Abstract des Autors

An increasing body of evidence has shown that strenuous exercise increases the formation of reactive oxygen species (ROS) in the muscle by a multitude of possible mechanisms. In order to prevent oxidative stress, the body contains a large number of non-enzymatic (e.g. antioxidant vitamins, polyphenols, glutathion) and enzymatic (e.g. superoxide dismutase, glutathion peroxidase, catalase) antioxidants that either prevent ROS formation or scavenge radical species and convert them to a lesser active molecule. Oxidative stress can lead to damage or destruction of cellular macromolecules such as lipids, proteins, nucleic acids and components of the extracellular matrix. Therefore, oxidative stress has been associated with decreased physical performance, muscular fatigue, muscle damage, and overtraining. It has been reported that the body's physiological amount of antioxidants is not sufficient to prevent exercise-induced oxidative stress and that additional antioxidants are needed to reduce oxidative stress, muscular damage or overshooting inflammation. However, the hypothesis that the rise in exercise-induced ROS is associated with oxidative stress has not been confirmed by all studies. Furthermore, a simple cause and effect relationship between plasma levels of several antioxidants, exercise-induced muscular, metabolic, hormonal or inflammatory stress markers on the one hand and oxidative stress on the other hand could not be found. At the moment, there is no clear evidence that subjects exercising on a regular basis would benefit in terms of reduced exercise-induced stress, increased performance or faster regeneration from additional antioxidants, exceeding the amount that is provided by a healthy, balanced nutrition. Verf.-Referat