprint protocol consisted of 2 sets of five 5-second sprints with 45 seconds of passive recovery. A 2-minute walking recovery at 1.5 mph on an adjacent motorized treadmill separated the 2 sets of sprints. Subjects were instructed to achieve maximal effort and maintain that effort for the entire 5 seconds of every sprint. Strong verbal encouragement was given to each participant. The test-retest reliabilities (intraclass correlation, ICC) of this repeat sprint protocol were r = 0.998 and r = 0.918 for mean power and peak power performance, respectively.

Blood Lactate

Fingertip capillary blood samples were taken before warm-up and 5 minutes after the last sprint. After puncturing the skin of the fingertip, the first drop of blood was wiped from the skin. The succeeding blood flow was collected in a heparinized capillary tube. Twenty-five microliters of blood was immediately removed from the capillary tube and mixed with 50 μl of NaF Triton buffer, which is used for red blood cell lyses and to prevent an increase in lactate after the whole blood sample was added to the buffer. Samples were immediately analyzed for lactate using a Yellow Springs Instruments 1500 Sport lactate analyzer (Yellow Springs, OH, USA). The test-retest reliability (ICC) of this method in our laboratory has been shown to be r ≥ 0.953.

Statistical Analyses

Based on a similar repeat sprint study design (31), we determined that 12 subjects would be necessary to achieve a statistical power of 0.80 for peak power performance and 8 subjects would be necessary to achieve this level for mean power performance (21). Because mean power is a more representative measure of sprint performance, we decided to recruit 10 subjects per group in this study.

Analysis of variance (2 × 2) with repeated measures on one factor (time: pre vs. post) was performed to determine if any significant main effects or interactions were present between time and between groups (BA and C) for analysis of HP, % fatigue (performance decrement), and blood lactate. All data are reported as mean ± SD unless otherwise indicated. The level of statistical significance was set at p ≤ 0.05, with meaningfulness of differences determined by the use of effect sizes. Effect sizes were calculated by determining the difference between pretest and posttest means, divided by the pretest SD, and interpreted according to a scale previously proposed by Rhea (24).


Review of supplement dosing journals indicated that all subjects met the required supplement dosage and demonstrated no side effects other than a mild prickling sensation in their neck and limbs due to the neural sensitivity from the supplement. This side effect is considered to be normal and typical of BA supplementation and dissipates with time.

Horizontal Power

Figure 1 shows the power output for peak (HPpeak) and mean (HPmean) horizontal power for each sprint by group. No significant differences were identified for HPpeak by time, group, or interaction of time × group (Table 2). We observed a significant main effect in HPmean by time such that there was a decrease in HPmean in both groups from pre- to posttesting; however, there was no significant difference between groups or time × group interaction (Table 2). Effect sizes for HP in both groups were trivial, ranging from 0.06 to 0.15. Figure 2 shows that there was a fairly consistent individual subject response to both the BA and C supplementation.

Table 2
Table 2:
HP for the BA and C groups pre and post supplementation (mean ±SD).†
Figure 1
Figure 1:
Peak and mean HP output per sprint for the BA group (A) and C group (B) pre and post supplementation (mean values only,SD not shown for clarity). HP = horizontal power; BA = β-alanine; C = control.
Figure 2
Figure 2:
Individual response (lines) and group mean (bars) for average HPpeak and HPmean per sprint for the BA group (A, C) and control group (B, D) pre and post supplementation (mean values only,SD not shown for clarity). BA = β-alanine.


The performance decrements (% fatigue) seen in the BA group and C group pre and post supplementation are shown in Table 3. No significant differences were seen in the performance decrement for HPpeak or HPmean. Effect sizes for HP in both groups were trivial to small, ranging from 0.03 to 0.43. Figure 3 shows a large variation in both HPpeak and HPmean for the individual subject response in performance decrement for both groups of subjects.

Table 3
Table 3:
Performance decrement (% fatigue) for HP and velocity (V) for the BA and C groups pre and post supplementation (mean ±SD).*†
Figure 3
Figure 3:
Individual response (lines) and group mean (bars) for power decrement (% fatigue) during the sprint protocol for the BA group (A, C) and C group (B, D) pre and post supplementation for HPpeak (A, B) and HPmean (C, D) (mean values only,SD not shown for clarity). BA = β-alanine; C = control.


Blood lactate response to the repeat sprint protocol is shown in Figure 4. There were no significant differences observed by group (p = 0.562) or time (p = 0.809). There was also no significant group × time interaction (p = 0.585).

Figure 4
Figure 4:
Lactate response to repeat sprint protocol pre and post supplementation. BA = β-alanine; C = control (mean ±SD).


The aim of this study was to determine the effect of 5 weeks of BA supplementation on performance during repeated brief all-out sprints. Results indicate that 6 g per day of BA supplementation had no effect on HP or performance decrement (% fatigue) during repeated sprints. The decrease in HPmean from pre to posttesting in both groups may be attributed to a change in pacing strategy during the sprint. We observed that both groups produced a nonsignificant increase in HPpeak after supplementation, which may have led to earlier fatigue within each sprint, resulting in a lower HPmean. The BA group increased HPpeak 2.4%, whereas HPmean decreased 1.0%. Similarly, the C group increased HPpeak 1.9%, which was accompanied by a 0.9% decrease in HPmean. Although the small decrease in HPmean produced a significant main effect by time, it is unlikely that this decrease is practically significant for most field sport athletes. The lack of a group × time interaction indicates there was no difference in the improvement in HPmean due to BA supplementation.

One of the key outcomes of a repeat sprint protocol is the measure of performance decrement over the number of sprints. In this study, we looked at the power decrease over ten 5-second sprints with a 45-second recovery. To be able to conclude that BA provides some positive ergogenic properties, supplementation with BA should improve the performance decrement (smaller decrease in power) for both HPpeak and HPmean. Our results show that BA did not improve the performance decrement; however, the results should be interpreted with caution. As shown in Figure 3, the individual pre- to post-supplementation % fatigue responses for both BA and C groups are quite variable. Although the method used to determine performance decrement in this study has been evaluated and compared with other methods for reliability and validity and determined to be the most reliable and valid method, it has also been shown to have a test-retest variability in fatigue of about 30% (13).

The absence of an ergogenic effect may be related to the inability to increase muscle carnosine levels by the dosing strategy used in this study. Beta-alanine is likely the rate-limiting substrate and essential supplement required to increase carnosine levels within the muscle tissue (2). Previous research has demonstrated that BA supplementation can increase muscle carnosine levels and contribute to the acid-base buffering capacity of the muscle (8,12,14,15,18). For example, Harris et al. (16) found a 42% increase in carnosine levels after supplementing with 3.2 g per day of BA and a 64% increase with 6.4 g per day after 4 weeks of supplementation.

Active subjects show higher resting levels of carnosine in their muscles than untrained individuals, especially if they have a history of anaerobic training (30). Muscle carnosine levels have been determined to be twice as high in competitive bodybuilders as untrained individuals, possibly due to changes associated with prolonged repetitive exposure to low muscle pH, diet, or supplementation (30). The subjects in our study would be classified as highly active with the majority of their activity in anaerobic activities (strength training), although none would be considered elite athletes. Recently, Derave et al. (9) found that trained sprinters were able to increase intramuscular carnosine 47% in the soleus and 37% in the gastrocnemius after 4 weeks of 2.4-4.8 g per day of BA supplementation. Although an important limitation of this study was our inability to measure carnosine levels, the dosage and supplement periods used in our study (6 g per day, 5 weeks) are equal to or in excess of previous studies that have shown a significant increase in muscle carnosine levels in both trained and untrained subjects. Therefore, the lack of ergogenic benefits observed in the present study is not likely attributed to an inappropriate BA supplementation protocol.

An increase in carnosine levels and muscle buffer capacity from BA would likely increase the ability to withstand and maintain performance during high-intensity activity where fast glycolysis is an important energy system. An increased reliance on fast glycolysis means a greater concentration of H+ ions and drop in pH. In the present study, we did not measure blood or muscle pH. However, sprint-type activity is known to recruit high-threshold motor units during high force production in muscles required in sprinting (25). The fast-twitch fibers that make up the high-threshold motor units are characterized by greater intramuscular acidosis during their activation than slow-twitch fibers (32). Therefore, during repeated all-out sprint exercise, the involvement of fast glycolysis in fast-twitch fibers, as evidenced in our study by moderately high blood lactate levels, indicates a likelihood that the muscle is in a state of acidosis during this repeat sprint protocol. As the pH of the muscle drops, power output may be impaired due to muscular fatigue (9). It is known that the fatiguing effects attributed to a decreasing pH during intense exercise include inhibition of rate-limiting enzymes involved with fast glycolysis (phosphofructokinase and phosphorylase), decreased release of Ca++ from the sarcoplasmic reticulum, and a decrease in cross-bridge interactions in the muscle (22,26), leading to a drop in HP.

The presumed increase in muscle carnosine levels associated with BA supplementation used in this study should have increased the ability to buffer H+ ions and maintain muscle pH and sprint performance. However, it is possible that the H+ produced may have exceeded the capacity of carnosine to be an effective intramuscular buffer because it is estimated that during intense exercise, muscle pH will drop from 7.2 at rest to 6.5 or lower at fatigue (16). However, the suggestion of exceeding the capacity of carnosine may be somewhat controversial because there is disagreement to the extent of the buffering capacity of carnosine. According to Mannion et al. (23) carnosine may be of little importance to pH maintenance by only contributing approximately 7% to the total muscle buffer capacity. However, findings by Davey (7) suggest that carnosine can contribute as much as 40% to buffering capacity when the physiological pH is between 6.5 and 7.5.

Although previous research has shown an improvement in performance after BA supplementation (9,17,18,29), it might be concluded from those studies that the ergogenic benefit may be more related to the dominant energy system used during the performance and as a result depend on the duration of the maximal effort. For example, Hill et al. (18) demonstrated a 16% increase in total work performed at 110% of maximum cycling power to exhaustion (∼150 seconds) after BA supplementation for 4 weeks. In addition, Derave et al. (9) demonstrated that BA improved performance of intermittent exercise bouts of isokinetic leg extensions (5 bouts of 30 maximal repetitions with 1-minute rest between bouts) where each bout lasted approximately 45 seconds. The ergogenic benefits however were not noticed until the last 2 sets of the intermittent protocol. Stout et al. (29) demonstrated an increase in neuromuscular fatigue threshold using an incremental cycling challenge that used four to five 2-minute stages after BA supplementation of 1.6 g per day for 28 days. Although many previous studies support the use of BA supplementation as a performance-enhancing ergogenic aid for some types of anaerobic exercise, this is the first study to investigate the effects of BA supplementation on repeat sprint exercise performance.

Our findings of the inability of BA supplementation to maintain HP during repeat sprint exercise in the present study are consistent with other studies using all-out efforts for less than 1 minute (9,19). For example, Hoffman et al. (19) found no additional benefit of supplementing with BA along with creatine compared with creatine alone when performing two 30-second Wingate tests separated by 3 minutes of active recovery. In the same study (19), the supplementation of BA did not improve the maintenance of jumping power during a 20 consecutive jump test. In addition, after 4 weeks of 4.8 g per day of BA (which significantly increased intramuscular carnosine), Derave et al. (9) found no change in performance time (average ∼52 seconds) in a single 400-m sprint in trained sprinters.

These findings, along with the results of our study, suggest that factors other than changes in pH may be more important than the accumulation of H+ ions for producing fatigue during repeated brief sprints with short recovery periods. During a single bout (6 seconds) of high-intensity exercise, use of PCr and fast glycolysis each account for approximately half of the total energy needed; however, during repeated sprints, a greater depletion of PCr is observed than during a single maximal effort (9). The rate of PCr resynthesis is influenced by the metabolic environment of the muscle, H+ ion concentrations of the muscle and blood, and ATP concentration within the muscle (27). It has been demonstrated that short recovery periods (30-180 seconds) may not provide adequate time to restore PCr values to resting levels, thus leading to an increased need for additional energy from fast glycolysis (2,9). Indeed, Bogdanis et al. (6) reported that the halftime for PCr resynthesis was 57 seconds, considerably longer than the recovery period (45 seconds) used in the present study. The incomplete resynthesis of PCr may explain the relatively high levels of blood lactate observed in our study but also suggest that changes in pH may not be the sole explanation for muscle fatigue during our sprint protocol. The availability of PCr may be the limiting factor in multiple sprint performance (4,5,9). During repeated sprints, PCr may only be partially restored if the recovery bouts are less than 1-2 minutes long and may take more than 6 minutes to fully recover (4,9). It is likely that the 45-second recovery periods used in our study did not allow for sufficient PCr resynthesis to maintain a considerable contribution to power output beyond the first couple of sprints. Therefore, BA supplementation may not have a large effect on repeated sprint performance because the lack of PCr resynthesis may have a greater effect on fatigue and decrease in performance than the accumulation of H+. In support of this notion, Bishop et al. (3) found that the physiochemical buffering in the muscle during a 5 × 6-second sprint protocol with 24-second recovery had no relationship to repeated sprint ability. They suggest that the contribution from the metabolic reactions that consume H+, the sarcolemmal lactate/H+, and Na+/H+ exchange mechanisms; capillarization; muscle blood flow; and changes in the intracellular strong ion difference may be a greater influence than the physiochemical buffering in the muscle. They also suggest that the individuals with the best repeated sprint ability are likely the ones who produce fewer H+, especially in the first few sprints (3).

In conclusion, it was determined that BA supplementation does not have an ergogenic effect on repeated brief sprints. The lack of PCr resynthesis associated with short recovery periods may more likely explain the limiting factors for performance.

Practical Applications

The ability to produce and maintain bouts of high-power output during periods of multiple sprint work is important to many field-based sports. Previous research using repeat high-intensity sprint performance has attributed fatigue to the availability and resynthesis of PCr. Phosphocreatine depletion may be a greater cause of fatigue in this protocol than acidosis, and as a result, any effects of BA were not noticeable. Although this area requires more investigation, the results of this study suggest that sports such as football, soccer, lacrosse, and others with repeated sprint efforts should probably not rely on BA supplementation for performance enhancement.


The authors would like to thank the University of Wisconsin-La Crosse Graduate Research Grant Program for assisting with funding for this project. The authors would also like to acknowledge Athletes Edge Nutrition, Miami, FL, for their help in providing supplementation. The results of the present study do not constitute endorsement of the product by the authors or the National Strength and Conditioning Association.


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carnosine; high-intensity exercise; buffer capacity; fatigue

© 2010 National Strength and Conditioning Association