Published: August 2020

Author: Trent Stellingwerff, PhD 

INTRODUCTION

Athletes participating in high-intensity sports/events (~1-10 min of all-out effort), or in sports where athletes are required to make repeated high-intensity efforts, have unique performance determinants. All of these sports use large amounts of anaerobically derived adenosine triphosphate (ATP) energy production from phosphocreatine and anaerobic glycolysis, the latter resulting in large amounts of lactate accumulation (>10 mmol/L). The diversity of these unique high-intensity performance determinates is especially prevalent in the middle-distance/high-intensity based events, which feature a blend of aerobic, anaerobic and neuromuscular/mechanical characteristics (Sandford & Stellingwerff, 2019) and many of these determinates are linked to nutritional interventions (Stellingwerff, Bovim, & Whitfield, 2019). Indeed, the limits to high-intensity performance are multifactorial, but a major limiting factor is the ability to tolerate ever increasing levels of muscle acidosis; both intra- and extra-cellular. To enhance extra-cellular buffering, sodium-bicarbonate loading has been researched and utilized by athletes for many decades. However, it was only in the mid-2000’s that pioneering work by Prof. Roger Harris and colleagues (2006) demonstrated that augmenting intra-cellular (within muscle) buffering was also possible via chronic (several weeks) beta-alanine supplementation, which significantly increased muscle carnosine (b-alanyl-L-histidine) and high-intensity performance (Hill et al., 2007) (Figure 1). Since this time, there has been an explosion of research examining the efficacy of beta-alanine supplementation to optimally augment the muscle carnosine content and enhance subsequent performance. 

KEY POINTS 

·       Fatigue during ~1-10 min of high-intensity sports/events is multifactorial, but there are strong mechanistic underpinnings demonstrating skeletal muscle acidosis, via accumulating hydrogen ion (H+), to be a key performance limiter. Accordingly, skeletal muscle has various innate intra- and extra-cellular buffering mechanisms to address exercise-induced acidosis.

·       Carnosine is a key intra-cellular buffer due to its nitrogen containing imidazole side ring, which can accept (buffer) H+and slow the decline in muscle pH during intense exercise and contribute as much as ~15% to total buffering capacity.

 ·       Beyond its role in buffering, carnosine has also been shown to be a diffusible calcium (Ca2+)/H+ exchanger, delivering Ca2+ back to the sarcoplasmic reticulum and H+ away to the cell membrane, suggesting that it might also enhance muscle Ca2+ sensitivity and contraction efficiency.

·       Carnosine in muscle is synthesized by carnosine synthase, in which the plasma beta-alanine concentration is the rate limiting substrate; consistent data has demonstrated that ~3-6 g beta-alanine over at least 4 weeks of supplementation can augment muscle carnosine stores by 30-60%.

·       Several meta-analyses have shown moderate effect sizes for exercise capacity, and smaller effect sizes for exercise performance over ~1-10 min duration. This translates into ~2-3 % performance benefits in non-elite subjects, but ~0.5-1% increases in elite subjects. However, more data is required in elite athlete cohorts.

·       Despite significant increases in scientific knowledge regarding beta-alanine supplementation protocols and performance efficacy since 2006, there are many prevailing questions and future applied research directions that remain.