NUTRITION IN SPORT

nisms into one mechanism involving the central
serotoninergic pathway in central fatigue.
There is considerable evidence that depletion
of muscle glycogen results in fatigue. In middle-
distance events, aerobic and anaerobic metabo-
lism both contribute to adenosine triphosphate
(ATP) generation. The athlete can use the aerobic
system towards its maximum capacity, i.e. that
which is limited by oxygen supply to the muscle
but, in addition, further ATP can be produced
from the conversion of glycogen to lactate. So
what causes fatigue in this situation? It is
suggested that it is either depletion of glycogen
or the accumulation of protons in the muscle;
whichever occurs will depend upon the distance
of the event, the class of the athlete and his/her
fitness. If the rate of conversion of glycogen to
lactate is greater than the capacity to lose protons
from the muscle, protons will eventually accu-
mulate sufficiently to cause fatigue (Newsholme
et al.1994). However, it is also possible that
depletion of glycogen before the end of the event
can result in fatigue. As glycogen levels fall, fatty

acid mobilization will occur and increase the

plasma fatty acid level. In a prolonged event such

as the marathon, fatty acids must be mobilized

since there is not enough glycogen to provide the

energy required for the whole event. For an

optimum performance, the marathon runner

must oxidize both glycogen and fat simultane-

ously, but the rate of utilization of the latter

should be such as to allow glycogen to be used

for the whole of the distance—and for depletion

to occur at the finishing post. Consequently,

precision in control of the rates of utilization of

the two fuels, fat and glycogen, is extremely

important.

An interesting question is why glycogen

depletion should result in fatigue. If, as is already

known, it were possible to switch to the enor-

mous store of fat as a fuel, this would delay

fatigue dramatically: theoretically, the runner

should then be able to maintain a good pace for a

considerable period of time—possibly several

days. At least two explanations have been put

forward to account for the fact that this does not

amino acids, fatigue and immunodepression 155

Table 11.1A ‘contemporary’ view of dispensable and non-dispensable amino acids.

Category Amino acid

Totally non-dispensable Lysine, threonine

Oxoacid non-dispensable* Branched-chain amino acids†,

methionine, phenylalanine,

tryptophan

Conditionally non-dispensable‡ Cysteine, tyrosine

Acquired non-dispensable§ Arginine, cysteine, glutamine, glycine,

histidine, serine

Dispensable¶ Alanine, asparagine, aspartate,

glutamate

• The carbon skeleton of these amino acids cannot be synthesized by the body. However, if the oxo(keto) acids are
  provided, the amino acids can be synthesized from the oxoacids via the process of transamination. The oxoacids
  can be provided artificially.
  †The branched-chain amino acids may play a role in fatigue but, to place them in context, it is important to outline
  various explanations for fatigue (see text).
  ‡These are produced from other amino acids—cysteine from methionine and tyrosine from phenylalanine—
  provided that these amino acids are present in excess.
  §The demand for these amino acids can increase markedly under some conditions, e.g. infection, severe trauma,
  burns and in some premature babies.
  ¶It is assumed that all these amino acids can be synthesized at sufficient rates in the body to satisfy all require-
  ments. It is now beginning to be appreciated that this may not always be the case for glutamine.