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Does the intramuscular tendon act like a free tendon?
  1. Peter Brukner1,
  2. Jill L Cook1,
  3. Craig Robert Purdam2
  1. 1 La Trobe Sport and Exercise Medicine Research Centre, La Trobe University, Bundoora, Victoria, Australia
  2. 2 Physical Therapies, Australian Institute of Sport, Bruce, Australia
  1. Correspondence to Dr Peter Brukner, La Trobe Sport and Exercise Research Centre, La Trobe University, Melbourne, VIC 3086, Australia; peterbrukner{at}gmail.com

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There​ ​has​ ​been​ ​a​n​ ​upsurge​ ​of​ ​interest,​ ​and​ ​some​ ​confusion, about​ ​the​ ​role​ ​of​ ​the ​connective​ ​tissue​ ​condensations within​ ​the​​ ​lower​ ​limb​ ​muscles, notably​​ ​biceps​ ​femoris,​ ​rectus femoris, ​gastrocnemius​ ​and​ ​soleus.​ ​These​ ​bands​ ​are​​ ​variably referred​ ​to​ ​in the​ ​literature​ ​as ​intramuscular​ ​tendon, connective tissue, central tendon​ ​or​ ​aponeurosis, and can have a variable appearance (aponeurotic, cord-like) and vary between individuals.1​ ​

These intramuscular tendons (​IMTs) act as​ central​ ​supporting​ ​struts​ ​to​ ​which​ ​the​ ​muscle fibres​ ​attach​, and they smooth and amalgamate asynchronous motor unit contribution. ​ ​ ​Muscle strain may tear the myofibrillar attachments​​ ​from​ ​the​ intramuscular​ ​tendon, ​​ with resultant​ bleeding and oedema. Occasionally​, ​the​ ​damage​ ​may also involve a partial or complete tear of ​the​ ​ intramuscular​ ​tendon itself.

When​ ​the​ ​ intramuscular​ ​tendon ​is​ ​damaged, ​ ​the​ ​injury​ ​is​ ​regarded​ ​as​ a ​more severe strain. ​ Damage to​ ​the​ intramuscular​ ​tendon ​of​ ​the hamstring group ​ has been associated with a prolonged ​​return​ ​to​ ​play​​,2 3 although van​ ​der​ ​Made​ ​et​ ​al 4 reported​ ​only​ ​a​ modest increase in return to play duration. ​​​ Differences in the sporting demands of these cohorts may contribute to the discrepancy. ​Prolonged​ return to play​ ​has also been reported​ ​in​​ intramuscular​ ​tendon injuries to the ​rectus​ ​femoris​, ​gastrocnemius​ ​and​ ​soleus muscles.5

​​Specialised management​ (surgery, injection therapies, delayed rehabilitation) of an intramuscular tendon tear beyond standard muscle strain management has been proposed ​because​​ ​of​ ​perceived ​failure​ ​to​ ​heal​ intramuscular​ ​tendon due to its tissue properties. Despite the similarities in collagenous structure in free tendon and intramuscular tendon, there​ ​are​ ​several​ ​reasons​ ​why​ injury to ​the intramuscular​ ​tendon may not be analogous to​ ​free​ ​tendon.

How do free tendon and intramuscular​ ​tendon differ in structure, function and pathology?

Structurally, ​ ​the​ ​cross-sectional area ​of​ ​the​ isolated​ intramuscular​ ​tendon ​is​ ​substantially ​smaller​ ​than the free tendon it contributes to. At​ ​a histological​ ​level​,​​ ​it​ ​is​ ​unlikely​ ​to​ ​have​ ​the well-aligned fascicular ​bundles​ ​and the specialised​ ​interfascicular matrix seen​ ​in​ ​free​ ​tendon. The intramuscular​ ​tendon is composed primarily of type 1 collagen, organisationally more reticular at the endomyseal, perimyseal and epimyseal levels as it accumulates muscle forces from varying angles of pennation.6

Functionally, the free tendon can ​tolerate​ ​high​ ​strain​ ​rates​ ​to​ ​store​ ​and​ ​release​ ​energy. Resultant strains​ ​of up​ ​to​ ​8%–10% are ​mostly​ derived from movement ​between​ ​the​ ​fascicle​ ​bundles​ ​in the interfascicular matrix, ​ ​rather than​​ ​of tendon​ ​collagen​ ​fibres themselves​7​​.​ In contrast, the intramuscular​ ​tendon in an activated musculo-tendinous unit​ is considerably stiffer, with ​strains of ​ ​2%–2.6%6 reported for triceps surae. Further, there is reported variability in longitudinal strain (some areas may shorten) and lateral expansion of up to 5%; considered a result of oblique tension from pennate contributing fibrils as well as expansion of the whole muscle as it shortens.6 These properties may exist within other muscle groups. Ultimately, the lack of fascicular bundles and interfascicular matrix result in a functionally stiffer intramuscular​ ​tendon, which cannot ​store​ ​and​ ​release​ ​energy​ ​like​​ ​free​ tendon.

Pathologically, free​ ​tendon​ ​succumbs​ ​to​ ​an overuse​ ​tendon​ ​pathology, ​ ​eventually​ ​becoming​ ​​degenerative in nature with little capacity to repair ​as​ ​there​ ​is​ ​little or no bleeding. ​ Over time, the collateral regions of the tendon appear to remodel and increase tendon diameter to share load.8 Rarely, ruptures occur in the degenerative region, where an ​inflammation, ​ ​proliferation​ ​and​ ​maturation​ response is triggered, resulting in a new matrix ​ and considerably larger free​ ​tendon​.

It is unlikely that intramuscular tendons have an overuse pathology and a pre-existing degenerative pathology as they have a higher vascular perfusion than free tendon. However, unlike the satellite cell response of myotendinous repair and similar to rupture in free tendon, intramuscular tendon ruptures result​ ​in​ ​bleeding​ ​and an inflammation, proliferation and maturation response​,​ resulting in formation of hypertrophic intramuscular tendon scar tissue. Retraction of the stumps​ of intramuscular tendon lesions is generally limited as the​ ​surrounding​ ​​ ​muscle acts as a splint, which differs in free tendon ruptures. As such, surgery is rarely indicated.

Pain, generally localised at the tendon bone junction, is the presenting clinical feature of free tendon injury; this differs somewhat from recurrent structural failure and variable pain in IMT injury. While the sensory nerve supply of free tendons principally resides in the peritendon supplying the periphery of the tendon only, very​ ​little​ ​is​ ​understood ​about​ ​the neural​ ​supply of the intramuscular tendon; ​in​ ​particular, those​ ​Iintramuscular tendons​ ​that​ ​are​ ​deep​ ​within​ ​a​ ​muscle,​ ​as​ ​opposed​ ​to​ ​the​ ​more superficial​ ​aponeuroses.​ ​Clinically,​​ ​particularly​ ​in intramuscular tendon strains of soleus and hamstring,​ ​ ​presenting symptoms​ may be of ​​ ​progressive​ ​tightness​ ​or​ ​acute​ ​pain,​ ​which​ ​further clouds​ ​clinical ​assessment​ ​and​ ​prognoses.

This editorial highlights why intramuscular tendon does not behave like a free tendon either functionally or when injured. While many of the exercise progressions may be similar, there are symptomatic, structural and mechanical differences that should influence early and late phase rehabilitation principles. Perhaps the most appropriate term for the pathology should not include ‘tendon’ as it misleads our understanding of both the pathology and its management. ‘Intramuscular aponeurosis’ or ‘intramuscular connective tissue’ are appropriate terms that reflect the unique structural, behavioural and pathological properties.

References

Footnotes

  • Contributors All three authors have contributed equally to the writing of this editorial.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent Not required.

  • Provenance and peer review Not commissioned; externally peer reviewed.