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Clinical Trial Summary

Carnosine (made by bonding β-alanine and histidine) has been suggested to contribute to the extension of physical exercise, counteracting the decline in muscle performance due to fatigue. However this process is largely restricted by the levels of β-alanine available in the human body. Carnosine levels can be raised through long term ingestion of food products, such as meat, fish and poultry, however it can also be significantly increased by β-alanine supplementation. Improved β-alanine levels can potentially advance exercise capacity and exercise performance, which may have been previously limited. Recently research has demonstrated no beneficial effect of β-alanine supplementation on neuromuscular performance in active, healthy males when they were well rested, with no prior exercise or fatigue of the assessed muscle. It remains unknown if β-alanine supplementation would aid physical performance when the muscle has already been fatigued. This is currently being investigated in older adults (60-80 years), however there is no clear comparison between the potential effects in younger and older participants.

Therefore this investigation hopes to examine the effects of 4 week β-alanine supplementation on lower limb contractile and force properties, pre and post muscle specific fatigue in 18-30 year old males.


Clinical Trial Description

Carnosine (β-alanyl-L-histidine) is a naturally occurring dipeptide formed by bonding histidine and β-alanine in a reaction catalysed by carnosine synthase. One role of carnosine within the human system, is as an intracellular pH buffer due to its pKa of 6.83. Carnosine is suitable over the whole exercise induced intramuscular pH transit-range. Carnosine in untrained populations can neutralise 2.4 to 10.1mmol H+.kg-1 of dry mass muscle as intramuscular pH declines, adding at least 7% to 10% to total intramuscular buffering capacity. It has also been argued that carnosine in combination with anserine can contribute as much as 40% to the buffering capacity between pH ranges of 6.5 to 7.5. β-alanine has been suggested as the rate limiting factor for muscle carnosine synthesis, through ingestion of β-alanine in diet (meat, fish and poultry) or via short-term supplementation, demonstrating significant increases in muscle carnosine concentrations. Increases in carnosine concentrations between 40% and 80% have been shown, depending upon dose (between 3.2 and 6.4 g·d-1) and duration of administration (between 4 and 10 weeks). Increasing β-alanine concentrations therefore enhance carnosine synthesis with the muscle fibers and improves intramuscular buffering capacity. Exercise performance and capacity measurements that previously were limited by the accumulation of H+ have been demonstrated significant improvements through supplementation with β-alanine.

Research already conducted at Nottingham Trent University and approved by this ethical advisory committee has demonstrated no significant effect of β-alanine supplementation on neuromuscular performance in healthy, active males. However, this research was conducted with well rested participants, with no prior exercise or fatigue of the assessed muscle; therefore there was no accumulation of H+ demonstrated within the muscle. These previous investigations are therefore contemplating how β-alanine supplementation alters performance when intramuscular buffering has not been altered (at the start of the exercise), whereas the proposed study will examine the effect of β-alanine supplementation on performance when intramuscular pH has already been challenged (due to fatiguing exercise). It is hypothesised that β-alanine supplementation over 4 weeks will beneficially alter the contractile and force properties of the muscle fibres within the lower limb muscles, improving physical performance when the muscle is already fatigued.

Aims of the project:

To examine the effects of 4 week β-alanine supplementation on knee extensor contractile and force properties, pre and post induced muscle specific fatigue in 18-30 year old males. ;


Study Design

Allocation: Non-Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Investigator, Outcomes Assessor), Primary Purpose: Basic Science


Related Conditions & MeSH terms


NCT number NCT02819505
Study type Interventional
Source Nottingham Trent University
Contact
Status Completed
Phase Phase 4
Start date December 2014
Completion date August 2015

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