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Translational Rehabilitation from Human to Horse: Strategies for Tendon Rehabilitation
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All tendons connect muscle to bone to enable movement. However, some tendons additionally act as energy stores. They stretch like springs and store energy when loaded, recoiling on release to reduce the work a muscle must contribute to locomotion. The primary equine energy storing tendon is the SDFT, which stretches up to 20% during the landing phase of galloping, increasing galloping efficiency up to 36%. Under such extreme mechanical demands, it is not surprising the SDFT is prone to overuse injury, particularly amongst racehorses and other horses used for fast galloping disciplines. SDFT injuries are highly debilitating, requiring considerable rehabilitation periods and are often career limiting. There is little convincing evidence of efficacy for any current treatment, and even after extensive periods of rest and rehabilitation, re-injury rates are extremely high, with little knowledge of how best to safely reintroduce training.
Most studies agree that high SDFT injury rates are a function of mechanical demand. Like most natural materials no SDFT is fully elastic, losing energy during each loading/ unloading cycle (hysteresis) and accumulating fatigue damage. Building on this, we have a growing body of evidence proportionally linking SDFT elasticity with injury risk: The more efficiently the SDFT can function under stretch and recoil, the more efficient (hence potentially faster) galloping becomes, whilst a tendon with poor stretch and recoil is more injury prone. We know injury risk increases with age, and that one of the biggest risk factors for injury, is previous injury. Tendon does not fully regenerate following injury, but in fact replaces injured tendon tissue with fibrocartilaginous scar tissue which lacks the ordered hierarchical structure of longitudinally aligned collagen fibres, organized into fascicles, which are separated by an inter-fascicular matrix which provides most of the elastic function to the SDFT. It has been hypothesized that reinjury occurs as a consequence of the abrupt interface between the stiffer scarred fibrocartilage, and the more elastic surrounding normal tendon. [...]
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