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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

Central Fatigue

Lecture 18 Part I

slide2
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.
slide3
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.
slide4
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.
slide5
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.
slide6

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.
slide7
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.
slide8
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.
slide9

FFA

tryptophan

FFA

albumen

FFA

BCAA

slide10
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?
slide11
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.
slide12
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
slide13
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.
slide14
Bottom line: the evidence to suggest BCAA
  • supplements improve endurance performance is
  • almost non-existent. The best designed studies all
  • show negative results.