Two important enzyme complexes of glycoly-
sis and the citric acid cycle require TPP as a cofac-
tor, namely, pyruvate dehydrogenase (formation
of acetyl-coenzyme A from pyruvate) and a-
ketoglutarate dehydrogenase (formation of
succinyl-coenzyme A from a-ketoglutarate)
(Johnson Gubler 1984). If the decarboxylation of
pyruvate is inadequate to match the increased
speed of glycolysis, pyruvate will accumulate in
the tissue (Sauberlich 1967). The accumulation of
pyruvate will eventually lead to increased lactic
acid production (Johnson Gubler 1984), which
is lowered after thiamin supplementation
(Sauberlich 1967). By interfering with the citric
acid cycle, improper function of a-ketoglutarate
dehydrogenase would affect aerobic energy pro-
duction, and through feedback reactions, also the
overall rate of glycolysis.
Although the muscle tissue contains more
than 40% of the total body thiamin, the vitamin
concentration is much higher in the liver, kidney
and brain (Johnson Gubler 1984). Also, the
nerves contain a constant and significant amount
of TPP (Johnson Gubler 1984), and thiamin is
indeed very important for the function of the
brain and the nervous system (McCormick 1986;
Halsted 1993).
In addition to the two above-mentioned
enzyme complexes, thiamin is also needed in the
pentose phosphate pathway (PPP) as a cofactor
for transketolase (Johnson Gubler 1984). PPP is
important for production of pentoses for RNA
and DNA synthesis, and nicotinamide adenine
dinucleotide phosphate (NADPH) for biosyn-
thesis of fatty acids. The role of PPP in energy
production is minor (Johnson Gubler 1984).
However, the interesting feature about trans-
ketolase is that the activity of erythrocyte trans-
ketolase, with and without in vitroadded TPP,
is widely used as an indicator of thiamin status
(Bayomi & Rosalki 1976). Several papers have
been published on erythrocyte transketolase
activity in athletes (for a review, see Fogelholm
1995).
supply and metabolic functions
In subclinical thiamin deficiency, the exercise-
induced blood lactate concentrations are ele-
vated, especially after a pre-exercise glucose
load (Sauberlich 1967). The deterioration of
physical capacity in marginal deficiency is
less evident. Wood et al. (1980) did not find
decreased working capacity, neurophysiologi-
cal changes or adverse psychological reactions
in male students, despite a 5-week thiamin-
depleted diet. However, the erythrocyte trans-
ketolase activity decreased, showing that the
activity of this enzyme is affected faster than
the activity of the enzymes of glycolysis and
the citric acid cycle.
A combined depletion of thiamin, riboflavin,
vitamin B 6 and ascorbic acid has been found to
affect both erythrocyte transketolase activity and
aerobic working capacity (van der Beek et al.
1988). However, because of the multiple deple-
tion, the independent role of thiamin could not
be demonstrated. The uncertainty of the inde-
pendent role of thiamin was a concern also in
studies showing improved shooting accuracy
(Bonke & Nickel 1989) or neuromuscular
irritability (van Dam 1978) after combined
thiamin, riboflavin, vitamin B 6 or vitamin B 12
supplementation.
A 1–3-month vitamin B-complex supplemen-
tation (>7.5 mg · day–1) usually improves the
activity of erythrocyte transketolase (van Dam
1978; Guilland et al. 1989; Fogelholm et al. 1993b).
Nevertheless, despite improved erythrocyte
transketolase activity or increased blood thiamin
concentration, several studies have shown that
vitamin supplementation did not improve func-
tional capacity in athletes (Telford et al. 1992a,
1992b), young adults (Singh et al. 1992a, 1992b;
Fogelholmet al. 1993b) or in elderly subjects
(Suboticanecet al. 1989).safety of elevated thiamin intake
Adverse reactions of chronic, elevated oral
administration of thiamin are virtually unknown
(Marks 1989). Hypersensitivity reactions may
sometimes occur after very high oral loads (5–
10 g), or following much lower doses (5–10 mg)
by parenteral administration (Marks 1989). For
chronic oral use, the safe dose is at least 50–100