- Recent studies in men have shown plasma levels of vitamin B-6
and pyridoxal 5'-phosphate (PLP), the active form of vitamin B-6, to
increase with exercise. It was hypothesized that muscle glycogen
phosphorylase might be the source of these increases as this enzyme
has been shown to increase with increasing vitamin B-6 (B6) intake
in the rat, seemingly to store PLP. The investigation was designed
to study the effects of diet-altered glycogen stores and B6
supplements on B6 metabolism during controlled strenuous exercise.
The effect of exercise (EX) on the excretion of 4-pyridoxic acid
(4PA), the major B6 urinary metabolite, was also studied.
The study consisted of three experimental weeks during which
carbohydrate (CHO)-modified diets were fed and six EX tests were
administered (one each Wednesday and Saturday). Four trained male
cyclists (20-23 years) served as subjects. Week 1 a normal CHO
diet was fed (NC diet, 40% of total kilocalories as CHO). During
week 2, which began 7 days after week 1, a low CHO diet was fed
Sunday through Tuesday (LC diet, 11% CHO) to deplete muscle
glycogen. In the same week, the LC diet was followed by a high
CHO diet (HC diet, 71% CHO). The HC diet was fed Wednesday through
Saturday to replete, or load, glycogen stores. The NC, LC, and
HC diets contained 1.64, 1.55, and 1.82 mg of B6, respectively.
Week 3, beginning 14 days after week 2, was identical to week 2,
but with the daily addition of an 8 mg supplement of pyridoxine.
Daily exercise was encouraged Sunday through Tuesday to facilitate
glycogen depletion. The EX test consisted of 50 min of continuous
bicycle ergometer exercise (30 min at 60% HRmax (maximal heart rate),
15 min at 80% HRmax, and 5 min at 90% HRmax).
Blood samples were drawn prior to the exercise test (pre),
2 min prior to the 90% HR max interval (during), immediately post
EX (post), 30 min post, and 60 min post EX. Plasma samples were
analyzed for PLP, PB6, creatine kinase (a muscle enzyme), and
hematocrit and hemoglobin. Urine was collected in 24 hour
aliquots and analyzed for 4PA and creatinine.
The HC diet was associated with significantly lower pre
exercise PB6 and PLP levels than LC diet. This was attributed to
the high CHO content of HC.
Increased plasma PLP and PB6 levels (pre versus post) were
seen for all EX tests. This was significant for PB6 levels of all
EX tests. Exercise following LC resulted in smaller pre to post
increases in PB6 and PLP than other unsupplemented EX tests, but
this was significant only for EX following LC versus NC(Wed).
Supplementation resulted in greater pre to post increases in PLP
and PB6 than EX following unsupplemented diets, but this was
significant only for LC versus LC+B6. Plasma PLP and PB6 levels
dropped throughout the 60 min post EX period. The 60 min post
PLP levels were significantly below pre for the EX tests following
diets NC(Wed), LC, HC+B6. Neither plasma volume percent (%)
changes (calculated from hematocrit) nor creatine kinase % changes
correlated significantly with % changes in PB6 and PLP. Urinary
4PA was elevated on all EX test days as compared to non-test
days, except for EX following LC.
Tissue redistribution of B6 appears to be occurring with
exercise. With the LC diet, more B6 is needed for increased
amino acid catabolism in the liver. In this situation tissue
redistribution was not associated with increased conversion of B6
to 4PA. Greater increases in PLP with EX following supplementation
suggests increased storage may have occurred. These findings are
supportive of the hypothesis that increased PLP levels with
exercise may originate from PLP bound to phosphorylase. The need
for supplemental B6 for the athlete was not established, as status
was adequate with normal intakes.