Over the next several weeks, this newsletter series will serve as your runway to the Traverse City Tendon Summit.

Each installment highlights key ideas across the Summit’s three major content areas:

1. Foundational Science

2. Evaluation and Diagnostics

3. Management and Decision Making

The goal is simple. We want everyone arriving in April with a shared platform of understanding so that the conversations can move quickly past the basics and into the deeper, more meaningful discussions that drive real progress. None of the ideas introduced here should be taken as settled science. These nuances invite debate and discussion, and that exchange is central to the purpose of the Summit.

In the previous two installments covering Foundational Science, we have discussed the important structural considerations and multi level interactions giving rise to tendon function and how tendon design ensures that regulatory pathways are in place, mechanically responsive to the loading environments they are exposed to.

However, in doing so, we have made an error in oversimplification. We have discussed tendons as if they are interchangeable.

Foundational Science: Part III

KEY TAKEAWAYS

• Tendons are not interchangeable. Structural and metabolic differences create clear functional distinctions between energy‑storage and positional tendons. Each tissue responds to load and remodeling demands in its own way.

• The Achilles functions as a coordinated subtendon system. The tendon is composed of distinct units with their own geometry, stiffness, and neural control. These differences shape the non‑uniform strain patterns seen during dynamic tasks.

• Tendinopathy disrupts coordinated load sharing. Pathology alters subtendon stiffness, sliding behavior, and neural drive. These changes disrupt coordinated load sharing and alter how the tendon responds to mechanical demand.

• Controllable variables influence internal loading. Foot orientation, knee angle, and repetition parameters shift mechanical and neural contributions within the triceps surae. However, specificity is a tool to use when clinically indicated, not a universal requirement.

• Subtendon architecture informs more precise loading strategies. Understanding how load travels through the tendon clarifies when targeted exercise selection is warranted and when general loading is sufficient.

Not One Size Fits All

A primary distinction in tendon biology is the separation between positional tendons and energy storage tendons. This classification is not semantic. It reflects deep differences in functional intent, structural design, and adaptive capacity.

Positional tendons: designed for precision  

Positional tendons transmit force with accuracy and maintain joint position. They do not undergo large elongation during movement and are not intended to store elastic energy. The tibialis anterior tendon is a clear human example. It contributes to controlled dorsiflexion and fine postural adjustments, and it operates within a narrow strain window that prioritizes stability over elasticity [1].

Energy storage tendons: designed for locomotor efficiency  

Energy storage tendons stretch under load, store elastic strain energy, and return it during propulsion. The Achilles tendon is the primary human example. It experiences high strain during walking, running, and jumping, and its ability to store and return energy is central to economical locomotion [1].

These functional roles require fundamentally different structural solutions. The remainder of this section explains why.

Structural Differences That Create Functional Differences

The structural divergence between positional and energy storage tendons occurs at multiple hierarchical levels.

Fibril level  

Energy storage tendons contain collagen fibrils with trivalent crosslinks that limit molecular sliding and increase fatigue resistance. These fibrils stiffen at high strain and resist molecular disruption even when elongated to failure [2], which allows tissues like the Achilles to tolerate the long positional lengths and rapid stretch cycles of running and hopping without losing structural integrity. Positional tendons contain fibrils with divalent crosslinks, which permit greater molecular sliding and are more susceptible to structural disruption under load [2]. This sliding supports the precise, low strain force transmission required of tendons such as the tibialis anterior, but it also means these tissues are less suited to repetitive high strain environments.

Fascicle level  

Energy storage tendons exhibit a helical fascicle arrangement. This orientation increases compliance. The untwisting of these fascicles during loading provides an additional buffer that supports the stretch and recoil behavior seen in the Achilles during midstance and push off [3]. Positional tendons have minimal fascicle helicity and therefore behave as stiffer, more linear force transmitters [3], a structure that favors precision and stability over elastic recoil.

Whole tendon level  

Energy storage tendons operate under higher peak stresses and repetitive high strain cycles during locomotion. The Achilles, for example, experiences several bodyweights of force during walking and running [4,5].

Positional tendons operate in lower strain environments and participate in fine motor control and postural adjustments [1,4].

These global capacities are supported, in part, by differences in enzymatic susceptibility. Energy storage tendons show selective resistance to MMP mediated degradation, while positional tendons show broader enzyme sensitivity across fibril populations [6]. This regulatory distinction ties each tendon’s adaptive capacity to its functional role. Energy storage tendons guard against rapid change while positional tendons are highly responsive to shifts in their loading environment.

Functional Implications

These hierarchical differences form a coherent system in which each structural level reinforces the tendon’s functional role. Energy storage tendons prioritize durability under high strain, which makes them slower to remodel and more dependent on sustained, high load stimuli for adaptation [4,5,2,7]. Positional tendons, by contrast, are optimized for precision and rapid turnover, which supports fine motor control but leaves them poorly suited to repetitive high strain environments [1,3].

The pathophysiology of tendinopathy is multifaceted and remains an active area of investigation. Still, repetitive mechanical load is widely recognized as a major contributor to progression. The structural idiosyncrasies outlined above offer important clues for why that may be. Energy storage tendons frequently operate under high habitual strain and possess regulatory features that blunt rapid structural change. It becomes easy to envision scenarios in which loading demands shift faster than the tendon can adjust, microstructural disturbances accumulate, and dysfunction emerges.

With this in mind, it becomes increasingly valuable to examine the individual characteristics of each tendon to better understand the determinants of function. A more granular appreciation of these features creates opportunities to refine our approaches to performance enhancement, rehabilitation, and even tissue biofabrication. This is precisely the type of insight researchers like Dr. Stephanie Cone have provided for the Achilles tendon specifically.

Introducing Stephanie Cone: Advancing Achilles Subtendon Science

Among energy storage tendons, the Achilles stands out for its structural complexity and functional demands [1,4]. It is not a single homogeneous structure but a composite of three subtendons arising from the medial gastrocnemius, lateral gastrocnemius, and soleus [8,9]. This level of internal differentiation is uncommon among human tendons and gives the Achilles a uniquely complex architecture. The work of Dr. Stephanie Cone has fundamentally advanced our understanding of this architecture and clarified why these distinctions matter.

Three Dimensional Subtendon Mapping

Before Cone’s work, the internal organization of the Achilles was rarely considered and its subtendons could not be distinguished with any practical resolution. That left a conceptual gap. It was difficult to appreciate how each muscle contributed force through its own subtendon or how these units behaved during dynamic tasks.

Using high field MRI, Cone and colleagues demonstrated that the Achilles tendon contains three distinct subtendons with unique cross sectional areas, orientations, and twist patterns [8]. This work revealed substantial inter individual variability in subtendon geometry, including differences in twist magnitude and subtendon size.

Accessible In Vivo Identification

MRI is powerful for anatomical mapping, but on its own it offers limited actionable insight. Finni and colleagues built on this foundation by developing the Ultrasound and Electrical STIMulation (USTIM) method, a clinically accessible approach that uses ultrasound and targeted electrical stimulation to identify subtendon locations in vivo.

With these tools, the Achilles can finally be examined at the level at which it actually functions. Instead of treating it as a single structure, we can observe how each subtendon loads, lengthens, and interacts during dynamic tasks. This shift has meaningful implications for how we interpret strain patterns, identify vulnerable regions, and understand the origins of dysfunction.

How Subtendon Architecture Shapes Function

Subtendon structure and healthy load distribution

The subtendons differ in size, twist, and orientation [8,9], and these structural features shape how force is transmitted through the tendon. During dynamic tasks, the Achilles does not strain uniformly. Certain regions lengthen more than others, particularly during midstance and propulsion, where the soleus derived subtendon often experiences greater elongation while gastrocnemius derived regions behave more stiffly [11]. This non uniformity reflects a design that distributes load across the tendon in a context dependent manner.

Mechanical studies reinforce this interpretation by showing that these architectural differences translate into unique material behaviors. The soleus subtendon is significantly stiffer than either gastrocnemius subtendon, indicating that each unit plays a distinct role within the composite structure and contributes differently to how load is transmitted [12].

Neuromuscular evidence further supports the idea that each subtendon operates with its own mechanical identity. The triceps surae muscles do not contribute equally to Achilles loading. Each exhibits its own activation strategy, and these strategies shift with task demands. In healthy individuals, the lateral gastrocnemius, medial gastrocnemius, and soleus display distinct discharge behaviors that map onto their subtendon pathways [13,14,15]. These findings show that neural control mirrors the tendon’s internal structure, reinforcing the idea that each subtendon functions as a semi independent unit within a coordinated system.

Collectively, the architectural, mechanical, and neuromuscular evidence converge on a single point. The Achilles does not function as a uniform tendon but as a coordinated system of subtendons, each with its own mechanical properties and neural control. This organization allows the tendon to distribute load efficiently, adapt to changing demands, and maintain performance under high strain.

Pathological Disruption of Mechanical and Neural Coordination

Achilles tendinopathy disrupts this coordinated system. Multiple lines of evidence converge on the lateral gastrocnemius subtendon, where pathological changes include reduced intratendinous sliding during dynamic tasks and a selective loss of stiffness relative to the medial gastrocnemius and soleus [16,12]. Neural drive to the lateral gastrocnemius is similarly diminished, with lower discharge rates and reduced modulation across force levels [13]. The combined effect is a system that no longer distributes load effectively or adapts well to changing demands, increasing susceptibility to localized overload.

Controllable Variables and Emerging Opportunities

These behaviors highlight that load distribution within the tendon is not fixed. Even a basic heel raise contains several elements that can shift how the tissues are loaded. This naturally raises the question of whether specific clinical choices in the execution of the movement can influence that distribution to our advantage.

Many controllable variables appear to influence how the triceps surae contribute to tendon loading. Foot orientation is one example, with a toes out position increasing intratendinous sliding and biasing neural drive toward the medial gastrocnemius, whereas toes in shifts drive toward the lateral head [16,12].

Knee angle also modulates how force is shared within the calf complex. Flexing the knee shortens the gastrocnemius, producing consistent reductions in its activation and torque output across contraction modes, while soleus activation shows only small increases at low velocities that do not alter the overall loading pattern [17,18,19,20,21].

These mechanical and neural differences align with hypertrophy outcomes. Straight leg calf raises, which place the gastrocnemius at longer muscle lengths, produce substantially greater gastrocnemius hypertrophy than bent knee variations, whereas soleus hypertrophy remains similar across knee angles [22,23].

Exercise parameters further influence how load is dispersed within the plantarflexors. Variations in heel raise technique can shift how force is shared across the muscle group, and repetition characteristics such as loading rate and impulse determine how that force is expressed as tendon strain [24]. Range of motion studies reinforce these effects, showing that training in dorsiflexion, where the gastrocnemius operates at longer muscle lengths, produces the greatest hypertrophy of both heads [23].

Together, these findings show that joint configuration and ROM meaningfully alter muscle specific loading. Because these variables are easily measured and readily modified, they offer a practical way to influence the internal loading environment. This becomes relevant when considering that each muscle inserts into its own subtendon, a relationship that provides indirect but compelling support for the plausibility of influencing subtendon loading through deliberate exercise design.

Bringing The Evidence Together: What This Means For Practice

A system built for coordinated load sharing  

This coordinated subtendon system shows clear differences in stiffness, sliding behavior, neural drive, and hypertrophic responsiveness [12,16,13,23,22]. These differences are present in healthy individuals and become more pronounced in tendinopathy, where sliding decreases, stiffness loss is selective, and neural drive is altered. Understanding this organization is essential for clinical practice because it establishes the biological basis for why exercise choices may influence how load is distributed within the tendon.

Limits On Clinical Inference

It is important to recognize the limits of what can currently be assessed in the clinic. Subtendon strain, sliding, and stiffness cannot be measured at the point of care. Neural drive distribution requires specialized equipment, and subtendon geometry can only be mapped with advanced imaging [8,10]. These mechanisms are best viewed as conceptual tools that inform clinical reasoning rather than metrics that can be directly tested.

These limitations are compounded by meaningful inter individual variability. Subtendon size, twist, and orientation differ between people [8], and these structural differences likely influence how each individual responds to the same exercise, reinforcing the need for flexible clinical reasoning.

Symptom behavior adds further complexity. Mechanical deficits do not always map cleanly onto pain, and pain does not always reflect mechanical impairment. Even so, changes in load distribution can influence symptom irritability, particularly in energy storage tendons where localized overload is a common driver of symptoms.

When Specificity Is Unnecessary and When It Becomes Valuable

Not every clinical or performance goal requires this level of specificity. A well loaded standing calf raise places the gastrocnemius at a long muscle length, generates high tendon forces, and produces robust hypertrophy of the calf complex [22,23]. For many individuals, this may be entirely sufficient. The argument that we should not overcomplicate programming has merit, particularly when the primary goal is to increase general plantarflexor strength or provide a global stimulus to the Achilles tendon.

However, specificity becomes valuable when the clinical question becomes more specific. Joint configuration, muscle length, and foot orientation meaningfully alter how load is shared within the calf complex [16,12,22,23]. In some cases, tendinopathy may further alter how these pathways contribute to loading. These patterns matter when general loading is unlikely to address the particular structure or function of concern. In those situations, adjusting these variables provides a way to bias load toward the tissues that require focused attention.

This does not mean clinicians must micromanage every variable. It means that exercise selection can be used deliberately when a targeted effect is needed. If a patient presents with deficits in lateral gastrocnemius function, or if clinical reasoning suggests region specific tendon involvement, exercises that bias loading toward that pathway may be relevant. If tendinopathy has disrupted sliding or altered neural drive, restoring differential motion and muscle specific contributions may require more than a single exercise performed in a single configuration.

The evidence does not yet tell us that manipulating these variables improves outcomes. It does tell us that these variables change the internal loading environment in predictable ways. That alone justifies their consideration when the goal is to influence that environment deliberately. Specificity is not a requirement for everyone. It is a tool, and its value depends on the problem in front of us.

A Framework For More Precise Loading Strategies

Understanding subtendon architecture offers more than an anatomical detail. It provides a framework for interpreting how load is shared, how it can be influenced, and how it may become disrupted in tendinopathy. This perspective encourages clinicians to consider not only the magnitude of load, but the pathways through which that load travels. It also reinforces the importance of restoring both mechanical and neural components of load sharing when those pathways are altered. The result is a more precise approach to intervention, grounded in the structural and mechanical principles outlined in this series. This approach is built to address the specific demands of the clinical problem.

Looking Ahead

This installment concludes the Foundational Science section of the series. The goal has been to build a shared understanding of tendon structure, mechanics, and load distribution so that later discussions can move beyond surface level concepts.

The next installment marks a deliberate shift into the clinical domain. We will examine the pathophysiology of tendon related disorders, tracing how disruptions across biological scales emerge from the principles outlined so far and how they shape the symptoms and presentations clinicians encounter.

That discussion sets the stage for the evaluative framework developed by Ruth Chimenti. Her model organizes clinical findings around the biological and mechanical themes that define tendon pathology.

Miss a previous edition? Find our archive here.

Reference List 

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