Estimating peak strains associated with fast exercise in thoroughbred racehorses.

Abstract: The third metacarpal bones (MC3) of racing Thoroughbreds are a common site for bone damage. The midshaft dorsal cortex (DC) of MC3 thickens in response to fast exercise. It is not clear if it changes to a shape and size that limits the peak bone strains to a range associated with normal loading in other species. Objective: To relate the proportionate size of the DC cortex in racehorses exercising at racing speed to surface strains, and test whether the DC reached a plateau that was sustained through subsequent exposures to racing speed exercise. Methods: Standardised lateral MC3 radiographs were taken weekly for 2-5 years in 40 racehorses in race training (16-19 m/sec). DC, medulla (M), and palmar cortex (PC) thickness were measured. at 2.5 cm distal to the nutrient foramen. An index (RI) of the relative thickness of the DC was calculated for each radiograph (RI = [DC+PC]/ M multiplied by [DC/ PC]) and used to calculate strains at 12 m/sec from an equation published previously. Results: Mean time to plateau in DC thickness was 501 days, mean increase in DC was 3.9 mm on the left and 3.7 mm on the right. Rate of change was 8.8 microm/day on the left, and 8.4 microm/day on the right during this time. In most horses the medulla width did not change between the first and last measurements so these bone growth rates reflect periosteal bone growth on the DC surface. No further significant change in DC or RI was found, once they had reached a plateau. Mean DC thickness at the plateau was 14.7 mm on the left and 14.9 mm on the right. Mean RI at the plateau was 3.7. This equated to peak microstrains at 12 m/sec of -2492 and suggests that strains much greater than 3000 microstrains occur at racing speed in most horses. Conclusions: Experienced racehorses are likely to be exposed to peak strains beyond the normal limit for adult mammalian bone to resist without damage and strains associated with very fast exercise may not be sufficient stimulus to induce further bone modelling in these horses. Conclusions: Strains occur in the bones of experienced racehorses at a higher level than normal for other mammalian bones. Hence there may be other mechanisms operating in this particular bone in racehorses that protects the bone from failure when exposed to the high strains associated with fast exercise speeds. Investigation of such mechanisms may provide an insight on how to reduce the likelihood of damage to this bone during very fast exercise.