Functional Relevance of the Muscle-Specific Achilles Subtendons

“Should clinical interventions address the muscle-subtendon units independently?”

Stephanie Cone does an excellent job outlining current understanding of Achilles tendon micromorphology. She expertly discusses what we know to be true among healthy and pathological tendons, and how these factors drive functional consequences in those navigating tendinopathy.

At the end of her presentation, she raises the obvious question for anyone working in clinical care: should this knowledge change practice?

Depending on the population you’re examining, the timeframe in question, and the criteria used to be considered successful, estimates suggest that approximately 20 to 60 percent of patients do not respond to conservative treatment (1,2).

If we refer back to our prior editions of The Debrief (I and II), one theory is we see poor outcomes due to our inability to understand and interact with our biology in ways that could facilitate desired adaptations. One contention is that the rehabilitation of Achilles tendinopathy is inadequate because we often fail to zoom in enough to address contributing factors.

The literature contributing to this discussion is far too vast to cover in a simple newsletter. Instead, our goal here is to outline the cases for and against the idea of targeting subtendons independently. We will focus on what is known, what remains unclear, and what this means for clinicians who care more about outcomes than theory.

The Case For Subtendon‑Specific Rehabilitation:

In Foundational Science III, we highlighted the many ways in which the Achilles tendon is unique, both in terms of its anatomy and the functional implications those features allow. 

In short, the Achilles tendon comprises three subunits: one from the gastrocnemius medialis (GM), one from the gastrocnemius lateralis (GL), and one from the soleus.

Although each of these muscles have a similar role, it would be a mistake to ignore the distinctions. The muscles exhibit anatomical, neurophysiological, and functional differences, and their respective subtendons are indeed semi-independent structures with unique mechanical properties (3,4,5).

Each subtendon is not equally impacted by the pathological process.

When thinking about “isolating” individual tendon subunits, most likely default to grouping the gastroc subtendons vs. the soleus and look to bias either group by performing knee-extended or knee-flexed calf exercises. This would be defensible, as soleus dysfunction has historically been considered a primary factor contributing to plantarflexor strength and endurance deficits in runners with Achilles tendinopathy (6). Selective soleus weakness was implied to unevenly load the Achilles tendon, potentially contributing to pain and progression of the pathology (6,7). 

However, emerging evidence suggests that we may have been focusing on the wrong subunit. 

In tendinopathy, the soleus’ contribution to overall force production during submaximal contractions is often not reduced (6) and there are no major changes to the neural regulation or mechanical properties of the tendon (3,7). In stark contrast, there are noted alterations in neural drive, physiological cross sectional area, and sub-unit specific stiffness in the lateral gastroc (3,4,6,7).

Despite normal absolute force production, only in the lateral gastroc do we have evidence to suggest selective atrophy, reduced stiffness, and disrupted neural coordination (reduced firing rates at low intensities, increased discharge rates at higher intensities, and significantly elevated de-recruitment thresholds at higher intensities) (3,4,6).

This means our crude clinical measures regarding muscular strength and endurance may be unable to capture lingering deficits.

You may be inclined to say these discrepancies do not matter if output is sustained. But it is important to remember subtendons do not operate in isolation. Their behavior is embedded within a larger system that relies on coordinated load sharing. To understand why GL-specific changes matter, we need to consider how the Achilles tendon normally distributes stress and how this process is altered in tendinopathy.

The twisted architecture of the Achilles tendon leads to non-uniform strain patterns during loading, exposing it to inter-tendon shear stress (6). While there is often a knee-jerk reaction to view shearing forces as a negative, they are actually a powerful signal for tissue regulation. Shear forces lead to tenocyte synthesis, supporting tendon homeostasis and regeneration (1). 

However, the dosage makes the poison. Too much stress is considered a vehicle for microdamage and mal-adaptive tendon response (implicated in the development and progression of Achilles tendinopathy) (6).

To combat this, healthy Achilles tendons have methods to prevent excessive strain.  Intratendinous sliding occurs between different structural levels of the tendon (between the three subtendons) and/or within subtendons themselves (between fascicles, fibrils, and fibers) in order to reduce load through the individual fascicles. (1,3).

Importantly, in both Achilles tendinopathy and post Achilles tendon rupture, reduced sliding has been observed between tendon fascicles originating from different parts of the calf complex (1,8). What this means is there are mechanisms at play causing the subtendons to “pull” on their neighboring tissues (whether this is due to interfascicular adhesions, collagen reorganization, or other altered calf dynamics remains unclear), which results in more uniform displacement than the semi-independent behavior seen in healthy subtendons (1,8,9,10). This strain pattern potentially minimizes or removes an important mechanical signal to the tenocytes, which may exacerbate the dysregulation seen in tendinopathy. 

There are many ways to interpret these findings, and there is unlikely to be an easy, universal answer to the direction of causality and downstream implications. What we can say is that there appear to be specific changes to the GL muscle-subtendon behaviour and the typical load distribution between the segments is altered. The outlined changes may place individuals in a positive feedback loop in which it becomes increasingly difficult to deliver therapeutic loads to the tissues in need. This potentially perpetuates the pathological process, leaving individuals susceptible to prolonged dysfunction or recurrence of symptoms despite our best efforts.

In her lecture, Dr. Cone hints that they have been experimenting with NMES as a method to bias the different muscles of the calf complex. But additionally, a few simple, low-tech solutions have been proposed to assist in the isolation of the two main issues outlined as well.

Rather than focusing solely on knee position, several authors encourage us to think more about foot orientation. Fernandes showed that turning the foot in during plantarflexion exercises lengthens the GL subtendon and enhances neural activation (6). Lecompte showed that outward foot rotation counteracts the natural Achilles tendon direction of rotation, theoretically unwinding the tendon and allowing for greater sliding between segments (1).

So perhaps a small tweak in foot placement and exercise execution can unlock unrealized therapeutic potential. 

The Case Against Subtendon‑Specific Rehabilitation

The argument against subtendon‑specific loading is less about plausibility and more about epistemology. In clinical practice, we’ve repeatedly allowed mechanistic enthusiasm to outpace evidential certainty. Our current literature all discusses surrogate outcomes, not the end‑states of interest.

In science, this is the distinction that separates efficacy from effectiveness.

Efficacy tells us whether an intervention changes a proximal mechanism under controlled conditions. Effectiveness tells us whether that mechanistic change actually alters the outcomes that matter in real clinical practice. Medicine is full of examples where a drug produces a clean mechanistic effect in a lab yet fails to move the outcomes that matter once it leaves the confines of a controlled trial.

To put this in tendon terms, we may be able to differentially impact multi-level sliding mechanics and sub-tendon specific neuromuscular behavior in clinical trials without seeing any change in pain, function, or performance. 

Even if we make the generous assumption that these surrogate measures have a direct and meaningful causal relationship with the outcomes we care about, we still have to consider how well the current evidence reflects the physiological realities of real training.
Much of the subtendon‑sliding literature is built on loading conditions that bear little resemblance to the forces we actually impose in rehabilitation or sport. 

First, Strand’s work (9,10) relied on electrically stimulated contractions producing ~15 newtons (N) of force (a trivial load when compared to the ~190 N and ~1,600 N seen in the GL and soleus respectively during the simple task of walking) (2). Lecompte’s study involved no external loading, and Khair’s work only evaluated contractions at 30% MVC (1,8).

These studies collectively serve as a proof of concept, demonstrating that sliding exists and changes with the presence of pathology. However, they do not tell us whether the phenomenon persists under loading intensities that actually drive tendon adaptation.

Second, nearly all the studies discussed were performed in neutral or near‑neutral ankle postures. We have strong longitudinal evidence showing that meaningful muscle and tendon remodeling occurs when the unit is trained at longer lengths (12,13,14). Neural drive, fascicle behavior, and strain distribution all shift as we move into dorsiflexion, and it is entirely plausible that the subtendon‑level nuances observed in neutral are altered or erased once passive strain increases (15,16).

Third, substantial interindividual variability could drastically change the impact of our treatments. In Lecompte’s work, the absolute magnitude of sliding differed widely across participants, and in some individuals, the toes‑out posture actually produced less sliding than neutral (1). This suggests that human anatomy and subtendon behavior are highly variable, and without imaging, we have no reliable way to determine whether a given intervention is producing the intended mechanical effect.

Finally, and potentially most importantly, we lack longitudinal evidence that we can actually change these alterations. We have no data to suggest training within constraints that improve sub-tendon specific characteristics translate to chronic changes- much less that those adaptations result in improved outcomes more globally.

In summary, while subtendon behaviour may contribute to persistent symptoms, we do not yet have evidence that we can influence these features in a distinct or lasting way. The current data do not show that targeted attempts produce outcomes beyond what is already achieved through well-executed, progressively loaded rehabilitation. Until longitudinal work demonstrates otherwise, the most defensible position is that our existing best practices are likely addressing whatever subtendon-level processes matter in real clinical settings.

Practical Takeaways and Open Questions

Taken together, the arguments for and against subtendon‑specific rehabilitation leave us in a familiar position. There is biological plausibility suggesting that small adjustments in exercise execution could meaningfully influence how load is shared within the Achilles tendon and may even help us better target the processes that contribute to persistent symptoms. At the same time, the evidence is limited, and the substantial interindividual variability observed in sliding mechanics reminds us that we cannot assume these strategies will influence subtendon behavior in a consistent way.

Modifications such as altering foot orientation are easy to implement and unlikely to interfere with established best practice, but we should be honest about the limits of what we know.

As the field continues to evolve, clinicians will have to decide whether these nuances are worth exploring in their own settings or whether the current evidence supports staying the course with well‑executed, progressively loaded programs.

Next up, we review the lecture from Ruth Chimenti — a toolkit for Achilles assessment: from diagnosis to outcome tracking.

See you in two weeks!

Debrief written by: Jason Eure, PT, DPT, OCS, CSCS

Reference List

1) Lecompte L, Crouzier M, Bogaerts S, Vanwanseele B. Patients with Achilles Tendinopathy Show Reduced Intratendinous Sliding during Dynamic Exercises. Med Sci Sports Exerc. 2026 Jun 1;58(6):1149-1158. doi: 10.1249/MSS.0000000000003942. Epub 2026 Jan 22. PMID: 41572520.

2)  Funaro, A., Shim, V., Mylle, I. et al. Subject-specific biomechanics influences tendon strains in patients with Achilles tendinopathy. Sci Rep 15, 1084 (2025). https://doi.org/10.1038/s41598-024-84202-9

3) Crouzier M, Baudry S, Vanwanseele B. Achilles Subtendons Stiffness Differ in People with and without Achilles Tendinopathy. Med Sci Sports Exerc. 2025 Aug 1;57(8):1636-1645. doi: 10.1249/MSS.0000000000003717. Epub 2025 Apr 3. PMID: 40176287.

4) Contreras-Hernandez I, Falla D, Arvanitidis M, Negro F, Jimenez-Grande D, Martinez-Valdes E. Load and muscle-dependent changes in triceps surae motor unit firing properties in individuals with non-insertional Achilles tendinopathy. J Physiol. 2026 Jan;604(2):955-978. doi: 10.1113/JP287588. Epub 2025 May 11. PMID: 40349309.

5) Finni T, Khair R, Franz JR, Sukanen M, Cronin N, Cone S. A Novel Method to Assess Subject-Specific Architecture of the Achilles Tendon In Vivo in Humans. Scand J Med Sci Sports. 2025 Apr;35(4):e70042. doi: 10.1111/sms.70042. PMID: 40135396; PMCID: PMC11938201.

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8) M Khair R, Stenroth L, Péter A, Cronin NJ, Reito A, Paloneva J, Finni T. Non-uniform displacement within ruptured Achilles tendon during isometric contraction. Scand J Med Sci Sports. 2021 May;31(5):1069-1077. doi: 10.1111/sms.13925. Epub 2021 Feb 4. PMID: 33464638.

9) Strand KS, Hullfish TJ, Baxter JR. In vivo characterization of Achilles subtendon function and morphology within the tendon cross section and along the free tendon. J Appl Physiol (1985). 2025 Sep 1;139(3):812-822. doi: 10.1152/japplphysiol.00479.2025. Epub 2025 Aug 19. PMID: 40828574; PMCID: PMC12427142. 

10) Strand KS, Hullfish TJ, Wagner MM, Russo D, Zawel M, Schaubel DE, Humbyrd CJ, Baxter JR. A Novel Measurement of Altered Achilles Subtendon Load Sharing 6-12 Months Following Rupture. J Orthop Res. 2026 Apr;44(4):e70182. doi: 10.1002/jor.70182. PMID: 41889060; PMCID: PMC13022063.

11) Funaro, A., Shim, V., Mylle, I. et al. Subject-specific biomechanics influences tendon strains in patients with Achilles tendinopathy. Sci Rep 15, 1084 (2025). https://doi.org/10.1038/s41598-024-84202-9

12)  Kinoshita M, Maeo S, Kobayashi Y, Eihara Y, Ono M, Sato M, Sugiyama T, Kanehisa H and Isaka T (2023), Triceps surae muscle hypertrophy is greater after standing versus seated calf-raise training.Front. Physiol. 14:1272106. doi: 10.3389/fphys.2023.1272106

13) Wolf M, Androulakis Korakakis P, Piñero A, Mohan AE, Hermann T, Augustin F, Sapuppo M, Lin B, Coleman M, Burke R, Nippard J, Swinton PA, Schoenfeld BJ. 2025. Lengthened partial repetitions elicit similar muscular adaptations as full range of motion repetitions during resistance training in trained individuals. PeerJ 13:e18904 DOI 10.7717/peerj.18904

14)  McMahon, G., Sanderson, A., & Degens, H. (2025). Isometric training at longer muscle–tendon complex lengths: A potential countermeasure to impaired neuro-muscle–tendon function during space travel. Experimental Physiology, 1–13. https://doi.org/10.1113/EP092225

15)  Yu XS, Levine JT, Pons JL. Modulation of motor unit recruitment threshold and common synaptic inputs in triceps surae muscles: effects of ankle position. J Appl Physiol (1985). 2025 Jun 1;138(6):1638-1650. doi: 10.1152/japplphysiol.00029.2025. Epub 2025 May 27. PMID: 40421865.

16) Kunita Y, Ikeda N, Nishioka T, Yamaguchi S, Yoshikawa A, Hajima D, Yabuno N, Harato K, Inami T. Angle-specific stiffness profiles of the achilles tendon and Triceps surae muscles: a continuous characterization. Front Sports Act Living. 2026 Feb 18;8:1728114. doi: 10.3389/fspor.2026.1728114. PMID: 41783778; PMCID: PMC12956305.