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Harris R.C.,Junipa Ltd. | Sale C.,Nottingham Trent University
Medicine and Sport Science | Year: 2013

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 CO2 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 pKas within the intracellular exercise pH transit range. Carnosine (β-alanyl-l-histidine) is ideal for this role given that it occurs in millimolar concentrations within the skeletal muscle and has a pKa of 6.83. Carnosine is a cytoplasmic dipeptide formed by bonding histidine and β-alanine in a reaction catalysed by carnosine synthase, although it is the availability of β-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 β-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 β-alanine, and the available evidence relating to the effects of β-alanine supplementation on muscle carnosine synthesis and the subsequent effects of this on high-intensity exercise capacity and performance. Copyright © 2012 S. Karger AG, Basel. Source

Saunders B.,Nottingham Trent University | Sale C.,Nottingham Trent University | Harris R.C.,Junipa Ltd. | Sunderland C.,Nottingham Trent University
International Journal of Sports Physiology and Performance | Year: 2014

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. © 2014 Human Kinetics, Inc. Source

Stellingwerff T.,Nestle | Stellingwerff T.,Pacific Institute for Sport Excellence | Decombaz J.,Nestle | Harris R.C.,Junipa Ltd. | Boesch C.,University of Bern
Amino Acids | Year: 2012

Interest into the effects of carnosine on cellular metabolism is rapidly expanding. The first study to demonstrate in humans that chronic β-alanine (BA) supplementation (~3-6 g BA/day for ~4 weeks) can result in significantly augmented muscle carnosine concentrations (>50%) was only recently published. BA supplementation is potentially poised for application beyond the niche exercise and performance-enhancement field and into other more clinical populations. When examining all BA supplementation studies that directly measure muscle carnosine (n = 8), there is a significant linear correlation between total grams of BA consumed (of daily intake ranges of 1.6-6.4 g BA/day) versus both the relative and absolute increases in muscle carnosine. Supporting this, a recent dose-response study demonstrated a large linear dependency (R 2 = 0.921) based on the total grams of BA consumed over 8 weeks. The pre-supplementation baseline carnosine or individual subjects' body weight (from 65 to 90 kg) does not appear to impact on subsequent carnosine synthesis from BA consumption. Once muscle carnosine is augmented, the washout is very slow (~2%/week). Recently, a slow-release BA tablet supplement has been developed showing a smaller peak plasma BA concentration and delayed time to peak, with no difference in the area under the curve compared to pure BA in solution. Further, this slow-release profile resulted in a reduced urinary BA loss and improved retention, while at the same time, eliciting minimal paraesthesia symptoms. However, our complete understanding of optimizing in vivo delivery and dosing of BA is still in its infancy. Thus, this review will clarify our current knowledge of BA supplementation to augment muscle carnosine as well as highlight future research questions on the regulatory points of control for muscle carnosine synthesis. © 2012 Springer-Verlag. Source

Sale C.,Nottingham Trent University | Saunders B.,Nottingham Trent University | Hudson S.,Nottingham Trent University | Harris R.C.,Junipa Ltd. | Sunderland C.D.,Nottingham Trent University
Medicine and Science in Sports and Exercise | Year: 2011

Purpose: We examined the effect of β-alanine supplementation plus sodium bicarbonate on high-intensity cycling capacity. Methods: Twenty males (age = 25 ± 5 yr, height = 1.79 ± 0.06 m, body mass = 80.0 ± 10.3 kg) were assigned to either a placebo (P) or a β-alanine (BA; 6.4 g•d for 4 wk) group based on power max, completing four cycling capacity tests at110% of power max (CCT 110%) to determine time to exhaustion (TTE) and total work done. A CCT 110% was performed twice (habituation and baseline) before supplementation (with maltodextrin [MD]) and twice after supplementation (with MD and with sodium bicarbonate [SB]), using a crossover design with 2 d of rest between trials, creating four study conditions (PMD, PSB, BAMD, and BASB). Blood pH, Lactate, bicarbonate and base excess were determined at baseline, before exercise, immediately after exercise, and 5 min after exercise. Data were analyzed using repeated-measures ANOVA. Results: TTE was increased in all conditions after supplementation (+1.6% PMD, +6.5% PSB, +12.1% BAMD, and +16.2% BASB). Both BAMD and BASB resulted in significantly improved TTE compared with that before supplementation (P ≤ 0.01). Although further increases in TTE (4.1%) were shown in BASB compared with BAMD, these differences were not significant (P = 0.74). Differences in total work done were similar to those of TTE. Blood bicarbonate concentrations were significantly (P ≤ 0.001) elevated before exercise in PSB and BASB but not in PMD or BAMD. Blood lactate concentrations were significantly elevated after exercise, remaining elevated after 5 min of recovery (P ≤ 0.001) and were highest in PSB and BASB. Conclusions: Results show that BA improved high-intensity cycling capacity. However, despite a 6-s (∼4%) increase in TTE with the addition of SB, this did not reach statistical significance, but magnitude-based inferences suggested a ∼70% probability of a meaningful positive difference. © 2011 by the American College of Sports Medicine. Source

Saunders B.,Nottingham Trent University | Sunderland C.,Nottingham Trent University | Harris R.C.,Junipa Ltd. | Sale C.,Nottingham Trent University
Journal of the International Society of Sports Nutrition | Year: 2012

Background: β-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 β-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 β-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 β-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. © 2012 Saunders et al.; licensee BioMed Central Ltd. Source

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