Welcome back to the Biomechanics blog Seth O’Neil – aka the Achilles tendon twitter. He previously provided us with a fantastic synopsis of the 3rd scientific tendon symposium in Oxford held last year. In this post, Seth puts his tendon geek on once more, discussing the importance of soleus to the managing mid-portion Achilles tendinopathy. Over to you Seth ……..
Achilles tendinopathy (AT) commonly affects runners with prevalence rates around 10% reported but with some reporting rates as high as 50%.(1,2) Endurance runners are seemingly most at risk. AT is general accepted as being an active degenerative process, with some inflammation biochemical pathways involved. These changes eventually lead to tissue alterations, tendon pain and dysfunction. One of the main risk factors in otherwise healthy athletic individuals is repetitive high tendon load activity, such as running. During running Achilles tendon loads of around 4-5000N are normal,(3) but peaks as high as 9000N have been found.(4) It may be that one of the Plantarflexors is more involved than another.
Arguments for soleus involvement
1 = Soleus is an important force producer, especially for endurance athletes
Despite the common misconception that Gastrocnemius is the main force producer during running it is in fact Soleus. During running the Soleus muscle produces up to 50% of the total vertical support force(5), which is made possible by the fact it makes up 52% of the volume of the posterior calf.(6) The actual forces it produces are around 8 times body weight.(5) In comparison the Gastrocnemius produces forces around 3 times body weight.
2 = Soleus and gastroc function independently
Most clinicians and researchers seem to have assumed the muscles always work in unison, however they can and do work independently.(7-11) For example, during gait, some studies have found that Gastrocnemius functions largely isometrically whilst the Soleus tends to function eccentrically,(7,8,10) potentially leading to different strains and injury risk in in different parts of the tendon. Soleus is primarily the “endurance” muscle of the calf and as such has a higher level of slow twitch muscle fibres making it more likely to be essential for endurance running. These findings make the Soleus of primary importance to endurance runners- the highest risk group for AT.
3 = Soleus dysfunction in Achilles tendinopathy
When we examine the existing literature around calf function and AT it is really very limited. Wyndow et al (12)showed people with AT have an earlier offset of Soleus EMG activity during running compared to controls. Whilst this timing alteration may be an effect of pain and not a pre-cursor to injury it certainly shows different adaptations to induced tendon pain as per Henriksen’s seminal paper(13). Henriksen took healthy volunteers and injected Saline into their tendons to induce tendon pain. This injection produced quite widespread motor changes rather than the very specific motor control adaptations observed in Wyndow et al’s work, and also showed the Gastrocnemius to be most affected. However, we do not know how closely this links to in vivo tendon pain. We also currently know that reduced Plantarflexor muscle strength is predictive of tendinopathy development, based on Nele Mahieu’s (14)fantastic work. However, despite her study being published in 2006, all the later work on AT risk factors has failed to assess Plantarflexor function and instead often assesses other locomotive muscles
These studies formed the basis of my PhD work which centred on which of the Plantarflexors was primarily involved in AT. In our work we used isokinetic testing of individuals with AT and Healthy controls. 80 degrees of knee flexion was used to isolate Soleus force production, this position has been shown to inhibit Gastrocnemius*.(15) Our work highlighted that there were significant deficits in peak torque of the Plantarflexors in either position. Additionally, these deficits were so similar that our conclusion is that the Soleus is responsible for the majority of the observed deficits. Our study is not prospective so does not show pre-existing alterations, but it is worthwhile noting that these findings were bilateral. This may suggest that the peak torque reduction was a secondary motor response due to pain. However we must also note our concentric data was below the 50NM threshold identified by Mahieu as predictive of tendinopathy.
4 = Zone of pathology may relate to soleus
Using the images below we can clearly see which areas of the tendon are derived from fascicles continuous with the Soleus (note these images relate to the insertion and the degree of rotation will be less in the mid tendon). Current data suggests that the deep tendon (likely to be Soleus) experiences the most longitudinal displacement during gait (16)and imaging studies suggest 91% of symptomatic tendons have pathology in the medial part of the tendon- the part relating to Soleus.(17)
Image from Szaro et al(18)
Image from Edama et al 2014 (19)
Treatment of Soleus deficits
We currently have a strong suspicion that Soleus loading is necessary and essential to the resolution of Achilles tendon pain. In order to effectively rehab the Soleus muscle deficits we need to use knee bent calf raises -standing or seated, and incorporate concentric and eccentric loads and progress to eccentrics in isolation as this allows heavier loads to be used. Most runners with AT will need to use body weight + up to an additional 50-75%. Without this they will not be working at a high enough threshold to rehab to an eccentric strength of around 200% body weight (as shown to be the average for healthy runners).
Rehab obviously needs to be graded and gradually increased over time, and must also incorporate running and/or other stretch shortening cycle work.
The mechanism of effect is likely to be a combination of:
- Neuromuscular changes effecting the stretch shorten cycle
- Pain perception through a graded loading approach
There is sufficient evidence to substantiate the involvement of Soleus weakness in Achilles tendinopathy. However, further work needs to be completed to determine if it is a prospective risk factor. Neuromuscular alterations have been identified in a recent systematic review by Malliaras et al as the likely mechanism of effect of loading and we need to consider how we can change these deficits
A caveat on this blog is that not all patients will behave as the evidence suggests, i.e. with deficits in soleus. We need to convince ourselves that this is the case by finding clinical evidence of soleus dysfunction. For example, this could be poor function or endurance in knee bent standing calf raises, or poor seated soleus 8-10RM strength. Other clues may be very developed gastrocnemius and poor soleus bulk.
There are lots of other issues in Achilles rehab that we have not discussed in this blog, for example, running retraining, addressing other kinetic chain deficits, progressing to power loading – topics for future blogs, watch this space!
That’s all for now, and remember to consider soleus in your Achilles patients.
*( Our protocol has undergone rigorous reliability testing with 37 participants and has ICC values of 0.8 or better.)
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