times the recommended daily intake; that is,
above 100 mg daily.
Riboflavin
chemistry and
biochemical functions
Riboflavin (correct chemical name) or vitamin B 2
is composed of an isoalloxazine ring linked to a
ribityl side chain (Halsted 1993). Modification of
the side chain yields flavin mononucleotide
(FMN). When linked to adenine monophos-
phate, FMN forms flavin adenine dinucleotide
(FAD). FMN and FAD function as coenzymes in
numerous oxidation-reduction reactions in gly-
colysis and the respiratory chain (Cooperman &
Lopez 1984). Enzymes requiring FAD are, e.g.
pyruvate dehydrogenase complex (glycolysis),
a-ketoglutarate dehydrogenase complex and
succinate dehydrogenase (citric acid cycle). FAD
is also needed in fatty acid oxidation, whereas
FMN is necessary for the synthesis of fatty acids
from acetate (Cooperman & Lopez 1984).
Riboflavin has also indirect effects on
body functions by affecting iron utilization
(Fairweather-Tait et al. 1992). The mechanism is
still unknown in humans, but some results indi-
cate that correction of riboflavin deficiency also
raises low blood haemoglobin concentrations
(Cooperman & Lopez 1984; Fairweather-Tait
et al. 1992). Severe riboflavin deficiency can also
affect the status of other B-complex vitamins,
mainly by decreased conversion of vitamin B 6 to
its active coenzyme and of tryptophan to niacin
(Cooperman & Lopez 1984).
Like thiamin, the activity of an enzyme iso-
lated from the erythrocytes is widely used as an
indicator of riboflavin status (Bayomi & Rosalki
1976; Cooperman & Lopez 1984). The enzyme,
glutathione reductase, catalyses the reduction of
oxidized glutathione with simultaneous oxida-
tion of NADPH. The enzyme activity in vitrois
related to activity after saturation by FAD. The
better the vitamin status, the smaller the increase
in activity after added FAD (Bayomi & Rosalki
1976).
270 nutrition and exercise
supply and metabolic functions
Changes in riboflavin supply have been postu-
lated to affect both muscle metabolism and
neuromuscular function. Data on the effects of
marginal riboflavin supply are, however, scarce.
In three studies (Belko et al. 1984, 1985; Trebler
Winters et al. 1992), a 4–5-week period with mar-
ginal riboflavin intake resulted in lowering of the
erythrocyte glutathione reductase activity, but no
relation with aerobic capacity was found. Simi-
larly, Soares et al. (1993) did not find changes in
muscular efficiency during moderate-intensity
exercise after a 7-week period of riboflavin-
restricted diet.
In contrast to the above studies, van der Beek
et al. (1988) reported impaired maximal oxygen
uptake and increased blood lactate appearance
after a 10-week period with marginal thiamin,
riboflavin and vitamin B 6 intake. The indepen-
dent role of riboflavin was, however, uncertain.
Decreased urinary riboflavin excretion might
be one mechanism in preventing changes in
riboflavin-dependent body functions during
marginal depletion (Belko et al. 1984, 1985; Soares
et al. 1993). More severe riboflavin deficiency is
obviously likely to affect both maximal and sub-
maximal aerobic work capacity, as well as neuro-
muscular function (Cooperman & Lopez 1984).
A 1–3-month vitamin B-complex supplemen-
tation improves the activity of erythrocyte
glutathione reductase (van Dam 1978; Weight
et al. 1988b; Guilland et al. 1989; Fogelholm et al.
1993b) in athletes or trained students, even
without indications of impaired vitamin status
(Weight et al. 1988b). Two studies have suggested
that supplementation and improvement in
riboflavin status (judged by changes in erythro-
cyte glutathione reductase activity) were
related to improved neuromuscular function
(Haralambie 1976; Bamji et al. 1982).
Riboflavin supplementation, in combination
with one or more water-soluble vitamins, has
been shown to affect both erythrocyte enzyme
activity and maximal oxygen uptake (Buzina
et al. 1982; Suboticanec-Buzina et al. 1984) or
work efficiency (Powers et al. 1985) in children