Treatment of skeletal and cardiac muscle using gene transfer is a major goal for diseases such as Duchenne muscular dystrophy (1). However, recent developments have raised fears about the potential for abuse in athletic competition. Some of the uses of gene transfer are relatively easy to detect in standard samples, for example the glycosylation pattern of erythropoietin produced from skeletal muscle differs from that produced by the kidney (2). In contrast, local genetic modification of skeletal muscle may be much harder to detect without taking invasive biopsies which are not currently part of the testing regime for athletes. Improvements in viral vector technology have the potential to genetically modify large amounts of muscle to change phenotype or improve repair and the hypertrophic response to training. With current technologies one can produce increased gene expression that supports increased muscle mass, e.g. insulin-like growth factor-1, IGF-1 (3), or local production of agents that block the action of the negative regulator of muscle mass, myostatin. The presentation will review the limits currently in place that reduce the potential to exploit gene transfer/inhibition technology, as well as possible methods to detect such genetic manipulation. Provided the products do not leak out into the general circulation, this type of modification will be hard to detect indirectly except by looking for antibodies to the delivery system, for example an adeno-associated viral vector. An alternative approach will be to examine the metabolic profile of the individual looking for abnormal patterns of different proteins and/or metabolites, such as is used for the detection of testosterone abuse.