NUTRITION IN SPORT

used as a fuel in the gut (Souba 1991) or for gluco-
neogenesis in the liver (Ross et al. 1967), and the
other half is released and transported back to the
muscle. This glutamine–glutamate cycle pro-
vides a means to transport ammonia produced in
muscle in the form of a non-toxic carrier (gluta-
mine) through the blood to the splanchnic area
where it can be removed as urea.

Muscle amino acid metabolism

during exercise

Anaplerotic role of the alanine
aminotransferase reaction

During one- and two-legged cycling exercise at
intensities between 50% and 70% of Wmax.only
two amino acids change substantially in concen-
tration in the muscle free amino acid pool, i.e.
glutamate and alanine (Bergström et al. 1985;
Sahlinet al. 1990; Van Hall et al. 1995b). Gluta-
mate decreases by 50–70% within 10 min of
exercise, while alanine at that point in time is
increased by 50–60%. The low concentration of
glutamate is maintained when exercise is con-
tinued for periods up to 90 min or until exhaus-
tion, while alanine slowly returns to resting
levels. Substantial amounts of alanine, further-
more, are released into the circulation during the
first 30 min of exercise (Van Hall et al. 1995b).
Alanine release is reduced again when exercise is
continued and the muscle glycogen stores are
gradually emptied (Van Hall et al. 1995b). The
functionality of the rapid fall in muscle gluta-
mate concentration most likely is conversion
of its carbon skeleton into a-ketoglutarate and
TCA-cycle intermediates. The sum concentration
of the most abundant TCA-cycle intermediates
in skeletal muscle has been shown to increase
rapidly by about 10-fold after the start of exer-
cise (Essen & Kaijser 1978; Sahlin et al. 1990).
Although the mechanisms of metabolic control
of the flux in the TCA cycle are not exactly under-
stood today because of the complexity of this
multienzyme system, both allosteric activation
mechanisms (increases in the concentration of
mitochondrial free ADP and calcium among

others activate a-ketoglutarate dehydrogenase)

and increases in the concentration of some of the

TCA-cycle intermediates (the substrates of the

TCA-cycle enzymes) most likely both contribute

to the increased TCA-cycle flux during exercise.

The increase in the sum concentration of the most

abundant TCA-cycle intermediates, in other

words, may be needed for an optimal aerobic

energy production and to meet the increased

energy demand for contraction.

The high rate of alanine production during the

first 30 min of exercise (Van Hall et al. 1995b) and

the temporary increase in muscle alanine concen-

tration after 10 min of exercise indicate that

the alanine aminotransferase reaction (Fig. 9.3)

is used for the rapid conversion of glutamate

carbon into TCA-cycle intermediates. The ala-

nine aminotransferase reaction is a near equilib-

rium reaction. At the start of exercise the rate of

glycolysis and thus of pyruvate formation is

high, as indicated by a temporary increase of the

muscle pyruvate concentration (Dohm et al. 1986;

Sahlinet al. 1990; Spencer et al. 1992) and an

increased release of pyruvate and lactate from

the exercising muscle during the first 30 min

(Van Hall 1996). The increase in muscle pyruvate

automatically forces the alanine aminotrans-

amino acid metabolism in exercise 125

Increased

TCA cycle

activity

Fatty acids

Acetyl-CoA

α-ketoglutarate

Pyruvate + glutamate Alanine + α-ketoglutarate

Alanine aminotransferase

+ Exercise

Muscle glycogen

Fig. 9.3The alanine aminotransferase reaction feeds

carbon into the tricarboxylic acid (TCA) cycle during

the first minutes of exercise.