This important article, by veterinarian Nancy Loving, is a must read! Originally posted in the Horse magazine.
Bone was once considered an inert material with its structure defined by genetics. But it turns out there’s a lot more at work, explained Larry Bramlage, DVM, MS, Dipl. ACVS: “Selective breeding dictates the initial skeleton, but adaptive training in response to exercise modifies it further.” He and other racehorse surgeons are striving to better understand the balance between tolerable and excessive damage—the adaptive kind that occurs naturally and the type that sidelines animals or ends their careers.
During his presentation at the 2013 American Association of Equine Practitioners’ Convention, held Dec. 7-11 in Nashville, Tenn., Bramlage, of Rood & Riddle Equine Hospital, in Lexington, Ky., explained that bone is the only tissue capable of entirely reconstituting itself. With this capacity to change, he noted, there are several ways long bones strengthen themselves in response to training, including modeling and remodeling. Modeling is the process in which bone adds to itself, both inside and out, while remodeling is how existing bone tissue alters itself.
Bramlage started by describing the dynamic nature of bone activity on a cellular level. Two types of bone cells are involved in bone modeling and remodeling: osteoblasts and osteoclasts. Osteoblasts become trapped in the bone and become osteocytes, which are key to sensing biomechanical loads on the skeleton during exercise and directing bone tissue response accordingly. As they detect mechanical loads, they prompt additions to (formation) or reductions in (dissolution) bone mass, to achieve correct bone density for current athletic demands. Osteoclasts then tunnel through and cut canals into the bone, with osteoblasts following to make new bone.
It’s important to note that bone becomes stiffer as it ages. “This can become a problem when bone formation stops for a time and then is reinitiated due to changing stimuli,” said Bramlage. As bone loses its homogeneous structure, a distinct interface forms between new and old bone that can promote failure, similar to the interface of two types of pavement in a patched pothole. “Bone trains in a stair-step fashion with adaptations being work-specific,” Bramlage stressed. “Overloading results in microfractures that stimulate bone to strengthen (by way of osteoblasts creating new tissue to fill and repair the microfractures), but if there is inadequate repair in the face of exercise, damage accumulates.”
He refers to this as “exercise debt” that must be paid. Rest is an effective treatment, he said, as it enables overlying new bone to become as stiff as the underlying, older bone, to repair any damage, and to add more bone to better stand the level of exercise seen.
Researchers have shown in numerous studies that it’s ideal to train 2-year old Thoroughbreds; otherwise, their bone growth stops, and when they begin training later and start accumulating new bone, the interface between the old and new is more susceptible to stress fracture. “By converting growing bone into exercising bone before it stops growing, there isn’t the interruption in the bone formation and, therefore, quality,” he explained.
Further, bone trains to the exercise level instead of amount. Bramlage said this is not true of the cardiovascular system, which requires the animal to complete a volume of work before improvements in cardiovascular capacity are observable. Therefore, cardiovascular development must be balanced with bone training and not progress faster than the bone can respond; in the horse the heart and lungs are capable of responding much faster than the bone to large exercise loads. Trainers developed interval training programs, which presented means of rapidly improving the cardiovascular system in people but resulted in too many destructive repetitive cycles on bone in horses.
“After a number of cycles necessary to stimulate bone strength, further repetitive work becomes traumatic,” Bramlage said. “We gallop too much and don’t vary gaits enough.”
Repetitive cycling stress from high-speed exercise causes damage that must be repaired and causes the bone to remodel to prevent the damage from occurring again, but Bramlage said this takes time. For instance, he noted that, a horse running 35 high-speed furlongs in a two-month period is four times more likely to experience fatal skeletal injury than a horse running 25 high-speed furlongs over the same time.
“All athletic horses get the same diseases in bone, but in the high-level racehorse the degree is magnified,” added Bramlage. This is particularly true in joints, he noted, because bones cannot enlarge or distort at joint surfaces because the body must preserve original joint anatomy. The bone must respond by changing internally, which it cannot do quickly enough during periods of too-intense training and repetitive stress. This can cause bruising at the ends of long bones, predisposing the areas to fractures and degeneration if there’s no intervention.
Bramlage also suggested that there might be a tendency among individuals in the racing industry to select against “durable” racehorses if the qualities they strive for favor early brilliance and speed over longevity. The skeleton is “dead weight” during exercise, so a lighter horse is faster, he said, if all else is equal. As horses are selected for more speed, their lighter structures might not be able to withstand the wear and tear of intense exercise. Shoeing appliances, like toe grabs, and various track surface types can add to the problem, by altering gait and concussion on the limb.
Increasing the rest time between races improves the opportunity for bone injury healing, but Bramlage stressed that “for treatment, nothing compares to paddock turnout to resolve cumulative stress injury in significantly damaged bone.”