Abstract
PurposeIn fresh muscle, supplementation with the rate-limiting precursor of carnosine, β-alanine (BA), results in a decline in muscle half-relaxation time (HRT) potentially via alterations to calcium (Ca2+) handling. Accumulation of hydrogen cation (H+) has been shown to impact Ca2+ signalling during muscular contraction, carnosine has the potential to serve as a cytoplasmic regulator of Ca2+ and H+ coupling, since it binds to both ions. The present study examined the effect of BA supplementation on intrinsic in-vivo isometric knee extensor force production and muscle contractility in both fresh and fatigued human skeletal muscle assessed during voluntary and electrically evoked (nerve and superficial muscle stimulation) contractions.MethodsTwenty-three males completed two experimental sessions, pre- and post- 28 day supplementation with 6.4 g.day−1 of BA (n = 12) or placebo (PLA; n = 11). Isometric force was recorded during a series of voluntary and electrically evoked knee extensor contractions.ResultsBA supplementation had no effect on voluntary or electrically evoked isometric force production, or twitch electromechanical delay and time-to-peak tension. There was a significant decline in muscle HRT in fresh and fatigued muscle conditions during both resting (3 ± 13%; 19 ± 26%) and potentiated (1 ± 15%; 2 ± 20%) twitch contractions.ConclusionsThe mechanism for reduced HRT in fresh and fatigued skeletal muscle following BA supplementation is unclear. Due to the importance of muscle relaxation on total energy consumption, especially during short, repeated contractions, BA supplementation may prove to be beneficial in minimising contractile slowing induced by fatigue.Trial registrationThe trial is registered with Clinicaltrials.gov, ID number NCT02819505.
Highlights
Carnosine (β-alanyl-L-histidine) is a cytoplasmic dipeptide, synthesised from β-alanine (BA) and histidine and is found in high concentrations in skeletal muscle
Post hoc analysis showed that the percentage change in fresh muscle half-relaxation time (HRT) was not significantly different between the BA (−2 ± 10 ms; −3 ± 13%) and PLA group (+8 ± 16 ms; 8 ± 16%) with a large effect reported (P = 0.06; Cohen’s d = 0.9)
The key findings from the present study are: (a) no effects of BA supplementation on isometric force production capacity in either fresh or fatigued skeletal muscle, (b) the confirmation of our previous findings (Hannah et al 2015) showing altered fresh muscle relaxation speed following 28 days of BA supplementation, and (c) that the skeletal muscle relaxation speed is reduced by BA supplementation following muscle fatigue in the absence of any change to peak force production or contraction time compared to the PLA group
Summary
Carnosine (β-alanyl-L-histidine) is a cytoplasmic dipeptide, synthesised from β-alanine (BA) and histidine and is found in high concentrations in skeletal muscle. The synthesis of carnosine is limited by the availability of BA from the diet, while supplementation with BA over a number of weeks results in significant increases in the skeletal muscle carnosine content (Harris et al 2006; Hill et al 2007). Increasing skeletal muscle carnosine concentrations via BA supplementation in both upper and lower limbs has consistently been shown to benefit high-intensity exercise capacity and performance, as highlighted by several reviews (Sale et al 2010, 2013) and a recent meta-analysis (Hobson et al 2012). With a pKa of 6.83 for the histidine imidazole ring when combined with BA and the abundance of carnosine within skeletal muscle, it has been proposed that the improvements in high-intensity exercise outcomes following BA supplementation are the result of increased muscle buffering capacity over the exercise pH transit range (Hill et al 2007). Research has been limited to rodent and in-vitro models
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