Blood alkalosis, as indicated by an increased blood bicarbonate concentration and pH, has been shown to be beneficial for exercise performance. Sodium bicarbonate, sodium citrate, and sodium or calcium lactate, can all result in increased circulating bicarbonate and have all independently been shown to improve exercise capacity and performance under various circumstances. Although there is considerable evidence demonstrating the efficacy of these supplements in several sports-specific situations, it is commonly acknowledged that their efficacy is equivocal, due to contrasting evidence. Herein, we discuss the physiological and environmental factors that may modify the effectiveness of these supplements including, (i) absolute changes in circulating bicarbonate; (ii) supplement timing, (iii) the exercise task performed, (iv) monocarboxylate transporter (MCT) activity; (v) training status, and (vi) associated side-effects. The aim of this narrative review is to highlight the factors which may modify the response to these supplements, so that individuals can use this information to attempt to optimize supplementation and allow the greatest possibility of an ergogenic effect.

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Supplementation with β-alanine (BA) increases muscle carnosine content, although the amount of BA used for muscle carnosine loading has been suggested to be low. However, methodological issues may have underestimated the amount of BA used. The aim of this study was to determine the estimated amount of BA converted to muscle carnosine, using a retrospective analysis from a 4-week randomized controlled trial investigating the effects of BA supplementation on muscle carnosine content of the m. vastus lateralis. Twenty-five males (age 27±5 years, height 1.74±0.09 m, body mass 77.4±11.5 kg) were supplemented with 6.4 g·day-1 of BA (N=17) or placebo (PL; N=8) for 28 days. Pre- and postsupplementation participants provided a muscle biopsy subsequently analysed for carnosine content using HPLC. Data were analysed using mixed-models and Pearson’s correlations. Muscle carnosine content increased by +11.0±6.7 mmol·kg-1dm (P<0.0001) in BA, with no change in PL (P=0.99). The estimated amount of BA converted to muscle carnosine was 2.1±1.2% (Range: 0.5 to 4.5%) of the total dose ingested. Pearson’s correlations showed that pre-supplementation carnosine was correlated to post-supplementation carnosine in the BA group (r=0.65, r2=0.38, P=0.009), but not the absolute change in carnosine (r=-0.28, r2=0.08, P=0.28) or the amount of BA used (r=-0.31, r2=0.10, P=0.22). The estimated amount of ingested BA used for carnosine synthesis was extremely low following 4 weeks of BA supplementation at 6.4 g·day-1. Data suggest that very little of the BA ingested is used for muscle carnosine synthesis and highlights the potential for further work to optimise BA supplementation in humans.

Supplementation with β-alanine (BA) increases muscle carnosine content, although the amount of BA used for muscle carnosine loading has been suggested to be low. However, methodological issues may have underestimated the amount of BA used. The aim of this study was to determine the estimated amount of BA converted to muscle carnosine, using a retrospective analysis from a 4-week randomized controlled trial investigating the effects of BA supplementation on muscle carnosine content of the m. vastus lateralis. Twenty-five males (age 27±5 years, height 1.74±0.09 m, body mass 77.4±11.5 kg) were supplemented with 6.4 g·day-1 of BA (N=17) or placebo (PL; N=8) for 28 days. Pre- and postsupplementation participants provided a muscle biopsy subsequently analysed for carnosine content using HPLC. Data were analysed using mixed-models and Pearson’s correlations. Muscle carnosine content increased by +11.0±6.7 mmol·kg-1dm (P<0.0001) in BA, with no change in PL (P=0.99). The estimated amount of BA converted to muscle carnosine was 2.1±1.2% (Range: 0.5 to 4.5%) of the total dose ingested. Pearson’s correlations showed that pre-supplementation carnosine was correlated to post-supplementation carnosine in the BA group (r=0.65, r2=0.38, P=0.009), but not the absolute change in carnosine (r=-0.28, r2=0.08, P=0.28) or the amount of BA used (r=-0.31, r2=0.10, P=0.22). The estimated amount of ingested BA used for carnosine synthesis was extremely low following 4 weeks of BA supplementation at 6.4 g·day-1. Data suggest that very little of the BA ingested is used for muscle carnosine synthesis and highlights the potential for further work to optimise BA supplementation in humans.