Skeletal muscle histidine-containing dipeptide contents are increased in freshwater turtles (C. picta bellii) with cold-acclimation.

Freshwater turtles found in higher latitudes can experience extreme challenges to acid-base homeostasis while overwintering, due to a combination of cold temperatures along with the potential for environmental hypoxia. Histidine-containing dipeptides (HCDs; carnosine, anserine and balenine) may facilitate pH regulation in response to these challenges, through their role as pH buffers. We measured the HCD content of three tissues (liver, cardiac and skeletal muscle) from the anoxia-tolerant painted turtle (C. picta bellii) acclimated to either 3 or 20 °C. HCDs were detected in all tissues, with the highest content shown in the skeletal muscle. Turtles acclimated to 3 °C had more HCD in their skeletal muscle than those acclimated to 20 °C (carnosine = 20.8 ± 4.5 vs 12.5 ± 5.9 mmol·kg DM-1; ES = 1.59 (95%CI: 0.16-3.00), P = 0.013). The higher HCD content shown in the skeletal muscle of the cold-acclimated turtles suggests a role in acid-base regulation in response to physiological challenges associated with living in the cold, with the increase possibly related to the temperature sensitivity of carnosine's dissociation constant.

Chronic pantothenic acid supplementation does not affect muscle coenzyme A content or cycling performance.

This study determined if supplementation with pantothenic acid (PA) for 16 weeks could increase skeletal muscle coenzyme A (CoASH) content and exercise performance. Trained male cyclists (n = 14) were matched into control or PA (6 g·day-1) groups. At 0, 4, 8, and 16 weeks, subjects performed an incremental time to exhaustion cycle with muscle biopsies taken prior to and following exercise. Prolonged PA supplementation did not change skeletal muscle CoASH and acetyl-CoA contents or exercise performance. Novelty: Supplementation with pantothenic acid for 16 weeks had no effect on skeletal muscle CoASH and acetyl-CoA content or exercise performance in trained male cyclists.

Comparison of sustained-release and rapid-release ß-alanine formulations on changes in skeletal muscle carnosine and histidine content and isometric performance following a muscle-damaging protocol.

ß-alanine supplementation increases muscle carnosine content and improves anaerobic exercise performance by enhancing intracellular buffering capacity. ß-alanine ingestion in its traditional rapid-release formulation (RR) is associated with the symptoms of paresthesia. A sustained-release formulation (SR) of ß-alanine has been shown to circumvent paresthesia and extend the period of supply to muscle for carnosine synthesis. The purpose of this investigation was to compare 28 days of SR and RR formulations of ß-alanine (6 g day-1) on changes in carnosine content of the vastus lateralis and muscle fatigue. Thirty-nine recreationally active men and women were assigned to one of the three groups: SR, RR, or placebo (PLA). Participants supplementing with SR and RR formulations increased muscle carnosine content by 50.1% (3.87 mmol kg-1ww) and 37.9% (2.62 mmol kg-1ww), respectively. The change in muscle carnosine content in participants consuming SR was significantly different (p = 0.010) from those consuming PLA, but no significant difference was noted between RR and PLA (p = 0.077). Although participants ingesting SR experienced a 16.4% greater increase in muscle carnosine than RR, fatigue during maximal voluntary isometric contractions was significantly attenuated in both SR and RR compared to PLA (p = 0.002 and 0.024, respectively). Symptoms of paresthesia were significantly more frequent in RR compared to SR, the latter of which did not differ from PLA. Results of this study demonstrated that only participants consuming the SR formulation experienced a significant increase in muscle carnosine. Differences in the muscle carnosine response between these formulations may have practical significance for athletic populations in which small changes may have important implications on performance.

Comparison of Two ß-Alanine Dosing Protocols on Muscle Carnosine Elevations.

OBJECTIVE: ß-alanine (BA) is a nonproteogenic amino acid that combines with histidine to form carnosine. The amount taken orally in individual doses, however, is limited due to symptoms of paresthesia that are associated with higher doses. The use of a sustained-release formulation has been reported to reduce the symptoms of paresthesia, suggesting that a greater daily dose may be possible. The purpose of the present study was to determine whether increasing the daily dose of BA can result in a similar increase in muscle carnosine in a reduced time. METHODS: Eighteen men and twelve women were randomized into either a placebo (PLC), 6-g BA (6G), or 12-g BA (12G) groups. PLC and 6G were supplemented for 4 weeks, while 12G was supplemented for 2 weeks. A resting blood draw and muscle biopsy were obtained prior to (PRE) and following (POST) supplementation. Plasma and muscle metabolites were measured by high-performance liquid chromatography. The loss in peak torque (ΔPT) was calculated from maximal isometric contractions before and after 250 isokinetic kicks at 180°·sec-1 PRE and POST. RESULTS: Both 12G (p = 0.026) and 6G (p = 0.004) increased muscle carnosine compared to PLC. Plasma histidine was decreased from PRE to POST in 12G compared to PLC (p = 0.002) and 6G (p = 0.001), but no group x time interaction (p = 0.662) was observed for muscle histidine. No differences were observed for any hematological measure (e.g., complete blood counts) or in symptoms of paresthesia among the groups. Although no interaction was noted in ΔPT, a trend (p = 0.073) was observed. CONCLUSION: Results of this investigation indicate that a BA supplementation protocol of 12 g/d-1, using a sustained-release formulation, can accelerate the increase in carnosine content in skeletal muscle while attenuating paresthesia.

ß-Alanine supplementation and military performance.

During sustained high-intensity military training or simulated combat exercises, significant decreases in physical performance measures are often seen. The use of dietary supplements is becoming increasingly popular among military personnel, with more than half of the US soldiers deployed or garrisoned reported to using dietary supplements. ß-Alanine is a popular supplement used primarily by strength and power athletes to enhance performance, as well as training aimed at improving muscle growth, strength and power. However, there is limited research examining the efficacy of ß-alanine in soldiers conducting operationally relevant tasks. The gains brought about by ß-alanine use by selected competitive athletes appears to be relevant also for certain physiological demands common to military personnel during part of their training program. Medical and health personnel within the military are expected to extrapolate and implement relevant knowledge and doctrine from research performed on other population groups. The evidence supporting the use of ß-alanine in competitive and recreational athletic populations suggests that similar benefits would also be observed among tactical athletes. However, recent studies in military personnel have provided direct evidence supporting the use of ß-alanine supplementation for enhancing combat-specific performance. This appears to be most relevant for high-intensity activities lasting 60-300 s. Further, limited evidence has recently been presented suggesting that ß-alanine supplementation may enhance cognitive function and promote resiliency during highly stressful situations.

Effects of beta-alanine supplementation on brain homocarnosine/carnosine signal and cognitive function: an exploratory study.

OBJECTIVES: Two independent studies were conducted to examine the effects of 28 d of beta-alanine supplementation at 6.4 g d(-1) on brain homocarnosine/carnosine signal in omnivores and vegetarians (Study 1) and on cognitive function before and after exercise in trained cyclists (Study 2). METHODS: In Study 1, seven healthy vegetarians (3 women and 4 men) and seven age- and sex-matched omnivores undertook a brain 1H-MRS exam at baseline and after beta-alanine supplementation. In study 2, nineteen trained male cyclists completed four 20-Km cycling time trials (two pre supplementation and two post supplementation), with a battery of cognitive function tests (Stroop test, Sternberg paradigm, Rapid Visual Information Processing task) being performed before and after exercise on each occasion. RESULTS: In Study 1, there were no within-group effects of beta-alanine supplementation on brain homocarnosine/carnosine signal in either vegetarians (p = 0.99) or omnivores (p = 0.27); nor was there any effect when data from both groups were pooled (p = 0.19). Similarly, there was no group by time interaction for brain homocarnosine/carnosine signal (p = 0.27). In study 2, exercise improved cognitive function across all tests (P < 0.05), although there was no effect (P>0.05) of beta-alanine supplementation on response times or accuracy for the Stroop test, Sternberg paradigm or RVIP task at rest or after exercise. CONCLUSION: 28 d of beta-alanine supplementation at 6.4 g d(-1) appeared not to influence brain homocarnosine/carnosine signal in either omnivores or vegetarians; nor did it influence cognitive function before or after exercise in trained cyclists.

ß-Alanine supplemented diets enhance behavioral resilience to stress exposure in an animal model of PTSD.

This study investigated the effects of ß-alanine (BA) ingestion on the behavioral and neuroendocrine response of post-traumatic stress disorder (PTSD) in a murine model. Animals were fed a normal diet with or without (PL) BA supplementation (100 mg kg(-1)) for 30 days. Animals were then exposed to a predator-scent stress (PSS) or a sham (UNEX). Behaviors were evaluated using an elevated plus maze (EPM) and acoustic startle response (ASR) 7 days following exposure to the PSS. Corticosterone concentrations (CS), expression of brain-derived neurotrophic factor (BDNF), and brain carnosine concentrations were analyzed a day later. Animals in PSS+PL spent significantly less time in the open arms and in the number of entries in the EPM than PSS+BA, UNEX+BA, or UNEX+PL. Animals in PSS+BA had comparable scores to UNEX+BA. Anxiety index was higher (p < 0.05) in PSS+PL compared to PSS+BA or animals that were unexposed. ASR and freezing were greater (p < 0.05) in animals exposed to PSS compared to animals unexposed. CS expression was higher (p < 0.05) in animals exposed to PSS compared to unexposed animals. Brain carnosine concentrations in the hippocampus and other brain sections were significantly greater in animals supplemented with BA compared to PL. BDNF expression in the CA1 and DG subregions of the hippocampus was lower (p < 0.05) in animals exposed and fed a normal diet compared to animals exposed and supplemented with BA, or animals unexposed. In conclusion, BA supplementation in rats increased brain carnosine concentrations and resulted in a reduction in PTSD-like behavior, which may be mediated in part by maintaining BDNF expression in the hippocampus.

Effect of sodium bicarbonate supplementation on 2000-m rowing performance.

UNLABELLED: The ability to buffer H+ could be vital to exercise performance, as high concentrations of H+ contribute to the development of fatigue. PURPOSE: The authors examined the effect of sodium bicarbonate (SB) supplementation on 2000-m rowing-ergometer performance. METHODS: Twenty male rowers (age 23 ± 4 y, height 1.85 ± 0.08 m, mass 82.5 ± 8.9 kg, 2000-m personal-best time 409 ± 16 s) completed two 2000-m rowing-ergometer time trials, separated by 48 h. Participants were supplemented before exercise with 0.3 g/kg body mass of SB or a placebo (maltodextrin; PLA). The trials were conducted using a double-blinded, randomized, counterbalanced crossover study design. Time to complete the 2000-m and time taken for each 500-m split were recorded. Blood lactate, bicarbonate, pH, and base excess were determined preexercise, immediately postexercise, and 5 min postexercise. Performance data were analyzed using paired t tests, as well as magnitude-based inferences; hematological data were analyzed using a repeated-measures ANOVA. RESULTS: Using paired t tests, there was no benefit of SB over PLA (P = .095). However, using magnitude-based inferences there was a likely beneficial effect of SB compared with PLA (PLA 412.0 ± 15.1 s, SB 410.7 ± 14.9 s). Furthermore, SB was 0.5 ± 1.2 s faster than PLA in the third 500 m (P = .035; possibly beneficial) and 1.1 ± 1.7 s faster in the fourth 500 m (P = .004; very likely beneficial). All hematological data were different between SB and PLA and were different from preexercise to postexercise. CONCLUSION: SB supplementation is likely to be beneficial to the performance of those competing in 2000-m rowing events, particularly in the second half of the event.

Effect of sodium bicarbonate and Beta-alanine on repeated sprints during intermittent exercise performed in hypoxia.

PURPOSE: To investigate the separate and combined effects of sodium bicarbonate and beta-alanine supplementation on repeated sprints during simulated match play performed in hypoxia. METHODS: Study A: 20 recreationally active participants performed two trials following acute supplementation with either sodium bicarbonate (0.3 g·kg-1BM) or placebo (maltodextrin). Study B: 16 recreationally active participants were supplemented with either a placebo or beta-alanine for 5 weeks (6.4 g·day-1 for 4 weeks, 3.2 g·day-1 for 1 week), and performed one trial before supplementation (with maltodextrin) and two following supplementation (with sodium bicarbonate and maltodextrin). Trials consisted of 3 sets of 5 × 6 s repeated sprints performed during a football specific intermittent treadmill protocol performed in hypoxia (15.5% O2). Mean (MPO) and peak (PPO) power output were recorded as the performance measures. RESULTS: Study A: Overall MPO was lower with sodium bicarbonate than placebo (p = .02, 539.4 ± 84.5 vs. 554.0 ± 84.6 W), although there was no effect across sets (all p > .05). Study B: There was no effect of beta-alanine, or cosupplementation with sodium bicarbonate, on either parameter, although there was a trend toward higher MPO with sodium bicarbonate (p = .07). CONCLUSIONS: The effect of sodium bicarbonate on repeated sprints was equivocal, although there was no effect of beta-alanine or cosupplementation with sodium bicarbonate. Individual variation may have contributed to differences in results with sodium bicarbonate, although the lack of an effect with beta-alanine suggests this type of exercise may not be influenced by increased buffering capacity.

Sodium bicarbonate and high-intensity-cycling capacity: variability in responses.

PURPOSE: To determine whether gastrointestinal (GI) distress affects the ergogenicity of sodium bicarbonate and whether the degree of alkalemia or other metabolic responses is different between individuals who improve exercise capacity and those who do not. METHODS: Twenty-one men completed 2 cycling-capacity tests at 110% of maximum power output. Participants were supplemented with 0.3 g/kg body mass of either placebo (maltodextrin) or sodium bicarbonate (SB). Blood pH, bicarbonate, base excess, and lactate were determined at baseline, preexercise, immediately postexercise, and 5 min postexercise. RESULTS: SB supplementation did not significantly increase total work done (TWD; P = .16, 46.8 ± 9.1 vs 45.6 ± 8.4 kJ, d = 0.14), although magnitude-based inferences suggested a 63% likelihood of a positive effect. When data were analyzed without 4 participants who experienced GI discomfort, TWD (P = .01) was significantly improved with SB. Immediately postexercise blood lactate was higher in SB for the individuals who improved but not for those who did not. There were also differences in the preexercise-to-postexercise change in blood pH, bicarbonate, and base excess between individuals who improved and those who did not. CONCLUSIONS: SB improved high-intensity-cycling capacity but only with the exclusion of participants experiencing GI discomfort. Differences in blood responses suggest that SB may not be beneficial to all individuals. Magnitude-based inferences suggested that the exercise effects are unlikely to be negative; therefore, individuals should determine whether they respond well to SB supplementation before competition.

Effect of ß-alanine supplementation on high-intensity exercise performance.

Carnosine is a dipeptide of ß-alanine and L-histidine found in high concentrations in skeletal muscle. Combined with ß-alanine, the pKa of the histidine imidazole ring is raised to ∼6.8, placing it within the muscle intracellular pH high-intensity exercise transit range. Combination with ß-alanine renders the dipeptide inert to intracellular enzymic hydrolysis and blocks the histidinyl residue from participation in proteogenesis, thus making it an ideal, stable intracellular buffer. For vegetarians, synthesis is limited by ß-alanine availability; for meat-eaters, hepatic synthesis is supplemented with ß-alanine from the hydrolysis of dietary carnosine. Direct oral ß-alanine supplementation will compensate for low meat and fish intake, significantly raising the muscle carnosine concentration. This is best achieved with a sustained-release formulation of ß-alanine to avoid paresthesia symptoms and decreasing urinary spillover. In humans, increased levels of carnosine through ß-alanine supplementation have been shown to increase exercise capacity and performance of several types, particularly where the high-intensity exercise range is 1-4 min. ß-Alanine supplementation is used by athletes competing in high-intensity track and field cycling, rowing, swimming events and other competitions.

Additive effects of beta-alanine and sodium bicarbonate on upper-body intermittent performance.

We examined the isolated and combined effects of beta-alanine (BA) and sodium bicarbonate (SB) on high-intensity intermittent upper-body performance in judo and jiu-jitsu competitors. 37 athletes were assigned to one of four groups: (1) placebo (PL)+PL; (2) BA+PL; (3) PL+SB or (4) BA+SB. BA or dextrose (placebo) (6.4 g day⁻¹) was ingested for 4 weeks and 500 mg kg⁻¹ BM of SB or calcium carbonate (placebo) was ingested for 7 days during the 4th week. Before and after 4 weeks of supplementation, the athletes completed four 30-s upper-body Wingate tests, separated by 3 min. Blood lactate was determined at rest, immediately after and 5 min after the 4th exercise bout, with perceived exertion reported immediately after the 4th bout. BA and SB alone increased the total work done in +7 and 8 %, respectively. The co-ingestion resulted in an additive effect (+14 %, p < 0.05 vs. BA and SB alone). BA alone significantly improved mean power in the 2nd and 3rd bouts and tended to improve the 4th bout. SB alone significantly improved mean power in the 4th bout and tended to improve in the 2nd and 3rd bouts. BA+SB enhanced mean power in all four bouts. PL+PL did not elicit any alteration on mean and peak power. Post-exercise blood lactate increased with all treatments except with PL+PL. Only BA+SB resulted in lower ratings of perceived exertion (p = 0.05). Chronic BA and SB supplementation alone equally enhanced high-intensity intermittent upper-body performance in well-trained athletes. Combined BA and SB promoted a clear additive ergogenic effect.

Carnosine: from exercise performance to health.

Carnosine was first discovered in skeletal muscle, where its concentration is higher than in any other tissue. This, along with an understanding of its role as an intracellular pH buffer has made it a dipeptide of interest for the athletic population with its potential to increase high-intensity exercise performance and capacity. The ability to increase muscle carnosine levels via ß-alanine supplementation has spawned a new area of research into its use as an ergogenic aid. The current evidence base relating to the use of ß-alanine as an ergogenic aid is reviewed here, alongside our current thoughts on the potential mechanism(s) to support any effect. There is also some emerging evidence for a potential therapeutic role for carnosine, with this potential being, at least theoretically, shown in ageing, neurological diseases, diabetes and cancer. The currently available evidence to support this potential therapeutic role is also reviewed here, as are the potential limitations of its use for these purposes, which mainly focusses on issues surrounding carnosine bioavailability.

Effect of beta-alanine, with and without sodium bicarbonate, on 2000-m rowing performance.

PURPOSE: To examine the effect of beta-alanine only and beta-alanine with sodium bicarbonate supplementation on 2,000-m rowing performance. METHODS: Twenty well-trained rowers (age 23 ± 4 y; height 1.85 ± 0.08 m; body mass 82.5 ± 8.9 kg) were assigned to either a placebo or beta-alanine (6.4 g · d(-1) for 4 weeks) group. A 2,000-m rowing time trial (TT) was performed before supplementation (Baseline) and after 28 and 30 days of supplementation. The post supplementation trials involved supplementation with either maltodextrin or sodium bicarbonate in a double-blind, crossover design, creating four study conditions (placebo with maltodextrin; placebo with sodium bicarbonate; beta-alanine with maltodextrin; beta-alanine with sodium bicarbonate). Blood lactate, pH, bicarbonate, and base excess were measured pre-TT, immediately post-TT and at TT+5 min. Performance data were analyzed using magnitude based inferences. RESULTS: Beta-alanine supplementation was very likely to be beneficial to 2,000-m rowing performance (6.4 ± 8.1 s effect compared with placebo), with the effect of sodium bicarbonate having a likely benefit (3.2 ± 8.8 s). There was a small (1.1 ± 5.6 s) but possibly beneficial additional effect when combining chronic beta-alanine supplementation with acute sodium bicarbonate supplementation compared with chronic beta-alanine supplementation alone. Sodium bicarbonate ingestion led to increases in plasma pH, base excess, bicarbonate, and lactate concentrations. CONCLUSIONS: Both chronic beta-alanine and acute sodium bicarbonate supplementation alone had positive effects on 2,000-m rowing performance. The addition of acute sodium bicarbonate to chronic beta-alanine supplementation may further enhance rowing performance.

Altering the rest interval during high-intensity interval training does not affect muscle or performance adaptations.

It has been hypothesized that exercise-induced changes in metabolites and ions are crucial in the adaptation of contracting muscle. We tested this hypothesis by comparing adaptations to two different interval-training protocols (differing only in the rest duration between intervals), which provoked different perturbations in muscle metabolites and acid-base status. Prior to and immediately after training, 12 women performed the following tests: (1) a graded exercise test to determine peak oxygen uptake (V(O2)); (2) a high-intensity exercise bout (followed 60 s later by a repeated-sprint-ability test; and (3) a repeat of the high-intensity exercise bout alone with muscle biopsies pre-exercise, immediately postexercise and after 60 s of recovery. Subjects performed 5 weeks (3 days per week) of training, with either a short (1 min; HIT-1) or a long rest period (3 min; HIT-3) between intervals; training intensity and volume were matched. Muscle [H(+)] (155 ± 15 versus 125 ± 8 nmol l(-1); P < 0.05) and muscle lactate content (84.2 ± 7.9 versus 46.9 ± 3.1 mmol (g wet weight)(-1)) were both higher after HIT-1, while muscle phosphocreatine (PCr) content (52.8 ± 8.3 versus 63.4 ± 9.8 mmol (g wet weight)(-1)) was lower. There were no significant differences between the two groups regarding the increases in , repeated-sprint performance or muscle Na(+),K(+)-ATPase content. Following training, both groups had a significant decrease in postexercise muscle [H(+)] and lactate content, but not postexercise ATP or PCr. Postexercise PCr resynthesis increased following both training methods. In conclusion, intense interval training results in marked improvements in muscle Na(+),K(+)-ATPase content, PCr resynthesis and . However, manipulation of the rest period during intense interval training did not affect these changes.

Reliability of a high-intensity cycling capacity test.

OBJECTIVES: To assess the reliability of the CCT110%, a high-intensity cycling capacity test performed to exhaustion. DESIGN: 27 recreationally active participants (age 23±4y; height 1.79±0.06m; body mass 78.0±8.8kg; Powermax 306±49W) performed the CCT110% on two occasions. METHODS: Performance measures determined from the CCT110% were time to exhaustion (TTE) and total work done (TWD). Blood pH, lactate, bicarbonate and base excess were determined before exercise, immediately after exercise, and 5min after exercise. Exercise capacity data were analysed using intra-class correlations (ICC), systematic bias ratio, ratio limits of agreement, coefficient of variation (CV) and t-tests. Blood variables were analysed using repeated measures ANOVA and Tukey tests for post hoc comparisons. RESULTS: TTE (mean±SD: 134±20s and 135±20s, P=0.75) and TWD (42.2±10.3kJ and 42.2±9.8kJ, P=0.97) were not different between trials. The ICC between trials was r=0.88 for TTE and r=0.94 for TWD, with the CV being 4.43% for TTE and 4.94% for TWD. There were no between trial differences in blood markers at any time point except immediately post-exercise pH (7.246±0.041 vs. 7.269±0.064, P=0.004). CONCLUSIONS: The CCT110% is a reliable exercise protocol that can be used for nutritional interventions designed to affect intracellular and extracellular pH changes. Although blood pH was significantly different between trials immediately post-exercise, the absolute differences are much smaller than those expected to be seen using nutritional interventions intended to alter extracellular pH during exercise.

Beta-alanine supplementation in high-intensity exercise.

Glycolysis involves the oxidation of two neutral hydroxyl groups on each glycosyl (or glucosyl) unit metabolised, yielding two carboxylic acid groups. During low-intensity exercise these, along with the remainder of the carbon skeleton, are further oxidised to CO(2) and water. But during high-intensity exercise a major portion (and where blood flow is impaired, then most) is accumulated as lactate anions and H(+). The accumulation of H(+) has deleterious effects on muscle function, ultimately impairing force production and contributing to fatigue. Regulation of intracellular pH is achieved over time by export of H(+) out of the muscle, although physicochemical buffers in the muscle provide the first line of defence against H(+) accumulation. In order to be effective during high-intensity exercise, buffers need to be present in high concentrations in muscle and have pK(a)s within the intracellular exercise pH transit range. Carnosine (ß-alanyl-L-histidine) is ideal for this role given that it occurs in millimolar concentrations within the skeletal muscle and has a pK(a) of 6.83. Carnosine is a cytoplasmic dipeptide formed by bonding histidine and ß-alanine in a reaction catalysed by carnosine synthase, although it is the availability of ß-alanine, obtained in small amounts from hepatic synthesis and potentially in greater amounts from the diet that is limiting to synthesis. Increasing muscle carnosine through increased dietary intake of ß-alanine will increase the intracellular buffering capacity, which in turn might be expected to increase high-intensity exercise capacity and performance where this is pH limited. In this study we review the role of muscle carnosine as an H(+) buffer, the regulation of muscle carnosine by ß-alanine, and the available evidence relating to the effects of ß-alanine supplementation on muscle carnosine synthesis and the subsequent effects of this on high-intensity exercise capacity and performance.

ß-alanine supplementation improves YoYo intermittent recovery test performance.

BACKGROUND: ß-alanine supplementation has been shown to improve high-intensity exercise performance and capacity. However, the effects on intermittent exercise are less clear, with no effect shown on repeated sprint activity. The aim of this study was to investigate the effects of ß-alanine supplementation on YoYo Intermittent Recovery Test Level 2 (YoYo IR2) performance. METHODS: Seventeen amateur footballers were allocated to either a placebo (PLA; N = 8) or ß-alanine (BA; N = 9) supplementation group, and performed the YoYo IR2 on two separate occasions, pre and post 12 weeks of supplementation during a competitive season. Specifically, players were supplemented from early to mid-season (PLA: N = 5; BA: N = 6) or mid- to the end of the season (PLA: N = 3; BA: N = 3). Data were analysed using a two factor ANOVA with Tukey post-hoc analyses. RESULTS: Pre supplementation scores were 1185 ± 216 and 1093 ± 148 m for PLA and BA, with no differences between groups (P = 0.41). YoYo performance was significantly improved for BA (+34.3%, P ≤ 0.001) but not PLA (-7.3%, P = 0.24) following supplementation. 2 of 8 (Early - Mid: 2 of 5; Mid - End: 0 of 3) players improved their YoYo scores in PLA (Range: -37.5 to + 14.7%) and 8 of 9 (Early - Mid: 6 of 6; Mid - End: 2 of 3) improved for BA (Range: +0.0 to +72.7%). CONCLUSIONS: 12 weeks of ß-alanine supplementation improved YoYo IR2 performance, likely due to an increased muscle buffering capacity resulting in an attenuation of the reduction in intracellular pH during high-intensity intermittent exercise.

ß-alanine supplementation improves isometric endurance of the knee extensor muscles.

BACKGROUND: We examined the effect of four weeks of ß-alanine supplementation on isometric endurance of the knee extensors at 45% maximal voluntary isometric contraction (MVIC). METHODS: Thirteen males (age 23 ± 6 y; height 1.80 ± 0.05 m; body mass 81.0 ± 10.5 kg), matched for pre-supplementation isometric endurance, were allocated to either a placebo (n = 6) or ß-alanine (n = 7; 6.4 g·d-1 over 4 weeks) supplementation group. Participants completed an isometric knee extension test (IKET) to fatigue, at an intensity of 45% MVIC, before and after supplementation. In addition, two habituation tests were completed in the week prior to the pre-supplementation test and a further practice test was completed in the week prior to the post-supplementation test. MVIC force, IKET hold-time, and impulse generated were recorded. RESULTS: IKET hold-time increased by 9.7 ± 9.4 s (13.2%) and impulse by 3.7 ± 1.3 kN·s-1 (13.9%) following ß-alanine supplementation. These changes were significantly greater than those in the placebo group (IKET: t(11) = 2.9, p ≤0.05; impulse: t(11) = 3.1, p ≤ 0.05). There were no significant changes in MVIC force in either group. CONCLUSION: Four weeks of ß-alanine supplementation at 6.4 g·d-1 improved endurance capacity of the knee extensors at 45% MVIC, which most likely results from improved pH regulation within the muscle cell as a result of elevated muscle carnosine levels.

L-glutamine absorption is enhanced after ingestion of L-alanylglutamine compared with the free amino acid or wheat protein.

Differences in plasma L-glutamine (L-Gln) concentrations from ingestion of different formulations of L-Gln were examined in 8 men (26.8 ± 4.2 years old, 181.1 ± 10.9 cm, 85.8 ± 15.4 kg). Subjects reported to the laboratory on 4 separate occasions and randomly consumed 1 of 4 drinks containing 60 mg/kg of L-Gln; 89 mg/kg of Sustamine (L-alanylglutamine [AlaGln]; Kyowa Hakko Europe GmbH, Düsseldorf, Germany), which contained an equivalent L-Gln dose as consumed in L-Gln); 200 mg/kg of an enzymatically hydrolyzed wheat protein (HWP) with an L-Gln content of 31 mg/kg; or a control that consisted only of water. It was hypothesized that the AlaGln trial would increase plasma glutamine concentrations greater than the other experimental trials. Ingestion of L-Gln, AlaGln, and HWP resulted in significant increases in the plasma L-Gln concentration, peaking at 0.5, 0.5, and 0.75 hours, respectively. The corresponding mean peak increases were 179 ± 61, 284 ± 84, and 134 ± 36 µmol/L, respectively. Concentrations returned to baseline in all subjects by 2 hours after L-Gln and HWP and by 4 hours after AlaGln. Mean areas under the plasma concentration curve, calculated between 0 and 4 hours, were 127 ± 61, 284 ± 154, and 151 ± 63 µmol∙h∙L⁻¹ for L-Gln, AlaGln, and HWP, respectively. When allowance was made for the lower L-Gln dose administered as HWP, the peak plasma concentration and area under the plasma concentration curve were approximately the same as for AlaGln. The results suggest a greater transfer from the gut to plasma of L-Gln when supplied as AlaGln and possibly also as HWP compared with when the same dose was provided as the free amino acid.