Welcome to to tendinopathy blog 11 for 2016. The audio lecture of my simplified view of tendon management will be emailed to subscribers imminently! – sign up here to receive it.
A super blog this week – all about the effects of detraining and deconditioning on tendon. An interesting topic so have taken the liberty to go off on a few tangents with some interesting clinical messages. Hope it is of interest to people – please leave a comment and let me know. Read the full blog here.
See you next time
Is detraining really that bad for tendons? Probably
What they did: Frizziero et al. systematically reviewed studies investigating detraining of tendons. We know that physiological loads are required to maintain tendon homeostasis. Mechanotransduction is the process by which mechanical load influences tendon cells and produces cell signalling that leads to adaptive changes (e.g. homeostasis, strengthening of material properties) or maladaptive changes (e.g. tendon pathology, weakening of material properties). The type of load on the tendon cells (compressive, shear, tensile) and parameters (e.g. duration) will influence the response. It is thought that the type of load most likely to lead to tendon maladaptive change is sudden changes in energy storage load (walking, running, jumping) +/- compression, but at the other end of the load spectrum, stress shielding or reduced may also lead to pathology – the figure below from the continuum model of Cook and Purdam presents this nicely.
Frizziero et al. were interested in exploring the mechanotransductive load spectrum; specificallt they looked at the effects of detraining after a period of training. They conducted a systematic review following the PRISMA guidelines and identified 8 studies that investigated the effects of cessation of training.
What they found: There were 4 human studies and 4 animal studies. The animal studies were on rat patellar tendon or chicken Achilles tendon and investigated 3-10 weeks of treadmill running followed by 2-4 weeks of no exercise. Training stimulates tenocytes and in some cases improved tendon structure. Detraining generally resulted in reversal of improvements and poorer quality and strength of collagen (e.g. more type III vs type I collagen). A key point with these studies is that they involve training with energy storage loads, ie running. It is also important to note that one of them actually looked at immobilisation rather than detraining (Foutz 2007).
In regards to the human studies, Kubo et al. (2010, 2012) has shown that 3 months of heavy slow resistance training increases tendon stiffness but then there is reduction in stiffness back to baseline levels with 2 months of detraining. McMahon et al. (2013) compared training at short knee range (0-50°), long range (40-90°) or large range (0-90°). They performed split squats, lunges, squats, leg extension and leg press. Patellar tendon stiffness increased more in the groups that trained at long or large range (40-90 or 0-90°), and these groups better maintained adaptations during detraining (which involved 4 weeks of no exercise). Kannas et al (2015) found that after performing plyometrics on a 15 degree incline the gastrocnemius aponeurosis (continuous with the Achilles tendon) strain increased, and after 4 weeks of detraining returned to baseline levels.
Clinical interpretation: This review summarises the effects that detraining has on tendon. Not dissimilar in some aspects to the negative effects that we are familiar with related to stress shielding or immobilisation (e.g. Arnoczky 2007).
I feel it needs to be separated in two parts. The animal studies mainly show detraining after energy storage load (running) and show that it may be detrimental to structure. The human studies show reversal of stiffness adaptation after stopping heavy slow resistance training, but it may take 2 months. The final human study, the Kannas study, is the odd one out, as they found increased tendon/aponeurosis strain (so reduced stiffness you would assume but not reported) after plyometric on an incline, and this reversed with 4 weeks of detraining. This is most likely a neuromuscular adaptation rather than a change in the tendon. So overall, the review actually provides evidence for neuromuscular and tendon detraining effects, and although evidence is limited neuromuscular detraining may occur faster – makes sense. This is consistent with reports of faster muscle immobilisation effects compared with tendon (Kannus 1997).
The adaptations seen with heavy slow resistance and plyometrics in humans are consistent with what is reported in the Bohm systematic review from last year (definitely worth a read). They found that heavy load regardless of contraction type (isometric, eccentric, concentric) lead to increased tendon stiffness, whereas effects of plyometric training were inconsistent.
A question that often comes up about stiffness is, is it good? Ie should we strive to increase tendon stiffness? Tendon acts like a spring during stretch shorten cycle activities such as walking, running and jumping (see figure below – Achilles tendon stretches during terminal stance so calf fascicles can function at the same length). The Achilles tendon is especially good at this spring like function. Because the tendon stretches during these activities the muscle can act more isometrically and this saves energy and can improve performance (Lichtwark 2007). Optimal tendon stiffness is task dependent. For example, a stiffer Achilles tendon is more optimal for running compared to walking economy (Lichtwark 2007). And tendon stiffness is only part of it. There is also muscle-tendon unit stiffness and leg stiffness that is also ‘tuned’ or specific to task. So clinically, we focus more on optimising performance and efficiency rather than influencing tendon stiffness, although in a novice athlete or someone with pathology this may be a consideration.
So let’s wrap up with some beefy clinical take homes…
How do the findings of this review relate to the detrained/deconditioned athlete?
The human studies in the Frizziero review train relatively untrained individuals for a relatively short term, so well trained athletes may respond differently. But we know from clinical experience deconditioned athletes are at risk of tendinopathy – is it it due to tissue deconditioning? Of course the tissue will decondition with time but perhaps in the very short term (e.g. 3 week injury break) we are dealing more with neuromuscular changes. On the other end of the spectrum, ie multiple / long term injury set backs, cognitive-emotional issues are really important, e.g. hypervigilance. I had a great example this week! A patellar tendon patient who presented with 6 months of pain, BUT, the pain came on when he was making a come back from a 4-year injury run.
So can we avoid detraining being a risk factor for tendon pain?
This will sound simplistic, because it is! The key principle is to avoid huge breaks and fluctuation in load, particularly for ‘at risk’ individuals (e.g. they have a past history of tendon pain). This basically means maintain as much of their ‘usual’ load as possible during the offseason and injury breaks. We know from the Bohm study that heavy isometric and isotonic load seems to have more of an adaptive tendon response than, for example, plyometric load. But as I have argued in this blog neuromuscular detraining may be even more important in some instances, so it’s important to maintain their energy storage function efficiency (clinical translation; keep up some running, or hopping, etc). As always, an eclectic approach is best, cover all bases, so you make sure you don’t give the tendon any reason to complain!
There are interesting parallels here with rehab. Silbernagel 2007 showed us that it is ok to maintain energy storage/sport loads (e.g. running) during Achilles rehab as long as this is done within a pain monitoring framework (see graph below – similar VISA outcomes at all time points in the group who stopped and the group who continued sport in the first 6 weeks).
Although clinical outcomes were not better (or importantly worse) if they continued sport, those that continued sport had improved drop countermovement jump and hop quotient at 6 months (not seen in the group that stopped sport). I think this is such an important finding as it clearly highlights the neuromuscular benefits of continued energy storage loads, of course as per a pain monitoring model.
Until next time, keep joining the dots
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