The landscape of inheritance shifts with each discovery, but at this point, I currently believe there is a correlation between elite athletic performance and the mitochondrial DNA in Thoroughbred racehorses. We've been cataloguing mitochondrial haplotypes in Thoroughbreds as an initial step. I've also built a database of racehorses associated with their haplotype.

While athletic performance in horses has yet to be investigated at the genetic level, some asumptions and intriguing possibilities can be inferred from research into human athletic performance. The mitochondrial genome (16,596 - 16,660 bp) appears to have a central role in athletic performance since it is deeply involved with adenosine triphophate (ATP), the fuel of the biological cell and the creature composed of those cells, however its mechanism and function have not yet been fully investigated. A slight difference in efficiency (perhaps, less than one-tenth of one-tenth percent difference, for example) in creating, converting, or utilizing adenosine triphophate conferred by evolutionary advantage to the founder matriarch of one of Bruce Lowe's female families, that may lie dormant or latent in her descendants, may then become activated or expressed by other genetic processes (selective mating, for example) in elite descendants.

A nuclear gene variant in humans (and all mammals), alpha-actin 3 (ACTN3), has been suggested to be associated with fast-muscle-fiber function that is vital to sprinting & power athletic performance. Elite athletes are three times more likely to have this gene as other sportspeople. Other nuclear genes that have been suggested as having an association with performance include the following.

There are two common variants of the nuclear ACE gene. ACE II seems to be endurance related and predominates in athletes engaged in endurance- or stamina-related sports. ACE DD seems to be related to sprinting.

PPAR-delta is associated with predominance of slow-muscle-fibers found in stamina or endurance athletes.

Different variants of CKMM may affect VO₂max – the rate at which an athlete converts oxygen into energy as a response to training.

A mutation in the gene, myostatin, stops functional myostatin from being produced and thereby causes athletes to have very large muscles.

Multiple copies of the gene, aquaporin 7 (AQP7), a transporter of water and sugary compounds into cells.

Loren Bolinger, November 23., 2007