Beta-Alanine supplementation augments muscle carnosine content and attenuates fatigue during repeated isokinetic contraction bouts in trained sprinters

University of Chichester, Chichester, England, United Kingdom
Journal of Applied Physiology (Impact Factor: 3.06). 12/2007; 103(5):1736-43. DOI: 10.1152/japplphysiol.00397.2007
Source: PubMed


Carnosine (beta-alanyl-l-histidine) is present in high concentrations in human skeletal muscle. The ingestion of beta-alanine, the rate-limiting precursor of carnosine, has been shown to elevate the muscle carnosine content. We aimed to investigate, using proton magnetic resonance spectroscopy (proton MRS), whether oral supplementation with beta-alanine during 4 wk would elevate the calf muscle carnosine content and affect exercise performance in 400-m sprint-trained competitive athletes. Fifteen male athletes participated in a placebo-controlled, double-blind study and were supplemented orally for 4 wk with either 4.8 g/day beta-alanine or placebo. Muscle carnosine concentration was quantified in soleus and gastrocnemius by proton MRS. Performance was evaluated by isokinetic testing during five bouts of 30 maximal voluntary knee extensions, by endurance during isometric contraction at 45% maximal voluntary contraction, and by the indoor 400-m running time. beta-Alanine supplementation significantly increased the carnosine content in both the soleus (+47%) and gastrocnemius (+37%). In placebo, carnosine remained stable in soleus, while a small and significant increase of +16% occurred in gastrocnemius. Dynamic knee extension torque during the fourth and fifth bout was significantly improved with beta-alanine but not with placebo. Isometric endurance and 400-m race time were not affected by treatment. In conclusion, 1) proton MRS can be used to noninvasively quantify human muscle carnosine content; 2) muscle carnosine is increased by oral beta-alanine supplementation in sprint-trained athletes; 3) carnosine loading slightly but significantly attenuated fatigue in repeated bouts of exhaustive dynamic contractions; and 4) the increase in muscle carnosine did not improve isometric endurance or 400-m race time.

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    • "popularity as an ergogenic aid is beta-alanine (BA), which is suggested to be effective for increasing high-intensity exercise performance (Derave et al. 2007; Hill et al. 2007). BA is a non-essential amino acid physiologically functioning as the precursor to carnosine (Culbertson et al. 2010; Smith et al. 2009), which increases the buffering capacity of H + (Derave et al. 2010; Eudy et al. 2013; Sale et al. 2010). "
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    ABSTRACT: Within the aging population, there exists a subset of individuals termed masters athletes (MA). As masters-level competition increases in popularity, MA must find methods to enhance individual athletic performance. Longitudinal beta-alanine (BA) supplementation is suggested to enhance physical capability during exercise; however, these effects have not been evaluated in MA. To examine the longitudinal effects of BA on time to exhaustion (TTE), total work completed (TWC), and lactate clearance in female MA cyclists. Twenty-two female MA (age = 53.3 ± 1.0) participated in this double-blind design. Subjects were randomly assigned to BA (n = 11; 800 mg BA + 8 g dextrose) or placebo (PLA; n = 11; 8 g dextrose) groups and supplemented 4 doses/day over 28 days. Every 7 days, subjects completed a cycling TTE at 120 % VO2max, and TWC was calculated. Blood lactate was measured at baseline, immediate post, and 20-min post each TTE. No significant differences existed between groups for any variable at baseline (p > 0.05). After 28 days supplementation, BA had greater TTE (23 vs 1 % change) and TWC (21 vs 2 % change) than PLA (p < 0.05). Following the 20-min TTE recovery, lactate was 24 % lower in BA compared to PLA (4.35 vs. 5.76 mmol/L, respectively). No differences existed for variables during intermittent weeks. 28 days of BA supplementation increased cycling performance via an enhanced time to exhaustion and total work completed with associated lactate clearance during passive rest in female MA.
    Amino Acids 08/2015; DOI:10.1007/s00726-015-2050-x · 3.29 Impact Factor
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    • "In skeletal muscle, carnosine increases with progressive glucose intolerance , suggesting that increased carnosine might be a compensatory mechanism to prevent cell damage in states of skeletal muscle insulin resistance (Stegen et al. 2015). Skeletal muscle is an important tissue in the development of insulin resistance (Abdul-Ghani and DeFronzo 2010; DeFronzo and Tripathy 2009) and over 99% of total body carnosine is located in skeletal muscle (Boldyrev 2006; Derave et al. 2007). Thus, it is possible that boosting endogenous muscle carnosine levels via carnosine administration antagonizes oxidation-and glycation-induced carbonylation and low-grade inflammation, which are characteristic of insulinresistant skeletal muscle (Bonnard et al. 2008; Kewalramani et al. 2010; Oh-Ishi et al. 2003). "
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    ABSTRACT: There is growing in vivo evidence that the dipeptide carnosine has protective effects in metabolic diseases. A critical unanswered question is whether its site of action is tissues or plasma. This was investigated using oral carnosine versus β-alanine supplementation in a high-fat diet rat model. Thirty-six male Sprague-Dawley rats received a control diet (CON), a high-fat diet (HF; 60% of energy from fat), the HF diet with 1.8% carnosine (HFcar), or the HF diet with 1% β-alanine (HFba), as β-alanine can increase muscle carnosine without increasing plasma carnosine. Insulin sensitivity, inflammatory signaling, and lipoxidative stress were determined in skeletal muscle and blood. In a pilot study, urine was collected. The 3 HF groups were significantly heavier than the CON group. Muscle carnosine concentrations increased equally in the HFcar and HFba groups, while elevated plasma carnosine levels and carnosine-4-hydroxy-2-nonenal adducts were detected only in the HFcar group. Elevated plasma and urine N(ε)-(carboxymethyl)lysine in HF rats was reduced by ∼50% in the HFcar group but not in the HFba group. Likewise, inducible nitric oxide synthase mRNA was decreased by 47% (p < 0.05) in the HFcar group, but not in the HFba group, compared with HF rats. We conclude that plasma carnosine, but not muscle carnosine, is involved in preventing early-stage lipoxidation in the circulation and inflammatory signaling in the muscle of rats.
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    • " 1 g ) of pure β - alanine was associated with symptoms of paresthesia most appropriately described as tingling and / or pins and needles . Previ - ous research has reported that , for most individuals , consuming an acute 400 - mg dose of pure β - alanine is symptom free with this dose frequently used in previous studies ( Baguet et al . , 2009 ; Derave et al . , 2007 ; Harris et al . , 2006 ) . With 500 - mg doses , no symptoms were reported and participants could not differentiate between β - alanine and placebo ( Van Thienen et al . , 2009 ) . With 800 - mg doses ( 10 mg·kg −1 ) , Harris et al . ( 2006 ) reported " mild symptoms of flushing " in two out of four partici - pants , beginning within 20"
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    ABSTRACT: β-alanine is a common ingredient in supplements consumed by athletes. Indeed, athletes may believe that the β-alanine induced paresthesia, experienced shortly after ingestion, is associated with its ergogenic effect despite no scientific mechanism supporting this notion. The present study examined changes in cycling performance under conditions of β-alanine induced paresthesia. Eight competitive cyclists (VO2max = 61.8 ± 4.2 mL·kg·min−1) performed three practices, one baseline and four experimental trials. The experimental trials comprised a 1-km cycling time trial under four conditions with varying information (i.e., athlete informed β-alanine or placebo) and supplement content (athlete received β-alanine or placebo) delivered to the cyclist: informed β-alanine/received β-alanine, informed placebo/received β-alanine, informed β-alanine/received placebo and informed placebo/received placebo. Questionnaires were undertaken exploring the cyclists’ experience of the effects of the experimental conditions. A possibly likely increase in mean power was associated with conditions in which β-alanine was administered (±95% CL: 2.2% ± 4.0%), but these results were inconclusive for performance enhancement (p = 0.32, effect size = 0.18, smallest worthwhile change = 56% beneficial). A possibly harmful effect was observed when cyclists were correctly informed that they had ingested a placebo (–1.0% ± 1.9%). Questionnaire data suggested that β-alanine ingestion resulted in evident sensory side effects and six cyclists reported placebo effects. Acute ingestion of β-alanine is not associated with improved 1-km TT performance in competitive cyclists. These findings are in contrast to the athlete’s “belief” as cyclists reported improved energy and the ability to sustain a higher power output under conditions of β-alanine induced paresthesia.
    European Journal of Sport Science 01/2015; Epub. DOI:10.1080/17461391.2015.1005696 · 1.55 Impact Factor
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