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acids. Vitamin C serves many diverse functions in the body. A vitamin C-deficient diet can cause deficiency symptoms after a few weeks and can cause death from scurvy in 5 to 7 months (Guyton, 1986).

In the following discussion, these topics will be addressed for each vitamin: its function, how an individual's status is determined, changes in status by chronic exercise, effects of restriction or supplementation on performance, and relationship to heat stress.

Thiamin

The importance of thiamin ingestion was noted in the late nineteenth century when it was found that adding meat and whole grain to sailors' diets aboard ship prevented the condition known as beriberi (Brown, 1990). Thiamin is absorbed from the small intestine, and some is phosphorylated to form pyrophosphate (the coenzyme form). Pyrophosphate and free thiamin are transported via the blood to tissues, with the highest concentrations occurring in the liver, kidney, and heart. Most thiamin is stored in the pyrophosphate form.

Thiamin plays a role in carbohydrate metabolism. It functions specifically as a coenzyme in the conversion of pyruvate to acetyl coenzyme A (CoA) and alpha-ketoglutarate to succinyl CoA, as well as the transketolase reaction of the pentose phosphate pathway.

A sensitive technique for assessing thiamin status is the use of an erythrocyte enzyme stimulation test performed on blood samples. Erythrocyte transketolase activity is assessed before and after addition of thiamin pyrophosphate (TPP). If a deficiency of TPP exists, then adding TPP to the blood will increase the activity of the enzyme. The level of erythrocyte TPP is also used to determine thiamin status. Sauberlich et al. (1979) reported that urinary excretion of thiamin was a reasonably reliable indicator of thiamin nutritional status, although its use has been questioned (Gubler, 1984).

Whether physical exercise, because of the greater metabolic challenge, will increase the need for thiamin has not been fully established. The few studies that have assessed possible biochemical deficiencies of athletes have reported minimal evidence of thiamin deficiency compared with controls (Cohen et al., 1985; Guilland et al., 1989; Weight et al., 1988). Nijakowski (1966) found that blood levels of thiamin were lower in male athletes compared with a control group, however, it is possible that the lower levels were due to plasma volume expansion in athletes. Athletes were also tested after a 12-km skiing expedition, and thiamin levels showed a further decrease, which Nijakowski (1966) suggested was due to increased bodily requirements.

The National Research Council (1989) recommended that thiamin intake be proportional to caloric intake such that 0.5 mg per 1000 kcal is



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