The racing Thoroughbred is trapped between a rock and a hard place. The rock is speed, which evolved slowly by natural selection for 50 million years, then rapidly by human hand the last 500. The hard place is where we find our ward today, beset by vulnerable feet, a grain-bothered gut, hot behavior, bleeding lungs, a sloping vulva, gastric ulcers, tying-up, crooked legs, and developmental orthopedic disease. The rock and the hard place appear to be linked genetically and positively and, if so, selecting against any of these undesirable traits will also reduce the genetic potential for speed.

Heritability or the genetically determined fraction of racing performance has been estimated as 0.1 to 0.2 based on racing times, and 0.3 to 0.4 based on earnings or handicap ratings. That leaves at least 0.6 of the variation in racing performance to be accounted for by environmental factors and genetic-environmental interactions. Annual genetic improvement of British Thoroughbreds has been estimated as 0.94 pounds of weight assigned in a free handicap. Slow improvement in winning times of English classics has been attributed to over-estimation of speed heritability or to physiological limits.

Heritability is probably higher for sprinting and for staying than for middle-distance performance, according to recent studies in Japan and Australia. This fits with physiological limits of performance, which are different for speed or stamina. Genetic studies have focused on high rates of production and clearance of lactic acid that enable sprinting, and maximal oxygen uptake for staying.

My hypothesis is different—the limits of breeding for speed are