Free Radicals In Sport

Highly intensive sport performance is characterized by a number of events, which make increased free radical production and related cell damage most probable. Oxygen consumption for aerobic energy production increases about 20-fold and so does free radical production since both processes are quantitatively interrelated.

Additionally, free radicals may result from energy depletion in skeletal muscle during which ATP is broken down to ADP 2 AMP 2 hypoxanthine, which finally leads to the formation of xanthine and uric acid in red blood cells and endothelial cells, resulting in the liberation of free radicals. This is the xanthine oxidase (XO) pathway. Also the autooxidation of catecholamines as well as the production of nitric oxide, substances that are increased during exercise, lead to free radical production.

From animal experiments as well as from surgery in humans it is known that a restriction of blood flow, followed by reperfusion (restoration of blood flow) is accompanied by an enhanced production of free radicals. Similarly, it may be that a significant reduction of the blood flow to the gastrointestinal tract, as takes place during endurance events in a dehydrated state, may cause similar effects. In marathon runners, a condition of gut ischaemia and gut mucosa necroses, leading to bloody diarrhoea after the race, has been observed and one may speculate that free radicals are associated with the damage of the epithelial gut cells. Also, iron released from red blood cells during haemolysis may induce free radical formation (290).

Muscle soreness after an intensive bout of exercise in less well trained subjects may be linked to free radicals. The micro-trauma (disruption at the Z band level of the sarcomeres) which results from acute overload cannot be avoided by antioxidant systems, because it is mechanical in nature. The repair process of mechanically damaged muscle fibres, however, involves an inflammatory process, which causes muscle pain, stiffness and loss of muscle strength, especially in the period 2-5 days after the sport event. It is suggested that free radicals play an important role during this inflammatory process and that supply with adequate amounts of antioxidants may lessen both the severity and the duration of this delayed muscle soreness (288).

Endurance exercise in polluted air, such as running a major city marathon on a hot summer day in the smog, has been suggested to lead to damage to the lung tissue induced by ozone. Free radicals are suspected to be the mediating mechanism. Accordingly, vitamin E supplementation is suggested to reduce such damage and lung function impairment (285).

Training is known to significantly increase the activity of the enzymatic defence mechanisms, a normal physiological adaptation (289, 299). One may speculate that such an adaptation in itself may be sufficient to offset possible effects due to increased free radical formation. If not, regular intensive exercise would lead to impaired health and body function.

The conclusions and consensus as listed below can be obtained from the above-cited reviews, in particular those of Sen et al. (276) and Li Li Ji (277).

Key points

  • Free radicals are involved in the aetiology of cell damage and tissue pathology.
  • The body possesses several defence mechanisms against free radicals, enzymatic and non-enzymatic, including nutrient derived cofactors
  • Free radical production during and after exercise is increased as a result of oxidative and metabolic stress, micro-trauma and ischaemia.
  • The body's defence mechanism capacity depends on nutritional status, especially the adequate supply of substances with free radical scavenging properties. Free radical damage to cells and tissues is assumed to be aggravated in cases of inappropriate defence mechanisms.
  • Marginal supply with cofactors, such as selenium, zinc, copper and manganese may limit enzymatic adaptations. Hard data, from athletic populations, showing that intake of such cofactors is insufficient and that this may impair free radical defence mechanisms is lacking, however.
  • Antioxidant supplementation may have an effect in cases of impaired defence mechanisms as seen with marginal nutritional intake leading to antioxidant vitamin or cofactor depletion.
  • In well trained healthy athletes there is no evidence of impaired body defence mechanisms
  • Vitamin E supplementation has been shown to reduce enzyme markers of tissue damage in the post-exercise phase. The effect of this observation on athletic performance or health status of the athlete remains unclear. Performance remains unaffected.
  • Vitamin C and Q10 when given in higher dosages can work as a pro-oxidant, which will potentiate free radical production. The role of both compounds on performance enhancement has not been proven.
  • There is lack of evidence for the role of beta carotene in performance and in antioxidant defence mechanisms in the exercising athlete.
  • Glutathione supplementation has been shown to improve performance in animal studies and to prevent exercise induced oxidation of GSH. As such GSH supplementation may be promising for further research to define possible benefits for the athlete.

IV Nutritional Ergogenics and Metabolism

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