One of the most interesting papers I have read all year! Highly recommended.
Dave
Abstract
Exercise causes oxidative stress only when exhaustive. Strenuous exercise causes oxidation of glutathione, release of cytosolic enzymes, and
other signs of cell damage. However, there is increasing evidence that reactive oxygen species (ROS) not only are toxic but also play an important
role in cell signaling and in the regulation of gene expression. Xanthine oxidase is involved in the generation of superoxide associated with
exhaustive exercise. Allopurinol (an inhibitor of this enzyme) prevents muscle damage after exhaustive exercise, but also modifies cell signaling
pathways associated with both moderate and exhaustive exercise in rats and humans. In gastrocnemius muscle from rats, exercise caused an
activation of MAP kinases. This in turn activated the NF- B pathway and consequently the expression of important enzymes associated with
defense against ROS (superoxide dismutase) and adaptation to exercise (eNOS and iNOS). All these changes were abolished when ROS
production was prevented by allopurinol. Thus ROS act as signals in exercise because decreasing their formation prevents activation of important
signaling pathways that cause useful adaptations in cells. Because these signals result in an upregulation of powerful antioxidant enzymes,
exercise itself can be considered an antioxidant. We have found that interfering with free radical metabolism with antioxidants may hamper useful
adaptations to training.
© 2007 Elsevier Inc. All rights reserved
Original Contribution
Moderate exercise is an antioxidant: Upregulation of antioxidant
genes by training
Mari-Carmen Gomez-Cabrera, Elena Domenech, Jose Viña
Department of Physiology, Faculty of Medicine, University of Valencia, Blasco Ibañez, 15, 46010 Valencia, Spain
Received 18 December 2006; revised 29 January 2007; accepted 1 February 2007
Available online 9 February 2007