Jones Rebecca Louise, Barnett Cleveland Thomas, Davidson Joel, Maritza Billy, Fraser William D, Harris Roger, Sale Craig
Musculoskeletal Physiology Research Group, Sport, Health and Performance Enhancement (SHAPE) Research Centre, School of Science and Technology, Nottingham Trent University, Erasmus Darwin Building, Clifton Lane, Clifton, Nottingham, NG11 8NS, UK.
Norwich Medical School, University of East Anglia, Norwich, Norfolk, UK.
Eur J Appl Physiol. 2017 May;117(5):867-879. doi: 10.1007/s00421-017-3569-1. Epub 2017 Mar 27.
In 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 (Ca) handling. Accumulation of hydrogen cation (H) has been shown to impact Ca signalling during muscular contraction, carnosine has the potential to serve as a cytoplasmic regulator of Ca 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.
Twenty-three males completed two experimental sessions, pre- and post- 28 day supplementation with 6.4 g.day of BA (n = 12) or placebo (PLA; n = 11). Isometric force was recorded during a series of voluntary and electrically evoked knee extensor contractions.
BA 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.
The 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.
The trial is registered with Clinicaltrials.gov, ID number NCT02819505.
在新鲜肌肉中，补充肌肽的限速前体β-丙氨酸（BA）可能会通过改变钙（Ca）的处理方式导致肌肉半松弛时间（HRT）下降。已表明氢离子（H）的积累会影响肌肉收缩过程中的钙信号传导，肌肽有可能作为Ca和H耦合的细胞质调节剂，因为它能与这两种离子结合。本研究考察了补充BA对新鲜和疲劳的人体骨骼肌内在体内等长伸膝力量产生及肌肉收缩性的影响，这些骨骼肌在自主收缩和电诱发（神经和浅表肌肉刺激）收缩过程中进行评估。
23名男性完成了两个实验阶段，分别在补充6.4克/天的BA（n = 12）或安慰剂（PLA；n = 11）28天之前和之后。在一系列自主和电诱发的膝伸肌收缩过程中记录等长力量。
补充BA对自主或电诱发的等长力量产生、抽搐机电延迟和峰值张力时间均无影响。在静息（3±13%；19±26%）和增强（1±15%；2±20%）抽搐收缩过程中，新鲜和疲劳肌肉状态下的肌肉HRT均显著下降。
补充BA后新鲜和疲劳骨骼肌中HRT降低的机制尚不清楚。由于肌肉松弛对总能量消耗的重要性，特别是在短时间重复收缩期间，补充BA可能被证明有助于最小化疲劳引起的收缩减慢。
该试验已在Clinicaltrials.gov注册，注册号为NCT02819505。
