Over the past eight weeks, this newsletter series has served as your runway to the Traverse City Tendon Summit.

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

1. Foundational Science

2. Evaluation and Diagnostics

3. Management and Decision Making

The goal has been 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 our previous installment, we explored the inseparable nature of context when addressing an athlete’s capabilities. We used Jarred Boyd’s overarching philosophy, along with his role as Director of Rehabilitation for the Memphis Grizzlies, to outline decision‑making processes for healthy athletes.

In this final installment of the Tendon Summit Insider, we draw inspiration from the Summit’s final presenter, Jarrod Antflick, to extend those same decision‑making principles to individuals navigating pathological tendons.

Management & Decision Making: Part III

As discussed in Newsletter VII, a comprehensive understanding of the athlete and their requirements is foundational. Like in healthy athletes, we must understand and quantify the systems contributing to movement quality, the task demands, and the global environment in which they operate. 

KEY TAKEAWAYS

• Tendinopathy is a multidomain condition that demands comprehensive evaluation. Tendinopathy extends far beyond local tendon structure. Failing to account for broader musculoskeletal, cardiovascular, neurological, and experiential consequences sets the stage for incomplete rehabilitation. 

• Intensity is the most direct clinical lever for generating tendon strain. In the absence of being able to directly observe tendon elongation, high‑effort contractions remain the most practical way to ensure the tendon experiences sufficient deformation for adaptation. 

• Volume and contraction type are valuable means to an end. These factors serve primarily to ensure the tendon receives adequate strain duration. When this requirement is met, the precise configuration of sets, reps, or contraction mode becomes far less consequential.

• Additional considerations act as modifiers that shape exercise prescription. Factors such as dorsiflexion range, joint position, and pain alter how loading should be applied, progressed, or constrained.

• A “good starting bet” anchors decision‑making when mechanisms are uncertain. Mechanistic evidence is fragmented and inconsistent. In spite of this, the most defensible position is to anchor management to loading principles displayed across the literature, as doing so offers the highest probability of success across populations.

Multidomain Disturbance

In practice, tendinopathy is a multidomain disorder affecting multiple interacting systems. Locally, pathological tendon tissue shows altered cellular strain responses and impaired mechanotransduction [1], reductions in stiffness and load‑bearing capacity [2], and downstream deficits in force production and functional performance [3]. These changes occur alongside broader neuromotor, muscular, and behavioral adaptations that shape how load is distributed through the limb.

Therefore, a comprehensive lens must extend beyond the tendon. Local associations such as plantaris involvement [4] and fat pad irritation [5] can meaningfully alter symptoms and shape treatment trajectory. Broader correlates such as postural deviations, range‑of‑motion limitations, and strength or endurance impairments across the kinetic chain have been implicated as both contributory and consequential factors in the development and propagation of tendinopathy [3,6,7,8,9,10]. Pain‑driven training modifications further compound this picture: even short reductions in loading can decrease neuromuscular efficiency, power output, and motor unit recruitment [11], while longer detraining periods reduce strength, speed, and metabolic capacity in trained athletes [12].

These interacting influences create multiple potential failure points. If local tissue‑specific functions are not restored, mechanical qualities may continue to degrade and the tendon will remain trapped in an inefficient regulatory state. If broader contributors are ignored, the individual may consciously or subconsciously shift the loading environment, producing the same stress‑shielding through different means. Either pathway reinforces a positive feedback loop of dysregulation that prevents full restoration and undermines the effectiveness of even well‑designed loading programs.

Assess, Don’t Guess

It is tempting to assume a uniform cascade of structural or functional changes when tendons become symptomatic, but the evidence does not support a single predictable pattern. Across studies, we see wide variability in stiffness, strain behavior, energy storage, and energy dissipation, with reported values differing substantially across cohorts and methodologies [13,14,3]. This same level of variability exists across the regional, kinetic‑chain, and systemic contributors just outlined.

These patterns make it clear there is no standardized phenotype. Clinicians begin with incomplete information and must assess qualities directly rather than infer them from the diagnosis. Our responsibility is to define the true deficits, collect accurate information with precision, and use ongoing accountability checks to keep decisions aligned with the athlete in real time. Ignorance at any point in this workflow introduces noise into the rehabilitative process and risks wasting time, resources, and therapeutic capital.

Considerations on Exercise Prescription

As with prior installments, the full scope of this condition exceeds what can be addressed here. Our focus will narrow to a single component of the broader framework: exercise interventions aimed at resolving local impairments.

Across lower‑limb tendinopathies, exercise remains the only intervention with consistent evidence of benefit. Many theoretical arguments exist, but adjunctive treatments rarely outperform exercise alone- more often simply adding cost or complexity without improving outcomes [21]. The broader evidence base is marked by low‑quality comparisons, heterogeneous study designs, and inconsistent findings. Despite this, one conclusion persists: meaningful clinical change is most reliably achieved through progressive loading.

As we exhaustively discussed in Newsletter II, specific loading criteria matter. Strain magnitude, distribution, and temporal characteristics each shape distinct cellular responses. However, as we have made clear throughout this discussion, pathological tendons may not demonstrate comparable responses. Their structure, cellular behavior, and mechanosensitivity differ in ways that limit the direct transfer of findings from healthy tissue. For this reason, it is essential to anchor clinical decision‑making to evidence that best approximates the state we aim to influence, rather than relying on assumptions drawn from intact, well‑organized tissue.

This is precisely where the clinical literature begins to reveal its limitations. Even when programs differ meaningfully in their loading parameters, the resulting outcomes often converge.

Habets’ 2021 study contrasting the Alfredson eccentric protocol with the Silbernagel combined concentric–eccentric program illustrates this point. The two interventions differ meaningfully in their loading parameters, yet, produced similar improvements in pain, function, and quality of life over twelve months [22]. When protocols that vary in contraction mode, progression strategy, and exercise structure yield comparable outcomes, it indicates the signal  responsible for change is being obscured.

The mediating factors common across implemented protocols are not being isolated, quantified, or assessed in a way that would refine our understanding of which loading characteristics actually matter. 

Resolving this ambiguity requires moving beyond labels and toward the specific loading variables that shape tendon behavior. Because protocol‑level comparisons hide the contribution of individual parameters, a structured process is needed to clarify which factors matter most. We once again turn to a Delphi consensus on this topic to provide guidance [23].

Intensity

In line with the mechanobiological principles outlined throughout this series, the Delphi panel reaffirmed that strain remains the primary driver of tendon adaptation, and that contraction intensity is one of the most direct interfaces clinicians can manipulate to elicit sufficient tendon elongation. The authors highlight that, in practice, this often corresponds to intensities above 90% MVIC for isometric contractions or above 70% MVC/RM for isotonic loading [23].

At the same time, the consensus is explicit that intensity is only a proxy. The true biological stimulus is tendon strain, and the relationship between external intensity and internal deformation is highly variable. As discussed previously, strain magnitudes within the adaptive window of 4.5–6.5% have been observed during contractions ranging anywhere from 30% to 90% MVC, underscoring why percentage‑based prescriptions cannot reliably guarantee a specific mechanical dose. 

Volume

The Delphi panel’s findings on loading volume reinforce that strain duration, not just strain magnitude, is a key determinant of tendon adaptation. Tendons behave as viscoelastic structures with time‑dependent force transmission, which means the deformation that reaches the cellular level depends on how long the tissue is held under tension [24; 25; 26; 27; 28]. Short and rapid contractions produce high strain rates but insufficient strain duration, while slower or sustained contractions allow more of the applied load to propagate through the extracellular matrix.

Although consensus varied across recommended sets and repetitions, contraction duration, and total time under tension, each parameter ultimately reflects a different way of ensuring adequate exposure to meaningful strain duration. 

Practically, the implication is straightforward. Volume should be organized to accumulate sufficient time under tension within the adaptive strain window. Slow isotonic or isometric contractions, typically three to six seconds per phase or thirty to forty five seconds per hold respectively, provide a reliable way to achieve this. Most rehabilitation sessions should accumulate several minutes of high quality loading for the involved tendon. Sets and repetitions are simply the delivery mechanism for this exposure and can be adjusted to match tolerance, desired neuromuscular adaptations, and stage of rehabilitation.

Contraction Type

The Alfredson protocol shaped an entire generation of clinical practice and eccentric loading became practically synonymous with Achilles tendinopathy management. However, recent evidence has shown that this reverence was likely misplaced. Studies now demonstrate comparable tendon loading during concentric and eccentric phases of dynamic tasks and similar clinical outcomes across isometric, concentric, and eccentric contractions.

The benefits historically attributed to eccentric loading likely reflect the mechanical conditions it created rather than any unique biological effect of the contraction type itself. In practice, eccentric movements simply made it easier to achieve the combination of high intensity and sufficient strain duration required for tendon adaptation.

The one clear exception is ballistic or plyometric exercise. As discussed earlier, these movements involve very short contraction times that limit the duration of strain transmitted through the extracellular matrix. They may be essential for restoring force rate, coordination, and task specificity, but when the goal is to influence tendon mechanical or morphological properties, there is little reason to prioritize them. Their value emerges when the objective shifts from tissue adaptation to preparing the athlete for the demands of sport.

Additional Considerations

Although intensity, volume, or contraction type are the primary pillars of rehabilitation, other factors still meaningfully shape intervention design and implementation. The Delphi panel highlighted two such considerations. 

Range of Dorsiflexion

Dorsiflexion meaningfully alters the balance of tensile and compressive load on the tendon, which makes its relevance highly dependent on the anatomical site of symptoms. The Delphi panel indicated that dorsiflexion is primarily influential for insertional Achilles tendinopathy, where avoiding dorsiflexion beyond neutral is generally recommended to limit compressive irritation.

Future work will likely clarify how joint position and external load interact, but current evidence already highlights a practical implication for clinical loading. Recent work has shown that training at longer muscle–tendon complex lengths produces higher internal forces and greater tendon strain for a given external load, reflecting clear biomechanical advantages over shorter‑length positions [15]. This relationship suggests that clinicians may be able to increase tendon strain by modifying the position of loading rather than relying solely on heavier external loads, offering greater flexibility when patient constraints, equipment access, or high‑frequency programming limit the use of traditional heavy resistance

Pain as a Regulatory Variable  

Pain serves as a feedback mechanism that helps calibrate load, volume, and intensity rather than acting as a direct driver of tendon adaptation. The Delphi panel ranked pain highly overall but it did not reach major‑influence consensus, reflecting its role as a regulator of dosage and patient behavior rather than a primary determinant of tendon response.

Task Constraints and Neural Drive

Although the Delphi group did not identify neurophysiological considerations, it is important to acknowledge emerging evidence that meaningfully shapes how athletes respond to loading interventions.

People with painful tendon conditions often report a disproportionate rise in pain relative to the external stimulus applied, indicating an up‑regulated nociceptive response. This heightened response corresponds with lower spinal excitability and reduced force output, constraining how much strength they can express at baseline [16].

Importantly, this limiting pattern is modifiable. A single session of resistance training can shift how the nervous system drives a muscle through both bottom up sensory processes and top down motor commands [17]. Akalu and colleagues showed that different loading styles facilitate distinct patterns of neural adaptation. When repetitions were externally paced and rhythm based, participants showed increased responsiveness in cortical pathways that support controlled and precise movement. When repetitions were self paced and performed with high effort, participants showed increased responsiveness in deeper brainstem pathways that support rapid and forceful contractions. 

These findings highlight that the way a task is performed influences which parts of the motor system contribute to force production. Changes in rhythm, attention, or cognitive focus can alter the balance between top down and bottom up influences during loading. 

In practice, this means clinicians may need both controlled, rhythm based tasks and high intent, effortful tasks to restore motor drive, because each targets a different part of the system that contributes to strength and performance [17].

Overlaying Philosophy

These parameters guide practice, but they sit on top of a foundation that is far less certain than the precision of our prescriptions implies. Despite the consistent clinical improvement observed across loading protocols, the mechanistic rationale behind these interventions remains underdeveloped. Many studies propose that exercise improves tendon strength, collagen synthesis, or muscle tendon function, yet only a small proportion measure outcomes that correspond to these proposed mechanisms [18] Murphy’s systematic review reinforces this uncertainty. In their review of the literature addressing mid portion Achilles tendinopathy, Murphy and colleagues found that no study examined whether changes in triceps surae structure or function were associated with changes in pain or disability, and the available physiological data were too limited and inconsistent to support any mechanistic conclusions [19].  Together, these findings caution attributing clinical benefit to presumed gains in muscle structure or strength. 

This uncertainty does not diminish the value of exercise. Instead, it clarifies how clinicians should think about the role of loading when mechanisms are unclear. Scot Morrison introduced the concept of a “good starting bet” to describe population level anchors that offer high‑probability entry points into complex clinical problems  [20]. The value of a good starting bet is not that it identifies a precise mechanistic pathway, but that it represents the most defensible initial position given current evidence and biological plausibility. 

In a landscape defined by incomplete mechanistic understanding, this approach allows clinicians to remain intellectually honest about uncertainty while still anchoring to interventions with the highest likelihood of benefit. High quality loading configurations remain good practice for Achilles tendinopathy because they reliably improve symptoms, carry no evidence of harm, and prepare the broader neuromuscular, physiological, and psychological systems required for return to sport.

Integrated Decision‑Making in Pathological Tendons

Management and decision making is not a search for perfect exercises. It is a process of making informed choices in the presence of biological noise, incomplete information, and shifting constraints. 

In healthy tendons, this means identifying the relevant context and providing consistent, reliable approaches that build movement capacity and expand the athlete’s affordances. In pathological tendons, the same logic applies, but it must also account for altered mechanobiology, protective strategies, and the reduced capacity that shapes how athletes interact with load and complexity.

A framework of thinking, whether the one outlined in this series or a different mental model, exists to help clinicians navigate uncertainty with clarity and discipline. Its value lies in structuring how we understand the athlete, how we interpret their responses, and how we guide them toward more efficient and resilient solutions.

Looking Ahead

This concludes the final installment of the Tendon Summit Insider. Our goal has never been to present a definitive or unquestioned authority on what is acceptable practice. The intention has been to highlight key areas of emerging evidence within a framework that is meaningful for those working in this space.

Whether these articles have aligned with your current thinking or challenged it, we hope they have sparked enough curiosity to bring these conversations forward in April. The value of the Summit lies in the collective expertise of those attending, and in our willingness to examine assumptions, debate ideas, and refine our understanding together.

- Research review written by: Jason Eure, PT, DPT, OCS, CSCS

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Reference List 

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