diet (100 IU per day) for about 6 months followed by vitamin A supplementation (25,000 to 75,000 IU per day) for 6 weeks (Wald et al., 1942). No significant difference in run to exhaustion on a treadmill was found between the deficient and supplemented condition. Because the subjects had supplemented their diets with 75,000 IU for 30 days prior to the depletion phase of the experiment, the 6-month period of vitamin deficiency may not have been long enough to deplete the body's stores of vitamin A. However, it seems that vitamin A stores are generally adequate to meet the demands of exercise.

An antioxidant supplement containing 10 mg beta-carotene, 1000 mg vitamin C, and 800 IU of vitamin E was given to subjects before a downhill running exercise on a treadmill (Viguie et al., 1989). Although the details of the study are not available because this was a published abstract, it seems that the subjects performed the same exercise twice, the first time without the supplement and the second time with the supplement. Results showed that the supplement enhanced glutathione status (antioxidant status) and reduced indicators of exercise-induced muscle damage. However, other studies have shown that when the same damage-inducing exercise was repeated, the indices of damage were always reduced on the second bout regardless of any treatment (Clarkson and Tremblay, 1988). Further studies of the effects of beta-carotene as an antioxidant to reduce muscle damage from strenuous exercise are warranted. Presently there is no information on the effects of heat stress on vitamin A requirements.

In the seventeenth century, rickets was scientifically described as resulting from a dietary deficiency (Norman, 1990). Later vitamin D was found to be synthesized by the body when skin was exposed to sunlight. The major function of vitamin D is its action as a hormone in the mineralization of bones and teeth (Keith, 1989). When the skin is exposed to ultraviolet radiation of the sun, a stero1 (7-dehydrocholesterol) is converted into vitamin D (cholecalciferol). Eventually vitamin D is converted to its hormone forms, 25-hydroxycholecalciferol (25(OH)D₃) and 1, 25-dihydroxycholecalciferol (1,25(OH)₂D₃), by the liver and kidney, respectively. Also, vitamin D is obtainable from a few food sources including fortified milk and milk products.

Biochemical status of vitamin D is generally assessed from measurement of 25(OH)D₃ in the blood; however, blood levels do not fully reflect the extent of storage. Although few studies have examined biochemical status of vitamin D in athletes (Adams et al., 1982; Cohen et al., 1985), vitamin D deficiencies generally are believed to be rare for those individuals with adequate milk consumption and exposure to sunlight.