The production of radicals in exercise was first established over 30 years ago in early studies undertaken by Dillard1 and Davies et al.2,3. But it was not until much later that McArdle4 first established that contractile activity in muscle released the superoxide radical (O2·-). Since these studies, discussion and debate on the role of reactive oxygen and nitrogen species (RONS) in exercise has continued. RONS are known to have the ability to interact with proteins, lipids and DNA5 to alter function and cause adduct formation. It is also now well established that transient increases in RONS are essential in cell signalling, muscle remodelling and regulation of gene expression6. The debate among exercise physiologists, concerning the relevance of ‘oxidative stress’ in exercise, and whether this term is really appropriate, has mirrored a wider debate in free radical biochemistry.

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