Medilas_content_vitamin Antioxidants form a front line defense against cell damage caused by free radicals, which are involved in muscle, joint and tendon damage and inflammation, degenerative arthritis and even in aging process.

The use of antioxidants can reduce free radical damage that occurs when we exercise and can also attenuate the ongoing damage to injured tissues caused by free radicals, thus accelerating the healing process.

Antioxidants, such as vitamins C and E (see under Vitamins below), selenium, green tea, reducedglutathione and N-acetyl-cysteine (NAC) can play an important role in reducing inflammation and fatigue, decreasing tissue damage, and in both preventing and treating injuries.

Various antioxidants, such as vitamin E, have been found to be useful in the treatment of some forms of arthritis and in dealing with the oxidative stress of exercise. As well, oxidative damage has been shown to contribute to the pathogenesis of injuries and arthritis, and the use of antioxidants, such as NAC, shown to have therapeutic value for reducing endothelial dysfunction, inflammation, fibrosis, invasion and cartilage erosion.

Vitamin C

Vitamin C is essential to proper collagen synthesis, and this is evident in the vitamin C deficiency disease scurvy, in which the collagen fibers synthesized in the body cannot form fibers properly, resulting in lesions, blood vessel fragility and poor would healing.

Vitamin C has been shown to have some anticatabolic effects that likely involves decreasing exercise induced cortisol but may also have some effects through its antioxidant action. Conversely, some of the anticatabolic effects of antioxidants may be mediated through a decrease in cortisol.

Antioxidants may be of some use in training induced muscle ischemia and injury. Research shows that exercise can adversely affect muscle tissue by increasing the formation of free radicals. These free radicals can then lead to muscle fatigue, inflammation and muscular damage.

During normal conditions free radicals are generated at a low rate and neutralized by antioxidant enzymes in the liver and skeletal muscle and other systems. Unfortunately, the increase in free radicals caused by exercise accompanies a simultaneous decrease in the supply of antioxidants to handle them.

Vitamin E

Vitamin E, for instance, can be severely decreased by training thus depleting muscle of its major antioxidant force.
A study examined the potential protective effect of pretreatment with corticosteroids or antioxidants (ascorbic acid or allopurinol) in rabbits with reperfusion-induced damage to skeletal muscle after ischemia.

Coenzyme Q10

Coenzyme Q10 acts as an electron carrier of the respiratory chain in mitochondria. As well, it has been shown that the reduced form of coenzyme Q10 is an important physiological lipid-soluble antioxidant and scavenges free radicals generated chemically within liposomal membranes.

Generation of free radicals and subsequent lipid peroxidation have been proposed to contribute to delayed tissue damage. One study has found that ascorbate and ubiquinol levels were decreased after trauma.


Zinc deficiency in humans is widespread and athletes may be particularly prone to lower plasma zinc levels. Zinc is a constituent of more than 100 fundamentally important enzymes, so zinc deficiency has many negative effects on almost every body function. As well, zinc deficiency can adversely effect the reproductive hormones and as such impair athletic efforts.

Zinc deficiency adversely affects protein synthesis. In one study the effects of zinc deficiency in rats, on the levels of free amino acid in urine, plasma and skin extract were investigated. Zinc deficiency adversely affected skin protein synthesis. Especially where a deficiency may be present, supplemental zinc has resulted in an increase the secretion of growth hormone and IGF-I, and testosterone and to raise plasma testosterone and sperm count.


Magnesium supplementation has been shown to increase protein synthesis and strength. In another study the authors felt that insulin sensitivity can be improved by reduction of excessive body weight, regular physical activity and, possibly, by correcting asubclinical magnesium deficiency.


Calcium permits the contractile filaments of the muscle cell -actin filaments and myosin filaments- to associate and produce the force that generates movement. When the nerve cell innervating a muscle cell signals that cell to contract, calcium is released from the sarcoplasmic reticulum into the region of the contractile filaments, thereby permitting contraction to occur. In one study calcium was shown to be effective in prolonging time of onset of fatigue in striated muscle.

Several studies have shown that calcium plays a key role in body weight regulation and especially on fat metabolism (with possible effects on lipolysis, fat oxidation, lipogenesis, energy expenditure, and appetite suppression) and thus is a useful supplement for those looking to decrease weight and body fat.

Another study published in November, 2004 found that a high intake of calcium may hinder weight and fat regain. The study found that after putting mice on a low calorie diet and producing weight and body fat loss, that those on a low calcium diet regained their weight after 6 weeks.

However, for those on a high calcium diet it was a different story. They found that the high calcium diets produced significant increases in lipolysis, decreases in fatty acid synthase expression and activity, and reduced fat regain. They also found that increasing calcium through the use of dairy products had significantly greater effects on fat regain.

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