An athletic phenotype have not yet been identified. Domestic animal species provide valuable opportunities to identify genes underlying phenotypes that have been strongly selected because discrete breeds have arisen relatively recently from a small number of founder animals. The Thoroughbred population is a Echinatin closed population established in the 16th and 17th centuries from crosses between local Galloway and Irish hobby horses with imported Eastern stock. As with many domesticates, the Thoroughbred originates from a small number of founders; just one founder stallion contributes to 95% of paternal lineages and ten founder mares account for 72% of maternal lineages. However, despite a limited number of founders and strong selection for racetrack performance some 35% of variation in performance is Butenafine hydrochloride heritable. These population demographics coupled with intense recent selection for athleticism offer a unique opportunity to identify genomic contributions to exercise-related traits. A number of approaches may be taken to 
identify genes underlying phenotypic adaptations. Whereas a candidate gene approach requires a priori knowledge of gene function and linkage mapping requires information about familial relationships as well as access to samples from large numbers of relatives, hitchhiking mapping using population genetics-based approaches evaluates the effects of natural or artificial selection across whole genomes in populations of unrelated individuals that have been subjected to differential selection pressures for the trait or traits of interest. Although it is generally considered that microsatellites themselves will not be subject to selection, loci closely linked to the microsatellites will influence their population genetic behaviour. Therefore we have employed a hitchhiking mapping approach to identify signatures of positive selection in the Thoroughbred genome and to localise genomic regions containing genes influencing exercise-related phenotypes. Mutations in ACTA1 have been found to disrupt sarcomere function in patients with congenital fibre type disproportion and other muscle weakness pathologies. In skeletal muscle a-actinin is responsible for cross linking actin filaments between adjacent sarcomeres and is known to interact with PI3K. Polymorphisms in the gene encoding a-actinin 3 are among the best characterised athletic-performance associated variants in human endurance athletes.