The relationship between ascorbic acid and exercise has been studied for a number of years, with several review articles having been written covering this topic.1-5 This chapter will further address the knowledge base concerning vitamin C and exercise. Such topics as the basic functions and deficiency symptoms of ascorbic acid as related to exercise will be covered. In addition, articles related to exercise and vitamin C requirements; immune function; cortisol secretion and stress; muscle soreness; supplementation and sports performance and intakes/needs of physically active persons for the vitamin will be reviewed.
While the existence of vitamin C has been known for only a relatively short time, the fact that a vitamin C deficiency could adversely affect physical performance has been documented for centuries.1,4 There are reports from the British Navy of the late 1700s concerning sailors with scurvy (vitamin C deficiency).4 These reports describe sailors who had good appetites and were cheerful, yet collapsed and died on deck upon the initiation of physical activity. During the Crimean War (1854-6) and the American Civil War, scurvy was reported among the soldiers. Those having scurvy were reported to have shortness of breath upon exertion and greatly reduced energy and powers of endurance.4 These are just a couple of examples of how ascorbic acid deficiency has adversely affected the physical ability of sailors and soldiers in the last several centuries, and other stories of scurvy's effects on physical performance exist.4 Thus, while the study of vitamin C and physical performance is a relatively new area, the fact that scurvy has caused decreases in physical performance has existed for centuries.
Vitamin C is a water-soluble vitamin for humans, primates and guinea pigs. Most other animal species can make ascorbic acid from the sugar glucose, but humans lack an enzyme necessary to convert glucose to ascorbic acid. Vitamin C exists in humans in two biologically active forms, ascorbic acid and dehydroascorbic acid. It is the ability to interconvert between these two forms that gives vitamin C antioxidant capabilities.6-10
Dietary intakes of vitamin C are absorbed in the upper small intestines by active transport mechanisms at physiological intakes (50-200 mg/day). Large intakes (gram doses) of the vitamin may be absorbed by passive diffusion. Most (80-90%) of a physiological dose will be absorbed. However, this absorbance value may drop to 10-20% for megadoses. Vitamin C is found in high concentrations in the adrenal glands, pituitary gland, white blood cells, the lens of the eye and brain tissue.6-10
Ascorbic acid has several important functions as related to physical activity. The vitamin has long been known to be necessary for normal collagen synthesis. Collagen, one of the most abundant proteins in the body, is a vital component of cartilage, ligaments, tendons and other connective tissue. Vitamin C is needed for the formation of the vitamin-like compound carnitine, which is necessary for the transport of long-chain fatty acids into the mitochondria. The fatty acids can then be used as an energy source. The neurotransmitters, norepinephrine and epinephrine also require vitamin C for their synthesis. Ascorbic acid seems to be needed for the proper transport of nonheme iron, the reduction of folic acid intermediates and for the proper metabolism of the stress hormone cortisol. Finally, vitamin C acts as a powerful water-soluble antioxidant. The vitamin seems to exert antioxidant functions in plasma and probably interfaces at the lipid membrane level with vitamin E to regenerate vitamin E from the vitamin E radical. Table 2.1 describes some of these functions in more detail.6-10
Through these various functions vitamin C can interface with physical activity at several levels. For example, poor development of connective tissue could result in increased numbers of ligament and tendon injuries and poor healing of these injuries. Inadequate production of carnitine would decrease a person's ability to utilize fatty acids as an energy source. This would force increased use on glycogen stores, exhausting these stores earlier during exercise and causing fatigue and decreased performance. With decreased production of norepinephrine and epinephrine, an athlete might not be able to properly stimulate the neural and metabolic systems necessary for optimal performance. Poor iron and folate metabolism would result in anemia's impairing the transport of oxygen to tissues. This would be a
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