How It Moves

In the first article of this series (The Horse of June 1995, page 21), I went on at some length about how much one could expect to predict performance based on the examination and evaluation of conformation. I tried to make it clear that, despite the many claims advanced, there is really not much accurate predicting of performance possible.

It is perfectly obvious, without any mechanical folderol, that a Shetland pony is not going to run as fast as a Thoroughbred. Why? If for no other reason, the short-legged Shetland has a much shorter stride length than the long-legged Thoroughbred. That such obvious differences are of limited predictive value may be shown by an experience I had many years ago.

In a Standardbred racing stable there was a black filly by Billy Direct that was a marvel of compact, powerful-looking pacer. She trained like a champion until about 2:18 or 2:20 for the mile. At that level she hung up and simply would not or could not go any faster. Watching her carefully, it was apparent that the frequency increased, but she didn't go any faster--the stride length did not increase. The effect was that she was working herself to death--legs just flying back and forth but going no faster. There was no lameness or any other apparent problem. Why? We'll never know; perhaps she just didn't want to go any faster and was increasing the frequency just to convince us she was doing the best she could.

In any case there was nothing that conformation could tell us about her lack of stride length. She was as big as her father, with better conformation (as one judges such things), and he was no mean pacing horse.

This gloomy picture is mitigated by the fact that conformation and other physical factors can be used to predict whether certain types of lamenes or singularly poor performance are probable. Let's begin with one of the most common lamenesses of racing horses--carpal arthrosis--often known as popped knee or bucked knee. It is a fact that this form of lameness is almost limited to racing horses: Thoroughbreds, Standardbreds, and Quarter Horses. It is rare in saddle horses, jumpers, draft horses, etc., but can be seen in certain extreme cases which we'll discuss later.

Postmortem examination of thousands of horses with carpal arthrosis has clearly shown that the primary damage in virtually all cases is damage to and destruction of the articular cartilage, particularly that cartilage between the radial carpal bone (in the upper or proximal row of bones making up the carpus) and the third carpal bone (in the distal row of bones of the carpus). When such damage occurs, the soft tissues around the joint become inflamed (swollen and hot), and the amount of synovial fluid in the joint increases. These are normal reactions to damage to any joint. One often hears of inflammation of the joint capsule (capsulitis or synovitis) as a primary site of damage, but that is simply incorrect. The cartilage is invariably damaged first, and the joint capsule changes are simply those of inflammation in response to the damage to the joint cartilage.

With time after the initial damage, the joint attempts to repair, and that leads to new bone formation on the front of the joint. This new bone, known as osteophytes, is often called "calcification," which it isn't. It is new bone forming as the joint attempts to repair the damaged cartilage.

In addition to the cartilage damage, the shearing forces applied to the small carpal bones can cause a small, shear fracture--usually called a "chip fracture." Sometimes the forces are so great that a slab fracture of the third carpal bone occurs, and we'll consider that later.

I believe it is clear to most people who study such things that the immediate cause of the damage to the cartilage of the radial and third carpal bone is too much dorsiflexion of the carpus. That is, the foreleg, rather than remaining almost straight as the load is on the leg, tends to bow or bend backward, doing so at the carpus (Figure 1). This is known as dorsiflexion.

Why does the carpus do this? Brace yourselves because we absolutely must do some mechanics now. In Figure 2, we have the foreleg at the middle of the support phase when the vertical force on the leg is greatest. That vertical force, and its line of action, is shown as F. That F force acts around the distance, 1, to cause what is called a moment or turning force, which is indicated by the curved arrow. It is apparent on inspection that this moment caused by the body weight acting on the leg will cause the leg to bow backward into dorsiflexion.

To resist or prevent that backward bowing, we must have an equal and opposite moment, indicated in Figure 2 by the dashed arrow. That moment is produced by the muscles and tendons on the back of the leg, indicated as a lumped force, T, acting around the distance, p. If the leg is to remain straight, as it should, these two moments--these two turning forces--must equal each other so that:

Tp-F1=0 or (the same thing) Tp=F1

When the moment Tp is too small, the leg bows back or dorsiflexes.

Next time we shall consider the relationship of all this to conformation.

About the Author

James R. Rooney, DVM

The late James R. Rooney, DVM, was Professor Emeritus of the Gluck Equine Research Center, Department of Veterinary Science, at the University of Kentucky. Rooney was a 1949 graduate of Dartmouth College with a bachelor's degree in English drama; a 1952 graduate of New York State Veterinary College at Cornell University; and a Diplomate, Emeritus, of the American College of Veterinary Pathologists. Rooney authored more than 100 articles and books on diseases and locomotion of horses, including: Biomechanics of Lameness in Horses, The Lame Horse, Clinical Neurology of the Horse, Autopsy of the Horse, and Mechanics of the Horse.

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