A suplementação com vitamina C e E pode inibir as adaptações ao treinamento físico aeróbio? / Does vitamin C and E supplementation inhibit aerobic exercise training adaptations?

Cronicamente, o exercício aeróbio promove inúmeros benefícios sobre o desempenho físico e a saúde. No entanto, sessões agudas de exercício aeróbio induzem a produção de Radicais Livres, cujo acúmulo está associado a diversos efeitos prejudiciais sobre a célula, e em última instância, sobre a saúde. Apesar da existência de defesas antioxidantes nas células musculares, e da sugestão de que a presença dos Radicais Livres funcionaria como um importante gatilho para algumas adaptações ao treinamento físico, é crescente o número de trabalhos investigando se a suplementação com antioxidantes, tais como as Vitaminas C e E, pode atenuar o surgimento dos Radicais Livres produzidos durante o exercício e treinamento aeróbio. É igualmente crescente o número de estudos averiguando se a suplementação com antioxidantes poderia interferir com certas adaptações ao treinamento aeróbio. Logo, o objetivo deste Ponto de Vista foi examinar se as evidências literárias permitem concluir se a suplementação com antioxidantes inibe a adaptação das defesas antioxidantes endógenas, de fatores relacionados ao conteúdo e função mitocondriais, e do consumo máximo de oxigênio. Observou-se escassez e controvérsia entre os diferentes estudos, onde fatores relacionados ao baixo número amostral, ao curto período de exposição aos protocolos de treinamento, e à ausência de padronização nas medidas fisiológicas sendo mensuradas bem como da caracterização do estado antioxidante basal ainda causam dificuldade no estabelecimento de conclusões definitivas. Entretanto, as poucas evidências oriundas de estudos bem controlados sugerem que algumas adaptações, em especial aquelas relacionadas à biogênese e atividade mitocondrial, podem ser inibidas com a adição das Vitaminas C e/ou E ao treinamento aeróbio...(AU)

Chronically, aerobic exercise promotes several benefits on exercise performance and health. However, acute sessions of aerobic exercise induce the production of Free Radicals, which accumulation is associated with several harmful effects on the cell, and ultimately on health. Despite the existence of antioxidant defenses within muscle cells, and the suggestion that the presence of Free Radicals would act as an important trigger for some adaptations to exercise training, there is a growing number of studies investigating whether supplementation with antioxidants, such as Vitamins C and E, can attenuate the occurrence of Free Radicals produced during exercise and aerobic training. The number of studies investigating whether antioxidant supplementation could interfere with certain adaptations to aerobic training is also increasing. Therefore, the aim of this Point of View was to examine whether evidence allow us to conclude if antioxidant supplementation inhibits the adaptation of endogenous antioxidant defenses, factors related to mitochondrial content and function, and maximal oxygen uptake. It was observed scarcity and controversy among the different studies, where factors related to the low sample size, the short period of exposure to the training protocols, and the lack of standardization in the physiological measures being measured as well as of the characterization of the basal antioxidant status still cause difficulty in establishing definitive conclusions. However, the few evidence from well-controlled studies suggest that some adaptations, especially those related to mitochondrial biogenesis and activity, may be inhibited with the addition of Vitamins C and/or E to aerobic training...(AU)

A Systematic Risk Assessment and Meta-Analysis on the Use of Oral ß-Alanine Supplementation.

ß-Alanine supplementation is one of the world's most commonly used sports supplements, and its use as a nutritional strategy in other populations is ever-increasing, due to evidence of pleiotropic ergogenic and therapeutic benefits. Despite its widespread use, there is only limited understanding of potential adverse effects. To address this, a systematic risk assessment and meta-analysis was undertaken. Four databases were searched using keywords and Medical Subject Headings. All human and animal studies that investigated an isolated, oral, ß-alanine supplementation strategy were included. Data were extracted according to 5 main outcomes, including 1) side effects reported during longitudinal trials, 2) side effects reported during acute trials, 3) effect of supplementation on circulating health-related biomarkers, 4) effect of supplementation on skeletal muscle taurine and histidine concentration, and 5) outcomes from animal trials. Quality of evidence for outcomes was ascertained using the Grading of Recommendations Assessment Development and Evaluation (GRADE) framework, and all quantitative data were meta-analyzed using multilevel models grounded in Bayesian principles. In total, 101 human and 50 animal studies were included. Paraesthesia was the only reported side effect and had an estimated OR of 8.9 [95% credible interval (CrI): 2.2, 32.6] with supplementation relative to placebo. Participants in active treatment groups experienced similar dropout rates to those receiving the placebo treatment. ß-Alanine supplementation caused a small increase in circulating alanine aminotransferase concentration (effect size, ES: 0.274, CrI: 0.04, 0.527), although mean data remained well within clinical reference ranges. Meta-analysis of human data showed no main effect of ß-alanine supplementation on skeletal muscle taurine (ES: 0.156; 95% CrI: -0.38, 0.72) or histidine (ES: -0.15; 95% CrI: -0.64, 0.33) concentration. A main effect of ß-alanine supplementation on taurine concentration was reported for murine models, but only when the daily dose was ≥3% ß-alanine in drinking water. The results of this review indicate that ß-alanine supplementation within the doses used in the available research designs, does not adversely affect those consuming it.

Dispelling the myth that habitual caffeine consumption influences the performance response to acute caffeine supplementation.

This study investigates the influence of habitual caffeine intake on aerobic exercise-performance responses to acute caffeine supplementation. A double-blind, crossover, counterbalanced study was performed. Forty male endurance-trained cyclists were allocated into tertiles, according to their daily caffeine intake: low (58 ± 29 mg/d), moderate (143 ± 25 mg/d), and high (351 ± 139 mg/d) consumers. Participants completed three trials in which they performed simulated cycling time trials (TTs) in the fastest time possible following ingestion of the following: caffeine (CAF: 6 mg/kg body mass), placebo (PLA), and no supplement (CON). A mixed-model analysis revealed that TT performance was significantly improved in CAF compared with PLA and CON (29.92 ± 2.18 vs. 30.81 ± 2.67 and 31.14 ± 2.71 min, respectively; P = 0.0002). Analysis of covariance revealed no influence of habitual caffeine intake as a covariate on exercise performance (P = 0.47). TT performance was not significantly different among tertiles (P = 0.75). No correlation was observed between habitual caffeine intake and absolute changes (CAF - CON) in TT performance with caffeine (P = 0.524). Individual analysis showed that eight, seven, and five individuals improved above the variation of the test in CAF in the low, moderate, and high tertiles, respectively. A Fisher's exact test did not show any significant differences in the number of individuals who improved in CAF among the tertiles (P > 0.05). Blood lactate and ratings of perceived exertion were not different between trials and tertiles (P > 0.05). Performance effects of acute caffeine supplementation during an ~30-min cycling TT performance were not influenced by the level of habitual caffeine consumption.NEW & NOTEWORTHY There has been a long-standing paradigm that habitual caffeine intake may influence the ergogenicity of caffeine supplementation. Low, moderate, and high caffeine consumers showed similar absolute and relative improvements in cycling time-trial performance following acute supplementation of 6 mg/kg body mass caffeine. Performance effects of acute caffeine were not influenced by the level of habitual caffeine consumption, suggesting that high habitual caffeine intake does not negate the benefits of acute caffeine supplementation.

Nutritional Strategies to Modulate Intracellular and Extracellular Buffering Capacity During High-Intensity Exercise.

Intramuscular acidosis is a contributing factor to fatigue during high-intensity exercise. Many nutritional strategies aiming to increase intra- and extracellular buffering capacity have been investigated. Among these, supplementation of beta-alanine (~3-6.4 g/day for 4 weeks or longer), the rate-limiting factor to the intramuscular synthesis of carnosine (i.e. an intracellular buffer), has been shown to result in positive effects on exercise performance in which acidosis is a contributing factor to fatigue. Furthermore, sodium bicarbonate, sodium citrate and sodium/calcium lactate supplementation have been employed in an attempt to increase the extracellular buffering capacity. Although all attempts have increased blood bicarbonate concentrations, evidence indicates that sodium bicarbonate (0.3 g/kg body mass) is the most effective in improving high-intensity exercise performance. The evidence supporting the ergogenic effects of sodium citrate and lactate remain weak. These nutritional strategies are not without side effects, as gastrointestinal distress is often associated with the effective doses of sodium bicarbonate, sodium citrate and calcium lactate. Similarly, paresthesia (i.e. tingling sensation of the skin) is currently the only known side effect associated with beta-alanine supplementation, and it is caused by the acute elevation in plasma beta-alanine concentration after a single dose of beta-alanine. Finally, the co-supplementation of beta-alanine and sodium bicarbonate may result in additive ergogenic gains during high-intensity exercise, although studies are required to investigate this combination in a wide range of sports.

Lactato: de causa da fadiga a suplemento ergogênico? / Lactate: from cause of fatigue to ergogenic supplement?

Durante anos, pesquisadores inseridos na área de fisiologia do exercício apontaram para o lactato como o principal causador da fadiga durante exercícios de alta intensidade. Hoje, por outro lado, já existem diversos estudos demonstrando que o lactato per se não possui qualquer efeito sobre a fadiga neste tipo de exercício, mas que a acidose muscular, ocasionada pelo acúmulo de íons hidrogênio no interior da célula muscular, seria o fator limitante para o desempenho físico durante exercícios físicos de alta intensidade. Assim, estratégias com o objetivo de atenuar a queda do pH intramuscular, como a suplementação de beta-alanina e bicarbonato de sódio, têm se destacado no cenário esportivo. Embora anteriormente destacado como vilão durante esforços intensos, a suplementação de lactato vem recebendo especial atenção em anos recentes. A suplementação com este composto teoricamente pode aumentar os níveis sanguíneos de pH e bicarbonato, aumentando a capacidade de tamponamento extracelular, e por consequência, o desempenho físico. A suplementação com lactato também pode aumentar os níveis sanguíneos deste composto, aumentando sua disponibilidade como substrato para a gliconeogênese. Assim, estudos tem surgido com o intuito de avaliar a eficácia do lactato como tamponante e como substrato energético. Os poucos estudos até agora conduzidos, entretanto, não nos permitem atestar a eficácia ergogênica desta estratégia nutricional. A falta de estudos dose-resposta sobre as variáveis sanguíneas que caracterizam o mecanismo de ação do lactato, bem como de aplicação de testes físicos com baixo coeficiente de variação e boa validade externa exemplificam a necessidade de mais estudos investigando a eficácia ergogênica desta estratégia nutricional.

For years, researchers from the exercise physiology field pointed to lactate as the main cause of fatigue during high-intensity exercises. Today, however, there are several studies demonstrating that lactate per se does not have any effect on fatigue during this type of exercise, but muscle acidosis occasioned by hydrogen ions accumulation inside the muscle cell would be the limiting factor for performance during high-intensity exercises. Therefore strategies aiming to attenuate the decrease of intramuscular pH levels, like beta-alanine and sodium bicarbonate supplementation, have been prominent in the sports scenario. Although previously highlighted as a villain during high-intensity exercises, lactate supplementation has received special attention in recent years. Supplementation with this compound can theoretically increase blood pH and bicarbonate levels, increasing the extracellular buffering capacity, and hence, performance. Lactate supplementation can also increase lactate blood levels, increasing its availability as a substrate for gluconeogenesis. Thus, studies have arisen aiming to assess the effectiveness of lactate as a buffering agent and as an energy substrate. The few studies so far conducted, however, do not allow us to attest the ergogenic effectiveness of this nutritional strategy. The lack of dose-response studies on blood variables that characterize lactate mechanism of action, as well as the application of physical tests with a low coefficient of variation and good external validity exemplifies the need for further studies investigating the ergogenic effectiveness of this nutritional strategy.

The effects of two different doses of calcium lactate on blood pH, bicarbonate, and repeated high-intensity exercise performance.

We investigated the effects of low- and high-dose calcium lactate supplementation on blood pH and bicarbonate (Study A) and on repeated high-intensity performance (Study B). In Study A, 10 young, physically active men (age: 24 ± 2.5 years; weight: 79.2 ± 9.45 kg; height: 1.79 ± 0.06 m) were assigned to acutely receive three different treatments, in a crossover fashion: high-dose calcium lactate (HD: 300 mg · kg(-1) body mass), low-dose calcium lactate (LD: 150 mg · kg(-1) body mass) and placebo (PL). During each visit, participants received one of these treatments and were assessed for blood pH and bicarbonate 0, 60, 90, 120, 150, 180, and 240 min following ingestion. In Study B, 12 young male participants (age: 26 ± 4.5 years; weight: 82.0 ± 11.0 kg; height: 1.81 ± 0.07 m) received the same treatments of Study A. Ninety minutes after ingestion, participants underwent 3 bouts of the upper-body Wingate test and were assessed for blood pH and bicarbonate 0 and 90 min following ingestion and immediately after exercise. In Study A, both HD and LD promoted slight but significant increases in blood bicarbonate (31.47 ± 1.57 and 31.69 ± 1.04 mmol · L(-1, respectively) and pH levels (7.36 ± 0.02 and 7.36 ± 0.01, respectively), with no effect of PL. In Study B, total work done, peak power, mean power output were not affected by treatments. In conclusion, low- and high-dose calcium lactate supplementation induced similar, yet very discrete, increases in blood pH and bicarbonate, which were not sufficiently large to improve repeated high-intensity performance.

The ergogenic effect of beta-alanine combined with sodium bicarbonate on high-intensity swimming performance.

We investigated the effect of beta-alanine (BA) alone (study A) and in combination with sodium bicarbonate (SB) (study B) on 100- and 200-m swimming performance. In study A, 16 swimmers were assigned to receive either BA (3.2 g·day(-1) for 1 week and 6.4 g·day(-1) for 4 weeks) or placebo (PL; dextrose). At baseline and after 5 weeks of supplementation, 100- and 200-m races were completed. In study B, 14 were assigned to receive either BA (3.2 g·day(-1) for 1 week and 6.4 g·day(-1) for 3 weeks) or PL. Time trials were performed once before and twice after supplementation (with PL and SB), in a crossover fashion, providing 4 conditions: PL-PL, PL-SB, BA-PL, and BA-SB. In study A, BA supplementation improved 100- and 200-m time-trial performance by 2.1% (p = 0.029) and 2.0% (p = 0.0008), respectively. In study B, 200-m time-trial performance improved in all conditions, compared with presupplementation, except the PL-PL condition (PL-SB, +2.3%; BA-PL, +1.5%; BA-SB, +2.13% (p < 0.05)). BA-SB was not different from BA-PL (p = 0.21), but the probability of a positive effect was 78.5%. In the 100-m time-trial, only a within-group effect for SB was observed in the PL-SB (p = 0.022) and BA-SB (p = 0.051) conditions. However, 6 of 7 athletes swam faster after BA supplementation. The probability of BA having a positive effect was 65.2%; when SB was added to BA, the probability was 71.8%. BA and SB supplementation improved 100- and 200-m swimming performance. The coingestion of BA and SB induced a further nonsignificant improvement in performance.