Beta-alanine supplementation has been shown to increase skeletal muscle carnosine concentration resulting in the delay of neuromuscular fatigue and an increased aerobic and anaerobic capacity. The current study investigated the effects of beta-alanine supplementation on aerobic and anaerobic capacity in trained cyclists. Fourteen highly-competitive (sprint, endurance, road and track) cyclists underwent an 8 week 6.4g/day protocol (beta-alanine and maltodextrin). Pre and post supplementation testing included a VO₂max test (familiarization and characterization), maximum aerobic power test (aerobic capacity), and 30s wingate anaerobic test (anaerobic capacity). Aerobic capacity parameter measures included aerobic and anaerobic thresholds, and maximum aerobic power, while anaerobic capacity parameters included fatigue index, average power, peak power, watts per kilogram, and final lactate concentration. There was a lack of change in aerobic and anaerobic capacity parameters post supplementation for both groups. Assuming an increase in skeletal muscle carnosine concentration, results suggest 8 weeks 6.4g/day beta-alanine does not increase aerobic and anaerobic capacity in trained cyclists. This lack of change has 3 potential explanations; carnosines’ physicochemical H⁺ buffering ability was not substantially elevated to prevent muscular fatigue via acidosis, pH decrease is only one limiting factor in aerobic and anaerobic capacity, or other factors (neuromuscular junction failure, contractile failure, substrate depletion, metabolite accumulation, oxidative stress) influence muscular fatigue.

No description available.

<p>Muscle fatigue has always been of vital importance in most sports. A few possible factors have been reported to be the cause of muscular fatigue during high intensity exercise; depletion of glycogen, oxidative stress, disruption of contractile mechanisms and accumulation of metabolites. One of the theories of the cause of muscular fatigue, both in endurance and intermittent sports, is decreased pH levels due to increased concentration of H+ ions dissociated from lactic acid in muscle. Carnosine, a fairly unnoticed ergogenic aid, taken in the form of β-alanine has shown to potentially delay the onset of fatigue. Supplementation of β-alanine, would increase carnosine levels in muscle and may counteract the decrease in pH since carnosine functions as a H+ buffer. The purpose of the present study was to examine the effects of 8 weeks supplementation of β-alanine in distance runners and Swedish division four soccer players on aerobic capacity, intermittent recovery and muscular fatigue. The runners (n = 15) were tested in lactate profiling tests and the soccer players (n = 22) were tested in the Yo-Yo intermittent endurance test pre and post the 8-week test-period. The yo-yo test did not result in significant difference between the soccer players’ β-group and control-group (p = 0,29). Neither did the lactate test result in significant differences between the distance runners’ β-group and control-group in any of the five variables measured. However, a trend in difference was seen between groups in both velocity at lactate threshold (VLT) (p = 0,11) and recovery blood lactate (RBL) (p = 0,14) where the β-group had increased slightly from 16,8 ± 1,6 km/h to 17,0 ± 1,2 km/h in VLT and decreased from 4,5 ± 1,6 mmol∙L-1 to 3,1 ± 1,0 mmol∙L-1 in RBL. The results suggested that β-alanine may delay the onset of fatigue and improve performance in endurance sports such as running by increasing the removal of lactate acid from muscle.</p>

Early research with beta-alanine (beta-ALA) supplementation has shown increases in muscle carnosine as well as improvements in body composition, exercise performance and blood lactate levels. Creatine monohydrate supplementation has been extensively researched for its effects on anaerobic exercise performance. Recently, a new line of studies have examined the combined effects beta-ALA and creatine supplementation on anaerobic exercise performance and lactate threshold. The purpose of the present study is to examine the acute and chronic effects of beta-ALA supplementation with and without creatine monohydrate on body composition, aerobic and anaerobic exercise performance, and muscle carnosine and phosphagen levels in college-aged recreationally active females. Thirty-two females were randomized in a double-blind placebo controlled manner into one of four supplementation groups including beta-ALA only, creatine only, beta-ALA and creatine combined and placebo. Participants supplemented for four weeks and reported for testing at baseline, day 7 and day 28. Testing sessions consisted of a resting muscle biopsy of the vastus lateralis, body composition measurements, a graded exercise test on the cycle ergometer for VO2max and lactate threshold, and multiple Wingate tests for anaerobic exercise performance. Results showed all supplementation strategies increasing muscle carnosine levels over placebo after four weeks, but not between groups. Muscle creatine increased for all groups after four weeks, but not between groups. There were improvements for all groups with body composition after four weeks, despite the present study not including a specific training protocol. There were no group differences observed for aerobic exercise, blood lactate levels, lactate threshold, ventilatory threshold, peak power, mean power, total work or rate of fatigue. There were some trends for anaerobic exercise indicating groups supplementing with creatine may have greater improvements, however, these findings were not statistically significant. The present study failed to show any additive effects of beta-ALA and creatine supplementation for body composition, aerobic exercise, lactate threshold or anaerobic exercise measures. This could be due to the small sample size resulting in low power and effect sizes. Previous research has demonstrated that four weeks of beta-ALA and creatine supplementation was enough time to increase muscle carnosine and phosphagen levels. However, perhaps more time is needed for performance adaptations to occur, especially without the addition of an exercise training component.

Muscle fatigue has always been of vital importance in most sports. A few possible factors have been reported to be the cause of muscular fatigue during high intensity exercise; depletion of glycogen, oxidative stress, disruption of contractile mechanisms and accumulation of metabolites. One of the theories of the cause of muscular fatigue, both in endurance and intermittent sports, is decreased pH levels due to increased concentration of H+ ions dissociated from lactic acid in muscle. Carnosine, a fairly unnoticed ergogenic aid, taken in the form of β-alanine has shown to potentially delay the onset of fatigue. Supplementation of β-alanine, would increase carnosine levels in muscle and may counteract the decrease in pH since carnosine functions as a H+ buffer. The purpose of the present study was to examine the effects of 8 weeks supplementation of β-alanine in distance runners and Swedish division four soccer players on aerobic capacity, intermittent recovery and muscular fatigue. The runners (n = 15) were tested in lactate profiling tests and the soccer players (n = 22) were tested in the Yo-Yo intermittent endurance test pre and post the 8-week test-period. The yo-yo test did not result in significant difference between the soccer players’ β-group and control-group (p = 0,29). Neither did the lactate test result in significant differences between the distance runners’ β-group and control-group in any of the five variables measured. However, a trend in difference was seen between groups in both velocity at lactate threshold (VLT) (p = 0,11) and recovery blood lactate (RBL) (p = 0,14) where the β-group had increased slightly from 16,8 ± 1,6 km/h to 17,0 ± 1,2 km/h in VLT and decreased from 4,5 ± 1,6 mmol∙L-1 to 3,1 ± 1,0 mmol∙L-1 in RBL. The results suggested that β-alanine may delay the onset of fatigue and improve performance in endurance sports such as running by increasing the removal of lactate acid from muscle.

No description available.

No description available.

A disponibilidade de beta-alanina é o fator limitante para a síntese intramuscular de carnosina. Dessa maneira, aumentar a disponibilidade de beta-alanina para o músculo esquelético é a estratégia mais eficaz para aumentar o conteúdo de carnosina muscular. Postula-se que o transportador de beta-alanina (TauT) possa ser estimulado pela insulina. Para testar essa hipótese, examinamos se a captação de beta-alanina pelo músculo esquelético de humanos é influenciada pela hiperinsulinemia, controlando as concentrações de insulina e beta-alanina no plasma através de infusão intravenosa aguda de beta-alanina. Realizamos um estudo crossover e contrabalanceado em 12 homens jovens e saudáveis (27,5±5,1 anos). Os participantes compareceram ao laboratório em duas ocasiões separadas por 10 semanas de whashout. A beta-alanina foi infundida por via intravenosa em ambos os ensaios por 150 min a uma taxa de 0,11 g.kg.min-1. Em um ensaio, a técnica de clamp euglicêmico hiperinsulinêmico foi usada para obtermos concentrações elevadas de insulina (AI), enquanto que no outro ensaio, foram mantidas concentrações de insulina em jejum (BI). Antes e 30 minutos após a infusão de beta-alanina, amostras de músculo (biópsias percutâneas) foram coletadas para determinar o conteúdo de beta-alanina e carnosina. Coletas sanguíneas foram realizadas antes (0), 10, 30, 60, 90, 120, 150 e 30 min (180) após a infusão para análise de insulina e beta-alanina plasmáticas. Urina 24 h foi coletada após o período de infusão para análise de beta-alanina. Não houve diferenças significantes entre os ensaios na concentração de beta-alanina plasmática (p=0,20), de beta-alanina muscular (p=0,72), de carnosina muscular (p=0,82) e de beta-alanina urinária (p= 0,92). A hiperinsulinemia não aumentou a captação de beta-alanina para o músculo esquelético, nem aumentou a retenção de beta-alanina corporal, pelo menos quando as concentrações de beta-alanina excederam a Vmax do TauT. Nossas descobertas sugerem que as estratégias de suplementação de beta-alanina que manipulam as concentrações de insulina provavelmente apresentam relevância clínica limitada / Beta-alanine availability is limiting for the intramuscular synthesis of carnosine. Thus, increasing beta-alanine availability to skeletal muscle is the most effective strategy to increase muscle carnosine content. It has been postulated that the transmembrane transporter of beta-alanine (TauT) could be stimulated by insulin. To test this hypothesis, we examined whether the beta-alanine uptake by human muscle is influenced by hyperinsulinemia by controlling both insulin and beta-alanine concentrations in plasma via intravenous infusion of beta-alanine. We conducted a counterbalanced crossover study in 12 young men (27.5 ± 5.1 yr). Participants attended to the laboratory on two separated occasions, 10 weeks apart. beta-alanine was intravenously infused on both trials for 150 min at a rate of 0.11 g.kg.min-1. In one trial, a hyperinsulinemic-euglycemic clamp was used to main high insulin concentrations (HI) whereas fasting insulin concentrations (LI) was maintained in the other trial. Before and 30 min after infusion, muscle samples (percutaneous biopsies) were taken to determine beta-alanine and carnosine content. Blood samples were taken before (0), 10, 30, 60, 90, 120, 150 e 30 min (180) after the infusion for plasma insulin and beta-alanine analysis. 24 h urine was colleted after infusion for beta-alanine analysis. No significant differences in plasma beta-alanine (p=0.20), muscle beta-alanine (p=0.72), muscle carnosine (p=0.82) and urinary beta-alanine (p=0.92) were shown between conditions. Hyperinsulinemia did not increase beta-alanine uptake to muscle tissue and bodily tissues, nor did it increase whole-body beta-alanine retention, at least when beta-alanine concentrations exceed the Vmax of TauT. Our findings suggest that beta-alanine supplementation strategies that maniupulate insulin concentrations are probably of limited clinical relevance

Estudos recentes têm demonstrado que a suplementação de beta-alanina (BA) pode melhorar o desempenho físico. O mecanismo proposto para tal resultado envolve o aumento das concentrações intramusculares de carnosina, um dipeptídeo cuja função mais bem atribuída é a de manutenção do equilíbrio ácido-básico. Apesar do emergente corpo literário acerca dos efeitos ergogênicos da suplementação de BA, a maior parte das evidências provém de estudos conduzidos com indivíduos não treinados ou fisicamente ativos, enquanto os estudos com indivíduos treinados são escassos, e seus resultados, controversos. Tem sido especulado que a diferença na capacidade tamponante muscular entre indivíduos treinados e não treinados é um possível fator mascarando o efeito ergogênico da suplementação de BA em indivíduos treinados, já que têm sido demonstrado que este perfil de indivíduos possui maior capacidade tamponante e conteúdo muscular de carnosina. Assim, o objetivo do presente estudo foi investigar a influência do estado de treinamento sobre o desempenho físico intermitente de membros inferiores em resposta à suplementação de BA. Para tanto, 40 homens jovens e saudáveis foram recrutados para participar do estudo, e divididos em dois grupos de acordo com o seu estado de treinamento [ciclistas treinados (T) ou indivíduos não treinados (NT)]. Os participantes foram aleatoriamente designados a um grupo suplementado com BA ou placebo (dextrose - PL), provendo quatro condições experimentais: NTPL, NTBA, TPL e TBA. A suplementação foi realizada com a ingestão de 6.4 gramas de BA ou PL por dia, durante 4 semanas. Antes e após o período de suplementação, os participantes completaram 4 séries do teste de Wingate para membro inferior, com 30 segundos de duração cada uma e 3 minutos de descanso entre elas. O trabalho total realizado foi significantemente aumentado após o período de suplementação em ambos os grupos NTBA (+1349 ± 1411 kJ; P = 0.03) e TBA (+1978 ± 1508 kJ; P = 0.002), foi significantemente reduzido no grupo NTPL (-1385 ± 2815 kJ; P = 0.03), e não se alterou no grupo TPL (-219 ± 1507 kJ; P = 0.73). Comparada ao período pré-suplementação, a potência média no período pós-suplementação foi significantemente maior na série 4 para o grupo NTBA (P = 0.0004), enquanto a mesma foi maior nas séries 1, 2 e 4 (P <= 0.05) para o grupo TBA. Não foram observadas diferenças na potência média entre o período pré- e pós-suplementação para os grupos NTPL e TPL. Em conclusão, quatro semanas de suplementação de BA foram efetivas em melhorar o desempenho físico intermitente de membros inferiores em ambos os participantes treinados e não treinados. Estes dados ressaltam a eficácia ergogênica da suplementação de BA para exercícios de alta-intensidade, independentemente do estado de treinamento do indivíduo / Recent studies have demonstrated that beta-alanine (BA) supplementation can improve performance. The proposed mechanisms for this result involve an increased muscle carnosine content, a dipeptide whose function is attributed to the maintenance of acid-base balance. Even though the body of evidence surrounding the ergogenic effects of BA supplementation is increasing, most of the evidences come from studies conducted with physically active or untrained individuals, while studies with trained participants are scarce, and their results, controversial. It has been speculated that the difference in muscle buffering capacity between trained and untrained individuals is a possible factor masking the ergogenic effect of BA supplementation in trained individuals, who have already been demonstrated to have greater buffering capacity and muscle carnosine content. Therefore, the aim of this study was to investigate the influence of training status on intermittent lower-body performance in response to BA supplementation. For this purpose, forty young males were divided into two groups according to their training status (trained - T, and untrained - NT cyclists). Participants were further randomly allocated to BA or placebo (dextrose - PL) groups, providing four experimental conditions: NTPL, NTBA, TPL, TBA. BA or PL was ingested by 6.4 g·d-1, during for 4 weeks. Before and after the supplementation period, participants completed four 30-seconds lower-body Wingate bouts, separated by 3 minutes. Total work done was significantly increased following supplementation in both NTBA (+1349 ± 1411 kJ; P = 0.03) and TBA (+1978 ± 1508 kJ; P = 0.002), and it was significantly reduced in NTPL (-1385 ± 2815 kJ; P = 0.03) with no difference for TPL (-219 ± 1507 kJ; P = 0.73). Compared to pre-supplementation, post-supplementation mean power output was significantly higher in bout 4 for NTBA (P = 0.0004), and higher in bouts 1, 2 and 4 (P <= 0.05) for TBA. No differences were observed in mean power output for NTPL and TPL from pre- to post-supplementation period. In conclusion, four weeks of BA supplementation was effective at improving intermittent lower-body performance in both untrained and trained individuals. These data highlight the efficacy of BA as an ergogenic aid for high-intensity exercise regardless of the training status of the individual

A &#946;-alanina tem se tornado um suplemento nutricional bastante popular entre atletas de diferentes modalidades esportivas. A razão para tal popularidade deve-se ao grande número de evidências indicando que sua suplementação pode aumentar as concentrações intramusculares de L-carnosina. Com a interrupção da suplementação de &#946;-alanina (BA), a degradação e eliminação da carnosina prevalecem sobre sua síntese, ocorrendo assim o chamado washout. O objetivo o presente trabalho foi avaliar a cinética de washout da carnosina durante 16 semanas após a suplementação de BA, associando as mudanças no conteúdo de carnosina muscular com o desempenho em exercício de alta intensidade. Foram recrutados 15 homens fisicamente ativos, não vegetarianos, a qual foram designados aleatoriamente em dois grupos, BA (n= 11) ou PL (n= 4). Cada participante recebeu a suplementação de BA ou PL (dextrose) em tabletes de liberação prologada (NAI®, USA) na dose de 6,4/d durante 8 semanas em um desenho duplo-cego. Amostras do músculo vasto lateral foram colhidas por meio de biópsia muscular, realizadas antes (S01) e após as 8 semanas (S02) de suplementação, bem como na 1ª (W01), 2ª (W02) 4ª (W03), 8ª (W04), 12ª (W05) e 16ª (W06) semanas após suplementação. Adicionalmente, um teste de tolerância ao esforço de alta intensidade (110% da potência máxima) foi aplicado no tempo S01 e S02, assim como nos tempos W03, W04, W05 e W06 para determinar o Tempo até a Exaustão (TTE). Após 8 semanas de suplementação, foi observada uma diferença significante do conteúdo de carnosina muscular entre o grupo BA (40,76± 12,29 mmol/Kg) e o grupo PL (18,74± 1,22 mmol/Kg; p= 0,0040). O delta médio absoluto observado do grupo BA foi de 18,73± 5,80 mmol/Kg (+ 85%) e, o grupo PL - 0,15± 1,78 mmol/Kg (- 0,7%). Após W02 o grupo BA apresentava 17,35± 8,99 mmol/Kg de carnosina (~ 79%; p= 0,4667) e após W03, o conteúdo médio verificado foi 12,43± 8,95 mmol/Kg (~ 56%) no grupo BA, (p= 0,0378). Após W04 o grupo BA apresentava o delta médio de 6,9± 8,30 mmol/Kg (~ 38%; p <0,0001) e após W05, 2,91± 6,76 mmol/Kg (~ 13%; p <0,0001). Após W06, o conteúdo de carnosina retornou próximo aos valores basais em 21,91± 7,99 mmol/Kg (p = 1,000). Após o período de suplementação (S02), o TTE não apresentou diferença significante entre o grupo BA, 150,95± 19,31 segundos, e o grupo PL, 153,78± 13,08 (p= 0,8184). Foi possível observar uma forte correlação linear positiva (r= 0,8995) e significante (p= 0,01492) entre o conteúdo de carnosina muscular e o desempenho físico. Conclui-se que a carnosina é um dipeptídeo estável na musculatura esquelética, podendo levar um tempo de 16 semanas ou mais para retornar aos valores / &#946;-alanine has become a popular nutritional supplement among athletes of different sports modalities. The reason for such popularity is due to the large number of evidences indicating that its supplementation may increase intramuscular concentrations of L-carnosine. With the interruption of &#946;-alanine (BA) supplementation, the degradation and elimination of carnosine prevail over its synthesis, thus occurring the washout. The aim of this study was to evaluate carnosine washout kinetics for 16 weeks after BA supplementation, associating changes in muscle carnosine content with high intensity exercise performance. Fifteen physically active, non-vegetarian males were randomly assigned in two groups, BA (n = 11) or PL (n = 4). Each participant received supplementation of BA or PL (dextrose) in sustained-release tablets (NAI®, USA) at a dose of 6.4g. d-1 for 8 weeks in a double-blind design. Samples of the vastus lateralis muscle were collected by muscle biopsy performed before (S01) and after 8 weeks (S02) of supplementation, additionally in the 1st (W01), 2nd (W02) 4th (W03), 8th (W04), 12th (W05) and 16th (W06) weeks after supplementation. In addition, a high intensity exercise test (110% of maximum power) was performed at time S01 and S02, W03, W04, W05 and W06 to determine Time to Exhaustion (TTE). After 8 weeks of supplementation, a significant difference in muscle carnosine content was observed between the BA group (40.76 ± 12.29 mmol.kg-1) and the PL group (18.74 ± 1.22 mmol.kg-1; p= 0.0040). The absolute mean delta of the BA group was 18.73± 5.80 mmol.kg-1 (+ 85%) and, the PL group - 0.15± 1.78 mmol.kg-1 (-0.7%). After W02 the BA group showed 17.35± 8.99 mmol.kg-1 carnosine (~ 79%, p= 0.4667), and after W03, the mean content was 12.43 ± 8.95 mmol.kg-1 (~ 56%) in the BA group, (p= 0.0378). After W04 the BA mean delta was 6.9 ± 8.30 mmol.kg-1 (~ 38%, p <0.0001) and after W05, 2.91± 6.76 mmol.kg- 1 (~ 13%, p <0.0001). After W06, the carnosine content returned to baseline levels in BA group 21.91 ± 7.99 mmol. Kg-1 (p = 1,000). After the supplementation period (S02), the TTE showed no significant difference between the BA group 150.95 ± 19.31 seconds and the PL group, 153.78 ± 13.08 (p= 0.8184). There was a strong positive linear correlation (r= 0.8995) and significant (p= 0.01492) between muscle carnosine content and performance. The present study shows that carnosine is a stable dipeptide in the skeletal muscle, which may take 16 weeks or longer to return to the baseline levels