Central Nervous System Fatigue is a type of fatigue caused by changes within the function of the central nervous system that can not be explained by dysfunction of the muscle. [1] It is brought about by prolonged exercise and the neurochemical changes in the brain- primarily of serotonin (5HT) and dopamine. Central Nervous System Fatigue plays an important role in endurance sports, and also highlights the importance of proper nutrition in endurance athletes.

Neurochemical Mechanisms

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While many neurochemical changes have been observed during central nervous system fatigue, no current method can provide a direct causal link between the changes and fatigue. However, existing methods have provided enough evidence to suggest that serotonin 5-HT and dopamine are significant drivers of central nervous system fatigue(cite). In the brain, serotonin is an inhibitory neurotransmitter and regulates arousal, behavior, sleep, and mood [2]. During prolonged exercise where central nervous system fatigue is present, serotonin levels in the brain are higher than normal physiological conditions; these higher levels can increase perceptions of effort and peripheral muscle fatigue [2]. The increased synthesis of brain serotonin occurs because of a higher level of tryptophan (serotonin precursor) in the blood and, in turn, larger amounts of tryptophan crossing the blood-brain barrier. An important factor of serotonin synthesis is the transport mechanism of tryptophan across the blood-brain barrier. The transport mechanism for tryptophan is shared with the branched chain amino acids (BCAAs), leucine, isoleucine, and valine. During extended exercise, BCAAs are consumed for skeletal muscle contraction, allowing for greater transport of tryptophan across the blood-brain barrier. None of the components of the serotonin synthesis reaction are saturated under normal physiological conditions, allowing for the increased production of the neurotransmitter. Dopamine is an excitatory neurotransmitter that regulates arousal, motivation, muscular coordination, and endurance performance [3]. Dopamine levels have been found to be lower after prolonged exercise [4]. A decrease in dopamine can decrease athletic performance as well as mental motivation. Dopamine and its precursors are too large to cross the blood brain barrier; the neurotransmitter is completely synthesized within the brain. Fatigue can be examined by investigating the ratio of serotonin t-HT to dopamine. A high ratio of serotonin 5-HT/dopamine would amount to central nervous system fatigue, whereas a low ratio would optimize performance.

Manipulating CNS Fatigue

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Controlling central nervous system fatigue could help athletes improve and develop a greater understanding for fatigue in of itself. Numerous approaches have been taken to manipulate neurochemical behavior or levels in order to improve athletic performance. Caffeine has been shown to delay the onset of fatigue in exercise, and possibly does so by obstructing adenosine receptors in the central nervous system[5] . Adenosine is a neurotransmitter that decreases arousal and increases sleepiness. Preventing adenosine from acting removes a factor that promotes rest, causing fatigue to delay. A study conducted by the Institute of Food, Nutrition, and Human Health at Massey University investigated the effect of consuming a carbohydrate and electrolyte solution on muscle glycogen use and running capacity on subjects that were on a high carbohydrate diet [6]. The group that consumed the carbohydrate and electrolyte solution before and during exercise experienced greater endurance capacity. This could not be explained by the varying levels of muscle glycogen; however, higher plasma glucose concentration may have led to this result. Dr. Stephen Bailey posits that the central nervous system can sense the influx of carbohydrates and reduces the perceived effort of the exercise, allowing for greater endurance capacity. Several studies have attempted to decrease the synthesis of serotonin by increasing BCAAs and inhibiting the transport of tryptophan across the blood brain barrier[7]. Unfortunately, the studies resulted in little or no change in performance between increased BCAA intake and placebo groups. One study in particular administered a carbohydrate solution and a carbohydrate + BCAA solution [8]. Both of the groups were able to run for longer before fatigue compared to the water placebo group. However, both the carbohydrate and the carbohydrate + BCAA groups had no differences in their performance. Branch chained amino acid supplementation has proven to have little to no effect on performance. There has been little success utilizing neurotransmitter precursors to control central nervous system fatigue. However caffeine and carbohydrates have seen success.

Role in the Body

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Central nervous system fatigue is a key component in preventing peripheral muscle injury [9]. There is much value in understanding it. The brain has numerous receptors, such as osmoreceptors, to track dehydration, nutrition, and body temperature. With that information and peripheral muscle fatigue information, the brain can reduce the amount of motor commands sent from the central nervous system. This is crucial in protecting the homeostasis of the body and keeping it in a proper physiological state by increasing the amount of perceived effort to continue exercise. Knowing when to ceasing exercise when at potentially dangerous core temperatures and nutritional lows is an important brain function, as hyperthermia and dehydration can be fatal.


References

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  1. ^ Davis, J. M., & Bailey, S. P. (1997). Possible mechanisms of central nervous system fatigue during exercise. Medicine & Science in Sports & Exercise, 29(1), 45-57.
  2. ^ a b Young, S. N. The clinical psychopharmacology of tryptophan. In: Nutrition and the Brain. Vol. 7, R. J. Wurtman and J. J. Wurtman, (Eds.). New York: Raven, 1986, pp. 49-88
  3. ^ Chaouloff, F., D. Laude, and J. L. Elghozi. Physical exercise: evidence for differential consequences of tryptophan on 5-HT synthesis and metabolism in central serotonergic cell bodies and terminals.J. Neural Transm. 78:121-130, 1989.
  4. ^ Bailey, S. P., J. M. Davis and E. N. Ahlborn. Neuroendocrine and substrate responses to altered brain 5-HT activity during prolonged exercise to fatigue. J. Appl. Physiol. 74:3006-3012, 1993
  5. ^ Central nervous system effects of caffeine and adenosine on fatigue. J. Mark Davis , Zuowei Zhao , Howard S. Stock , Kristen A. Mehl , James Buggy , Gregory A. Hand. American Journal of Physiology - Regulatory, Integrative and Comparative Physiology Published 1 February 2003 Vol. 284 no. R399-R404DOI: 10.1152/ajpregu.00386.2002
  6. ^ Foskett, A., Williams, C., Boobis, L., & Tsintzas, K. (2008). Carbohydrate availability and muscle energy metabolism during intermittent running. Med Sci Sports Exerc, 40(1), 96-103. doi: 10.1249/mss.0b013e3181586b2c
  7. ^ Meeusen, R., & Watson, P. (2007). Amino acids and the brain: do they play a role in "central fatigue"? Int J Sport Nutr Exerc Metab, 17 Suppl, S37-46
  8. ^ Blomstrand, E., S. Andersson, P. Hassmen, B. Ekblom, and E. A. Newsholme. Effect of branched-chain amino acid and carbohydrate supplementation on the exercise-induced change in plasma and muscle concentration of amino acids in human subjects. Acta Phys. Scand. 153:87-96, 1995
  9. ^ Fatigue is a Brain-Derived Emotion that Regulates the Exercise Behavior to Ensure the Protection of Whole Body Homeostasis. Timothy David Noakes. Front Physiol. 2012; 3: 82. Prepublished online 2012 January 9. Published online 2012 April 11. doi: 10.3389/fphys.2012.00082.