IN-DEPTH: RACING-RELATED LAMENESS


bending; therefore bone enlarges its cylindrical shape whenever it has the opportunity.14 The adaptation of bone to training is different


than most tissues because it trains to the level of work rather than the volume.17 Bone requires only a limited number of loads in a specific exercise pe- riod to stimulate its response. Experimentally, this has been determined to be approximately 36 similar cyclic loads.17 Two thousand similar loads were no better than the first 36 loads at producing hypertro- phy of the bone. In fact, in an exercise period of more than 36 similar cycles, the excess cycles be- come destructive, adding excess damage that can then begin to accumulate overwhelming the bone’s ability to repair the damage.10,17 The end result of this can be destruction of the bone rather than hy- pertrophy and eventually injury in the form of a stress fracture.10 Soft tissues such as the heart and muscles require a volume of work to train. The “interval training” of these tissues to increase the volume of work at a higher level revolutionized the training of people, but, when tried in the Thor- oughbred racehorse, the skeleton could not with- stand the volume of work. Endurance horses and Standardbred racehorses are able to somewhat more successfully apply the interval training principles, but it results in too much skeletal damage in the Thoroughbred to be successfully applied.4 Because damage and response to training is work- specific, the damage to a racehorse’s bone can be mitigated somewhat by varying the gait and the training surface. Mixing more trotting and the use of different training surfaces varies the load the bone encounters and therefore varies the type of damage done by the training. This allows the volume of work to be increased without as much cumulative damage to the bone. Monotonous large volumes of similar training, such as lots of repetitive galloping over the same surface, becomes damaging to bone rather than stimulating of bone adaptation.21 As the level of exercise increases, the tolerable volume decreases. Epidemiologic data shows “a horse that had accumulated a total of 35 furlongs of race and timed-work distance in 2 months, com- pared with a horse with 25 furlongs accumulated, had an estimated 3.9-fold increase in risk for racing- related fatal skeletal injury (95% confidence inter- val2.1, 7.1).”19 Mindlessly ignoring the ability of the horse’s bone to respond to the amount of exercise it is performing will eventually result in damage accumulation and injury.10,22 The diaphysis of the metacarpus provides a dra-


matic example of the adaptation to exercise in a more macro-example of the adaptation that is occur- ring in the entire skeleton and how it can be dis- rupted if the adaptation does not occur fast enough or completely enough to maintain soundness.10,21 Exercise produces new bone at sites of compression but not at sites of tension strain during exercise. The best evidence indicates that this is an active “biologic” process mediated by the osteocytes in the


416 2013  Vol. 59  AAEP PROCEEDINGS


Fig. 2. Metacarpal (left) and tibial (right) stress fractures show the typical 45° configuration of a stress fracture.


loaded bone that monitor the loading by means of their large dendritic networks within the canaliculi of the cortical bone.3,9,11 Compression loading re- sults in new bone production that models the bone to best resist the compression (Fig. 1). Bone is pro- duced in the areas of the most compression.4 This new bone then reduces the compression differential until the load is balanced on the long axis of the bone and the bone receives neutral forces during loading. Overload of compressed bone results in the classic stress fracture configuration that occurs in all ma- terials.10 The shear stress of compression results in an oblique fracture at 45 ° to the long axis of the bone (Fig. 2). It propagates into the bone until a lamellar plane that is of different stiffness is en- countered, and the fracture then propagates along that plane in the long axis of the bone. If no lamel- lar plane is encountered, the stress fracture may propagate through the cortex into the medullary cavity (Fig. 3). In the young training horse, radio- graphically evident multiple stress fractures can sometimes be identified in horses that have pain and lameness originating from the metacarpus (Fig. 4). When training is proceeding faster than the bone can ossify and strengthen, the newly formed bone is


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