toxicity, cholestatic jaundice, an increased serum
concentration of uric acid, cardiac dysrhythmias
and various dermatologic problems (Alhadeff
et al. 1984). The safe chronic dose appears to be
at least 50 times the recommended allowance,
i.e. 1 g · day–1(Marks 1989).
biotin
The main function of biotin is as cofactor in
enzymes catalysing transport of carboxyl
units (McCormick 1986). In the cytosol, a
biotin-dependent enzyme, acetyl-coenzyme A
carboxylase, catalyses the formation of malonyl-
coenzyme A from acetyl-coenzyme A. Malonyl-
coenzyme A is used for fatty acid synthesis. In
the mitochondria, biotin is an integral part of
pyruvate carboxylase. This enzyme catalyses the
conversion of pyruvate to oxaloacetate, which is
an intermediate in gluconeogenesis and the citric
acid cycle.
Through the function of pyruvate carboxylase,
biotin has a critical role in maintaining the level
of citric acid cycle intermediates. Although it is
likely that aerobic performance would be
impaired by biotin deficiency, the physical per-
formance of biotin deficient patients has never
been investigated. Moreover, excluding individ-
uals with an excessive intake of raw egg-white
(which contains avidin, a biotin-binding
glycoprotein), dietary biotin deficiency is almost
impossible in practice (McCormick 1986).
There are no reported toxic effects of biotin
intake up to 10 mg · day–1(>100 times the recom-
mended allowance) (Marks 1989; Halsted 1993).
pantothenic acid
Pantothenic acid functions as a cofactor in
coenzyme A, which, as acetyl-coenzyme A, is in a
central position for both energy production
and fatty acid synthesis (McCormick 1986).
Pantothenic acid is also needed in the 4¢-
phosphopantetheine moiety of acyl carrier
protein of fatty acid synthetase.
Pantothenic acid deficiency due to dietary
reasons has never been reported. Deficiency
274 nutrition and exercise
symptoms have been induced with a semisyn-
thetic diet practically free of pantothenate.
Symptoms include general fatigue and increased
heart rate during exertion (McCormick 1986).
Relations between pantothenic acid status and
physical performance capacity have not been
investigated.
Pantothenic acid has not been reported to
cause any toxic affects even at doses up to 10 g
daily, i.e. 1000 times the recommended intake
level (Alhadeff et al. 1984; Marks 1989).Vitamin Cchemistry and
biochemical functions
Vitamin C or ascorbic acid is a strong reducing
agent, which is reversibly oxidized to dehy-
droascorbic acid in numerous biochemical
reactions (Padh 1991). By its reducing capacity,
ascorbic acid stimulates enzymes involved in, for
instance, biosynthesis of collagen, carnitine,
pyrimidine and noradrenaline (McCormick
1986; Padh 1991).
In addition to the above biosynthetic path-
ways, ascorbic acid has a very important role as
an extracellular antioxidant against many types
of free radical compounds (see Chapter 22). In
the gastrointestinal tract, ascorbic acid enhances
iron absorption by keeping iron in a reduced
ferrous state (Gershoff 1993). In contrast, high
doses of ascorbic acid may suppress copper
absorption by reducing copper to a less
absorbable monovalent state (Finley &
Cerklewski 1983).supply and metabolic functions
Ascorbic acid is needed in carnitine synthesis,
and therefore indirectly for transfer of long-chain
fatty acids across the inner mitochondrial
membrane. A substantial decrease in muscle car-
nitine would theoretically decrease submaximal
endurance capacity by increasing the de-
pendence on glycogen instead of fatty acids
(Wagenmakers 1991). In one study (van der Beek