From the main blog: http://equinemechanics.com/
My last post covered a little about tendon structure, hysteresis and crimp and what all this means for the equine digital flexor tendons (link here). This time I’m going a little deeper into how tendons work, tendon creep, and how to make tendons (and ligaments) stronger. The main tissues I’m going to talk about are the superficial digital flexor tendon (SDFT), deep digital flexor tendon (DDFT), and the suspensory ligament or third interosseous muscle (SL), which despite its confused names is usually classed as a tendon. These form the suspensory apparatus, and I’ve talked a bit about what they do in the last post, but I’ve put a picture above so that we’re all on the same page (from one of my previous papers Lawson et al., 2007). The picture also has the main bones of the distal limb marked – the third metacarpal (MC3), proximal sesamoid bone (PSB), distal sesamoid bone (DSB), P1, P2 and P3.
Tendons are made up of a lot of different proteins, but the two main ones are collagen which resists loads and elastin which allows stretching. In tendons the collagen fibres are mostly parallel. This makes them effective in resisting forces from one predictable direction, and in turn being exposed to unidirectional forces encourages fibres to align and be more parallel, and we have a happy cycle. The collagen fibres in ligaments are less organised, as they can be pulled from more than one direction (see picture below of my lovely collateral ligament model). This makes ligaments weaker if we’re comparing stretching in one direction. In tendons and ligaments, collagen fibres are crimped when not under load, so they have an increased ability to lengthen and resist force without failing when they’re aligned in the right direction, more about that in the earlier post.
The amount a tissue can stretch compared to its original length is measured using strain (the ratio of new length to original length). The other thing we’re fond of measuring is stress, which is the load it’s exposed to as a proportion of its size (force per area). The amount a tissue will deform for any given load (stress divided by strain) is called the modulus of elasticity. This varies between tendons, and is one of the properties that will determine ultimate strength. The stress vs strain graph pictured shows the effect of modulus of elasticity on point of failure (ultimate tensile strength). The more a tendon can lengthen, the more load it can take before it fails.
So as tendons are not equally strong in all directions (anisotropic), the chance of them failing partly depends on the direction of the force and partly on the tendon’s (modulus of) elasticity. The final important factor is how quickly a force is applied (viscoelastic properties).
Creep is the effect that allows tendons to progressively lengthen under the same force which has the effect of releasing tension. It’s the reason you can get further if you hold a stretch and keep stretching. Does it matter? Well, it means that tendons are great with constant pull, lousy with sudden impact. This is the reason that I talk a lot about the initial impact spike of hoof hits ground, and its effect on the digital flexor tendons, despite the fact that peak tendon strain occurs in mid-stance (for SDFT and SL) or end-stance (DDFT). Sudden changes in length such as a tendon struck (and stretched) by a hoof or an unexpected footfall from uneven ground – whether that’s rabbit holes or inconsistent arena surfaces, this is what causes a lot of injuries. I have a deep resentment of inconsistent/patchy all-weather surfaces.
To try and understand how to develop stronger tendons, a lot of research has compared foals raised in stables and given different formal exercise regimes with those kept in fields. Pasture-kept foals, that live out 24/7, consistently grow stronger tendons not just in the short term but actually develop tendons with more collagen fibres – i.e. with a higher potential strength that they can achieve through training. Whilst increasing exercise in stable-kept foals does lead to stronger tendons, in all studies 24/7 pasture exercise induces more strengthening changes than controlled exercise combined with stabling. Foals that are shifted from box-kept to being field-kept will to some extent catch up, but are unlikely to ever reach the same extent of collagen structure and tenocyte metabolism as foals that have always been in the field. It’s worth mentioning that in research tests horses that live in but have access to 2-4 hours of field time a day are considered to be stable-confined. You just can’t get the same amount of stimulation in 3 hours as you can in 24. Similarly pasture-kept horses are rarely in “natural” conditions, as pasture-size and herd-size tends to be limited, which reduces the amount of movement horses experience. You get the picture.
Research looking at the effect of training on tendons of horses of different ages supports this. Contrary to popular belief early training whilst immature can reduce the risk of injury in the older horse, as younger tendon has a strong ability to adapt to exercise and older (mature) tendon less so. The equine digital extensor tendons do grow (hypertrophy) with sprint exercise, but not so much the flexor tendons. The SDFT and SL, with their role in elastic energy storage, do not appear to gain in collagen content or diameter with exercise once fully mature, and these tendons are mature by the time the horse reaches about two years old.
After maturity tendons get weaker with age, and so become more likely to fail at a lower strain rate. When the horse is 5 years old the SDFT has already started to degenerate, with changes in crimp angle and collagen levels causing a reduced total strength. From here on in exercise accelerates this age-related degeneration.
Some studies have shown exercise-induced increases in SDFT diameter in 2yo thoroughbreds (but not warmbloods), but not an improvement in crimp angles or biomechanical properties – in other words tendons got bigger but not stronger. Tendons can grow due to pathological changes, so in research studies an attempt is usually made to rule these out by biopsy or ultrasound (as it was in this case). Tendon can also increase in volume just due to gains in water content, which is an exercise-induced response, but not one that helps. In immature warmbloods, all tendons and ligaments adapt, improve and strengthen in response to exercise, all apart from the SDFT. In all horses the SDFT just behaves a little differently.
In elastic-energy storing tendons such as the SDFT, increased size increases stiffness so an increase in size actually reduces function. In these tendons being able to lengthen elastically rather than snap is more important, and so too much stiffness is dangerous. The improvement in the common digital extensor tendon with exercise is more helpful in improving the performance of the SDFT as these two tendons work together to help the SDFT hit the right stiffness for elastic-energy storage from hoof strike to push off. As I covered in the last post, the introduction of scar tissue in the tendon from overuse or previous injury is another potential source of increased stiffness.
Compared to hugely-responsive tissues like bone, tendon adapts slowly to exercise, and possibly not at all once mature. It may be that research in this area just isn’t precise enough at the moment to detect changes and predict optimal training regimes. In the great hierarchy of research funding, grants are keenly fought over and some excellent projects will always go unfunded. Understanding equine tendons is not the crocodile nearest the boat for many funding bodies, and not all human research can be directly translated as equine tendons are so unique. Research continues; slowly.
Images from my own research and graphs as before from Robi et al. 2013.