by Matt Samuels, RD
Athletes are quite familiar with localized fatigue. This can be observed during any weight training session when an exercise is taken to failure or during an endurance event when one body part fatigues before others. This localized fatigue occurs within the muscle itself and can be caused by the depletion of phosphocreatine, decreased neural stimulus to the muscle at the motor end plate,
disruption of calcium release and uptake within the sarcoplasmic reticulum (1), and the accumulation of metabolic byproducts such as lactate and ammonia (2).
While this kind of fatigue presents itself as sheer pain, another form of fatigue is central fatigue, which results from alterations in the central nervous system (CNS).
Central fatigue is critical to exercise performance since the lack of adequate CNS drive to the working muscles is the most likely explanation of fatigue in most people during normal activities (1). It is believed that central fatigue is the result of numerous physiological changes including decreased glycogen stores, decreased branched-chain amino acid (BCAA) concentrations, and increased
blood levels of free fatty acids (FFA), free tryptophan (fTryp), and serotonin (tryptophan is the precursor to serotonin).
It’s well established that when glycogen stores are depleted there is an increased utilization of FFA and BCAA as an energy source. Because FFA and tryptophan are transported in the blood attached to the same carrier (albumin), increased FFA levels will displace albumin-bound tryptophan and increase the concentration of fTryp. In turn, this leads to much larger concentrations of fTryp
in the blood. Concurrently, the increased utilization of BCAA (leucine, isoleucine, and valine) decreases the BCAA content of the blood. This is deleterious since fTryp and BCAA compete for the same transporter into the brain. Hence, when there is a decrease in BCAA concentrations, fTryp crosses the blood-brain barrier at a much higher rate leading to increased production of serotonin. As a result, the increased serotonin causes lethargy, depresses motor neuron excitability, alters autonomic and endocrine functions, decreases muscular contraction (3), and may impair judgement.
Nutritional Considerations to Delay Central Fatigue
Since glycogen stores and optimal concentrations of BCAA play such important roles in central fatigue, studies have been performed to determine if nutritional intervention can delay this process. These studies have focused on carbohydrate supplementation, BCAA supplementation, and carbohydrate combined with BCAA supplementation. The theories behind these nutritional interventions are that: (a) increasing blood glucose, and therefore decreasing glycogen depletion,
should decrease FFA utilization and prevent increased levels of fTryp and serotonin; (b) impeding the depletion of BCAA will decrease the fTryp/BCAA ratio, therefore decreasing fTryp from crossing the blood-brain barrier at an excessive rate; and (c) combining these two nutritional interventions should help prevent central fatigue via both mechanisms previously described. Detailed
descriptions of these studies are beyond the scope of this article. However, an excellent review of these three nutritional interventions can be found in reference 3.
Although the above theories are scientifically sound, findings are inconclusive, at least with regard to BCAA supplementation. Studies generally find that supplementation with glucose in the form of a sports drink (6-12% glucose-electrolyte solution) decreases the utilization of FFA as fuel and fTryp
concentrations (4), attenuates the depletion of BCAA and ammonia synthesis (5), and increases performance (6). In contrast, studies are mixed with regard to BCAA supplementation. Some studies show increases in plasma ammonia (7) and no benefits on cycling times to exhaustion or perceived exertion (8). However, other studies show that supplementation with BCAA (up to 10 g/hr) with or without carbohydrate minimize increases in the fTryp/BCAA ratio, decrease muscle protein breakdown, improve mental performance following exercise, and increase power output (3). Finally, researchers are mixed on the possibilities of gastrointestinal distress and toxic ammonia levels from supplementing with large doses of BCAA (1, 3). However, it should be noted that in solution, 7g/L of BCAA have been used safely (9).
Since adequate carbohydrate is essential for peak athletic performance, it is recommended that a high-carbohydrate diet be maintained (50-65% carbohydrate) and that a light carbohydrate-protein meal (30-50g carbohydrate and 5-10g protein) be consumed ~60 min prior to exercise to ensure adequate glycogen and amino acids levels (3). Although performance benefits of BCAA
mixed with a glucose solution are equivocal, the addition of BCAA (2-10g/hr) to a glucose solution during prolonged exercise bouts may help to decrease the fTryp/BCAA ratio and muscle protein breakdown, therefore decreasing fatigue and increasing recovery. Also, if carbohydrate nutrition is inadequate, BCAA supplementation may be helpful (9). Future studies will hopefully elucidate the
nutritional possibilities for delaying central fatigue.
1. Davis, JM (1996). Carbohydrates, branched-chain amino acids and endurance: The central fatigue hypothesis. Sports Science Exchange #61, 9 (2).
2. Volek, JS (1997). Energy metabolism and high intensity exercise: Dietary concerns for optimal recovery. Strength and Conditioning, October, pp. 26-37.
3. Kreider, RB (1998). Central fatigue hypothesis and overtraining. In RB Kreider, AC Fry, & ML O-Toole (Eds.), Overtraining in Sport (pp. 309-331). Champaign, IL: Human Kinetics.
4. Davis, JM, Bailey SP, Woods, JA, Galiano, FJ, Hamilton, MT, & Bartoli, WP (1992). Effects of carbohydrate feedings on plasma free tryptophan and branched-chain amino acids during prolonged cycling. European Journal of Applied Physiology, 65, 513-519.
5. Greenhaff, PL, Leiper, JP, Ball, D, & Maughan, RJ (1991). The influence of dietary manipulation on plasma ammonia accumulation during incremental exercise in man. European Journal of Applied Physiology, 63, 338-344.
6. Hargreaves, M (1997). Interaction between muscle glycogen and blood glucose during exercise. Exercise and Sport Sciences Review, 25, 21-39.
7. Vandewalle, L, Wagenmakers, AJM, Smets, K, Brouns, F, & Saris, WHM (1991). Effect of branched-chain amino acid supplements on exercise performance in glycogen depleted subjects. Medicine and Science in Sports and Exercise, 23, S116.
8. Galiano, FJ, Davis, JM, Bailey, SP, Woods, JA, & Hamilton, M (1991). Physiologic, endocrine and performance effects of adding branched-chain amino acids to a 6% carbohydrate-electrolyte beverage during prolonged cycling. Medicine and Science in Sports and Exercise, 23 (4), S14.
9. Williams, MH (1998). The ergogenics edge. Champaign, IL: Human Kinetics.