deviate from reference values (Fairbanks & Klee
1986). Folate is also needed in the nervous
system, and depletion during pregnancy might
cause lethal neural tube defects (Reynolds 1994).
Vitamin B 12 and cobalamin refer to a larger
group of physiologically active cobalamins
(Fairbanks & Klee 1986). Cyanocobalamin is the
principal commercial and therapeutic product
(Halsted 1993). Cobalamin is a cofactor for two
reactions: the synthesis of methionine and the
conversion of methylmalonic acid to succinic
acid (Halsted 1993). Through these reactions,
cobalamin is needed in normal red blood cell
synthesis and neuronal metabolism (Fairbanks &
Klee 1986).
Cobalamin deficiency leads to megaloblastic
anaemia and to neurological disorders. As in
anaemia caused by folate deficiency, erythrocyte
volume is usually increased, in contrast to frank
iron-deficiency anaemia (Fairbanks & Klee 1986).
Compared with the daily requirements, the 2–
3 mg body pool of cobalamin is very large. Even
with no dietary cobalamin, the body pool would
suffice for about 3–5 years (Fairbanks & Klee
1986).
supply and metabolic functions
There are only a few studies linking folic acid or
vitamin B 12 supply to sports-related functional
capacity. Folate supplementation and increased
serum folate concentration did not affect
maximal oxygen uptake (Matter et al. 1987),
anaerobic threshold (Matter et al. 1987), grip
strength (Suboticanec et al. 1989) or other
measures of physical performance (Telford et al.
1992a, 1992b). Together with thiamin and
vitamin B 6 supplementation, elevated intake of
vitamin B 12 was, however, associated with
improved shooting performance (Bonke &
Nickel 1989).
safety of elevated folic acid and
vitamin b 12 intake
The effects of high doses of folic acid have not
been studied very much, but some results indi-
cate a possible interference with zinc metabolism
(Marks 1989; Reynolds 1994). The current esti-
mate of the safety dose is between 50 and 100
times the daily recommended intake (Marks
1989). The safety margin for vitamin B 12 appears
to be much larger, because even doses as high as
30 mg · day–1 (that is, 10 000 times the recom-
mended intake) have been used without notice-
able toxic effects (Marks 1989).Other vitamins of the B-groupniacin
Niacinis used as a name for nicotinic acid as well
as for its derivatives nicotinamide and nicotinic
acid amide (McCormick 1986). About 67% of
niacin required by an adult can be converted
from the amino acid tryptophan; 60 mg of trypto-
phan is needed for the formation of 1 mg niacin.
Nicotinamide, as a part of nicotinamide
adenine dinucleotide (NAD) and NADPH,
participates in hundreds of oxidation-reduction
reactions (McCormick 1986; Halsted 1993). NAD
is needed as an electron acceptor in glycolysis
(enzyme: glyceraldehyde-3-phosphate dehydro-
genase) and the citric acid cycle (pyruvate
dehydrogenase, isocitrate dehydrogenase, a-
ketoglutarate dehydrogenase and malate dehy-
drogenase), and the reduced form of NADPH as
an electron donor in fatty acid synthesis.
Because of its important role in mitochondrial
metabolism, niacin deficiency has the potential
to affect both muscular and nervous function.
Unfortunately, there are no direct studies on the
effects of niacin deficiency on physical perfor-
mance. In contrast, high-dose supplementation
(e.g. intravenous administration) of niacin blocks
the release of free fatty acids from the adip-
ose tissue, and impairs long-term submaximal
endurance (Pernow & Saltin 1971).
Acute oral intake of at least 100 mg of nicotinic
acid per day (i.e. at least five times the recom-
mended daily allowance) causes vasodilatation
and flushing, which is a rather harmless effect
(Marks 1989). Very large, chronic supplementa-
tion of niacin has been reported to cause hepato-