Marginal vitamin B 6 supply has been related to
impaired aerobic functions only in combination
with a simultaneous thiamin and riboflavin
depletion (van der Beek et al. 1988).
In an interesting study, indices of vitamin B 6
status were examined during a 3-month sub-
marine patrol (Reynolds et al. 1988). The results
indicated deterioration in status and marginal
vitamin B 6 supply at the end of the patrol. Psy-
chological tests indicated pronounced depres-
sion after submergence and at the midpatrol
point. However, the depression measures were
neither correlated with indicators of vitamin B 6
status nor affected by vitamin supplementation.
Chronic supplementation of vitamin B 6
increases the erythrocyte ASAT activity (van
Dam 1978; Guilland et al. 1989; Fogelholm et al.
1993b) and plasma PLP-concentration (Weight
et al. 1988a; Coburn et al. 1991) even in healthy
subjects. However, an increase in the above indi-
cators of vitamin B 6 status is not necessarily asso-
ciated with a marked increase in intramuscular
vitamin B 6 content (Coburn et al. 1991).
It appears that vitamin B 6 , either as an infusion
(Moretti et al. 1982) or given orally as a 20 mg ·
day–1supplement (Dunton et al. 1993), has a
stimulating effect on exercise-induced growth
hormone production. The hypothetical mecha-
nism behind this effect is that PLP acts as the
coenzyme for dopa decarboxylase, and high
concentrations might promote the conversion of
L-dopa to dopamine (Manore 1994). The physio-
logical significance of the above effect is not
known (Manore 1994). Moreover, the effects of
chronic vitamin B 6 administration on the 24-h
growth hormone concentration of plasma have
not been studied.
Supplementation of vitamin B 6 , alone
(Suboticanecet al. 1990) or in combination with
other B-complex vitamins (van Dam 1978; Bonke
& Nickel 1989), has improved maximal oxygen
uptake in undernourished children (Suboticanec
et al. 1990), and shooting performance (Bonke &
Nickel 1989) and muscle irritability (van Dam
1978) in male athletes. In contrast, a number of
other studies did not find any association
between improved indicators of vitamin B 6
272 nutrition and exercise
status and maximal oxygen uptake (Suboticanec-
Buzinaet al. 1984; Weight et al. 1988a, 1988b),
exercise-induced lactate appearance in blood
(Manore & Leklem 1988; Weight et al. 1988a,
1988b; Fogelholm et al. 1993b), grip strength
(Suboticanecet al. 1989) or other tests of physical
performance (Telford et al. 1992a, 1992b).safety of elevated
vitamin b 6 intake
In contrast to thiamin and riboflavin, megadoses
of vitamin B 6 may have important toxic effects.
The most common disorder is sensory neuropa-
thy, sometimes combined with epidermal vesi-
cular dermatosis (Bässler 1989). The safe dose
for chronic oral administration of vitamin B 6
appears to be around 300–500 mg daily (Bässler
1989). However, it is recommended that
long-term supplementation should not exceed
200 mg · day–1—that is, 100 times the recom-
mended dietary allowance (Marks 1989).Folic acid and vitamin B 12chemistry and
biochemical functions
Folateandfolic acidare generic terms for com-
pounds related to pteroic acid. The body pool is
5–10 mg (Herbert 1987), and liver folate is a major
part of the total. Folate coenzymes are needed
in transportation of single carbon units in, for
instance, thymidylate, methionine and purine
synthesis (Fairbanks & Klee 1986).
Deficiency of folate results in impaired cell
division and alterations in protein synthesis.
The effects are most significant in rapidly
growing tissues (Herbert 1987). A typical
deficiency symptom is megaloblastic anaemia
(lowered blood haemoglobin concentration,
with increased mean corpuscular volume;
Halsted 1993). Decreased oxygen transport
capacity would affect submaximal and eventu-
ally also maximal aerobic performance. If iron
deficiency exists simultaneously with folate defi-
ciency, red cell morphology does not necessarily