Some 80% of the body's total vitamin B6 is as pyridoxal phosphate in muscle, and some 80% of this is associated with glycogen phosphorylase. This does not seem to function as a reserve of the vitamin and is not released from the muscle in deficiency.
Muscle pyridoxal phosphate is released into the circulation (as pyridoxal) in starvation as muscle glycogen reserves are exhausted and there is less requirement for glycogen phosphorylase activity. Under these conditions, it is potentially available for redistribution to other tissues, especially the liver and kidneys, to meet the increased requirement for gluconeogenesis from amino acids (Black et al., 1978). However, during both starvation and prolonged bed rest, there is a considerable increase in urinary excretion of 4-pyridoxic acid, suggesting that much of the vitamin B6 released as a result of depletion of muscle glycogen and atrophy of muscle is not redistributed, but rather is ca-tabolized and excreted (Coburn et al., 1995).
The normal muscle concentration of pyridoxal phosphate is of the order of 10 nmol per g; in patients with McArdle's disease (glycogen storage disease from congenital lack of glycogen phosphorylase), the muscle content of pyridoxal phosphate is reduced to one-fifth of this. There is some evidence that patients with McArdle's disease show signs of vitamin B6 deficiency, suggesting that the muscle pool of the vitamin is important in maintenance of vitamin B6 homeostasis (Beynon et al., 1995).
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