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Central Fatigue

Central Fatigue. Lecture 18 Part I. Define fatigue. operating definition : inability to maintain a desired level of intensity. We usually think of fatigue during exercise as occurring in the muscle; e.g. glycogen depletion or some other limitation decreasing the ability to

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Central Fatigue

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  1. Central Fatigue Lecture 18 Part I

  2. Define fatigue. • operating definition: inability to • maintain a desired level of intensity. • We usually think of fatigue during exercise as • occurring in the muscle; e.g. glycogen depletion or • some other limitation decreasing the ability to • produce ATP at the necessary rate.

  3. Some work suggests other factors are involved. • Coyle et al. infused glucose into the blood of trained • cyclists (to make sure they were never limited by • availability of carbohydrate) and, though they were • never depleted, they fatigued and stopped cycling.

  4. In 1987, Newsholme et al. proposed a novel • idea called the “central fatigue hypothesis”. • The basis for the idea is that fatigue during • endurance exercise is related to a buildup • of serotonin (a neurotransmitter) in the brain.

  5. In 1987, Newsholme et al. proposed a novel • idea called the “central fatigue hypothesis”. • The basis for the idea is that fatigue during • endurance exercise is related to a buildup • of serotonin (a neurotransmitter) in the brain. • It is true that increased levels of serotonin causes • drowsiness and fatigue (many sleeping aids work by • raising levels of serotonin in the brain). • Tryptophan is an amino acid • that is converted to 5- • OH tryptamine and then • to serotonin in the brain.

  6. Blood Vessel Transporter Brain • In order to get into the • brain, tryptyophan must • cross the blood-brain • barrier via a transporter. • The transporter is not • specific for tryptophan, • it also transports • branched chain amino • acids (BCAA), • so there is a • “competition” • for transport.

  7. During exercise, BCAA’s are taken up by muscle • and oxidized for energy. • Late in exercise, when muscle glycogen stores are • low, this process is accelerated. Greater uptake of • BCAAs late in exercise leads to lower blood BCAA • levels and increased ratio of tryptophan/BCAA. • So more tryptophan gets into the brain • = more serotonin production. • In addition, as exercise progresses, more free fatty • acids (FFA) are liberated from triglyceride stores • and blood level of FFA goes up.

  8. FFA’s and tryptophan are both • transported in the blood by • albumen (a common plasma protein). • As level of FFA’s goes up, more tryptophan is • displaced from binding sites on albumen and the • “free” tryptophan concentration rises. • So, increased BCAA uptake by muscle AND • decreased binding capacity by albumen greatly • enhances the transport of tryptophan into the brain • Hypothesis: increased tryptophan into brain = more • serotonin = central fatigue = stop exercise.

  9. FFA tryptophan FFA albumen FFA BCAA

  10. How do you test the central fatigue hypothesis? • What things do you need to know? • Does the ratio of tryptophan/BCAA in the blood • increase during exercise? • 2. Is there increased entry of tryptophan into the brain? • 3. Does it cause more production of serotonin? • 4. Does that change in serotonin cause more • fatigue?

  11. Because supplement industry is driven • by business and not scientific motives, • the FIRST studies actually done tested • the effects of supplements on humans. • A rational approach would have been • to supplement with tryptophan and see if it caused • MORE fatigue. But, b/c you can’t make money from • an ergolytic (inhibiting performance) compound, the • first studies tested the efficacy of BCAA supplements • to delay “time to fatigue” in athletes. • Complications: “time to fatigue” is easy to measure • in theory but hard to interpret.

  12. In mid-90’s, dozens of studies looking at effects of • BCAA (with and w/o CHO) on performance. Most • showed no effect. Some improved performance but • studies were usually seriously flawed. • e.g., Blomstrand et al. in 1991 studied effects of • BCAA ingestion vs. flavored water on marathon • runners. No effects unless divided group into “fast” • and “slow”, saw improvement in the “slow” runners. • Flaws: • 1. subjects in 2 groups not matched • 2. did not control energy or CHO intake • 3. division of runners arbitrary

  13. Finally, in about 2003, a group of investigators • infused tryptophan into the bloodstream of rodents • and looked at the uptake into the brain and time to • exhaustion. They found that the greatly elevated • levels of tryptophan in the blood did change the • BCAA/tryptophan ratio but had no effect at all on • endurance.

  14. Bottom line: the evidence to suggest BCAA • supplements improve endurance performance is • almost non-existent. The best designed studies all • show negative results.

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