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Do BCAAs and arginine prevent central fatigue during exercise?

Branched-chain amino acids and arginine improve performance in two consecutive days of simulated handball games in male and female athletes: a randomized trial

Study under review: Branched-chain amino acids and arginine improve performance in two consecutive days of simulated handball games in male and female athletes: a randomized trial

Introduction

Exercise fatigue is complex, stemming from both central (brain) and peripheral (muscular) origins. For example, skeletal muscle under repeated stress may deplete local energy stores and/or accumulate metabolites that disrupt enzymatic function and therefore may not be able to provide the necessary ATP in order facilitate contraction.

The skeletal muscle may also send inhibitory feedback to the brain under high effort loads via the golgi tendon apparatus in order to prevent injury, which may lead to muscular failure during resistance training. Alternatively, fatigue may involve the accumulation of serotonin[1] via tryptophan uptake into the brain. Tryptophan is the biological precursor to serotonin, and increasing levels of serotonin are linked with drowsiness, lethargy, and changes in motivation. Bioaccumulation of serotonin is the basis of the exercise-induced central fatigue[2] hypothesis, which is shown in Figure 1.

Figure 1: How BCAAs might combat central fatigue during exercise

The rate-limiting step in central serotonin synthesis is tryptophan transport into the brain. Tryptophan enters through the large neutral amino acid transporter (LNAAT). Therefore, it has been proposed that the competition between tryptophan and other compounds for the LNAAT may decrease intra-exercise serotonin production and decrease central fatigue.

Interestingly, branched chain amino acids (BCAAs) also use the LNAAT to pass through the blood-brain barrier (BBB), making them a viable option for competitive inhibition of tryptophan uptake. If this were the case, then BCAA supplementation would be an effective method for decreasing exercise-induced central fatigue via bioaccumulation of serotonin. However, previous studies on[3] humans[4] had[5] found[6] no[7] ergogenic[8] benefit[9].

In theory, BCAAs have a potential in inhibiting central fatigue. However, BCAA degradation leads to ammonia production. It has been postulated that the increase in circulating ammonia may be a limiting factor in applicability of BCAA supplementation to prevent central fatigue. Research groups may have come up empty handed due to the ammonia accumulation that occurs during periods of BCAA supplemented exercise[10]. It has been hypothesized that BCAA degradation into ammonia would effectively lead to exercise decrement[11] by affecting the brain’s central fatigue mechanisms. In this case, the introduction of arginine may mitigate the proposed effects of accumulated ammonia by stimulating the urea/ornithine cycle[12], converting the ammonia to urea and ornithine.

In addition, there has not been any data accumulated on the effects of BCAA supplementation and central fatigue with multiple days of controlled activity. A Taiwanese group proposed that BCAA and arginine would prevent the onset of central fatigue in consecutive days of exercise. This would imply that the serotonin synthesized during exercise would induce a refractory period that would affect performance on sequential day(s).

Who and what was studied?

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What were the findings?

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What does this study really tell us?

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The big picture

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Frequently Asked Questions

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What should I know?

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