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 our previous installments, we focused on the science that governs healthy tendon structure, function, and adaptation. That work established the baseline from which all pathological deviation must be understood. With that groundwork in place, we now shift toward clinical considerations. This entry examines what is currently known about tendon disorders, the contributory domains that help clinicians navigate the complexities associated with tendinopathy, and how these ideas converge into a modern evaluative framework. That framework will ultimately be anchored in the diagnostic model developed by Ruth Chimenti, whose Clinical Practice Guideline provides one of the most coherent, evidence‑aligned approaches to Achilles tendon evaluation available today.

Evaluation & Diagnostics: Part I

KEY TAKEAWAYS

• Tendinopathy reflects disruption across the entire tendon hierarchy. Cellular dysregulation, matrix disorganization, altered mechanotransduction, and impaired load transfer accumulate into tissue‑level changes that shape symptoms, mechanics, and functional performance.

• Microstructural disturbance creates a self‑reinforcing pathological loop. Increased compliance, unreliable mechanotransduction, and higher strain exposure amplify one another over time, making the pathological state progressively more entrenched and difficult to reverse.

• Structural and mechanical findings cannot fully explain symptom behavior. Tendinopathy reflects interactions across structure, mechanics, neuromotor behavior, sensory and neurovascular factors, psychological states, and contextual domains. No single domain reliably dominates across individuals or time.

• Evaluation must reflect this multidomain reality. Chimenti’s hierarchical framework integrates screening, classification, irritability, outcome measures, and intervention planning, with movement‑evoked pain serving as a central interpretive anchor because it captures the interaction of task demand, neuromotor strategy, and contextual influences rather than structure alone.

Pathology and Pathophysiological Development

In the Foundational Science editions, we outlined the hierarchical organization of tendons from the molecular level to the whole tissue. It follows that disruptions at any level of this hierarchy can have meaningful downstream effects. These alterations influence not only the mechanical characteristics of individual tissue components but also the dynamic interactions that coordinate tendon behavior across scales. To understand how pathological tendons differ from healthy tendons, and how these differences shape clinical presentation, we begin by examining the major structural and load‑transmitting properties affected by pathology. The discussion starts at the micro level and gradually widens to illustrate how these changes influence functional performance during real‑world loading.

Structure and Mechanical Features of Pathological Tendons

Cellular Disruption

Pathological tendons consistently show alterations in tenocyte morphology, density, and behavior. In asymptomatic athletes undergoing ACL reconstruction, abnormal tenocyte morphology was the most common histopathological feature, present even when collagen bundles showed only mild disruption [1]. Similar findings appear across tendinopathy samples, including ovoid nuclei, disrupted nuclear organization, and early chondroid transformation [2]. These morphological changes reflect shifts in cytoskeletal and nuclear mechanics that influence chromatin organization and gene expression. Although the precise temporal sequence in human tendinopathy is not fully defined, these cellular alterations are consistently associated with impaired load sensing and altered matrix maintenance, marking an early loss of tendon homeostasis.

Building on these cellular changes, further research has characterized the biochemical consequences of these changes in tenocyte number, shape, and organization. Proteoglycan synthesis rises, collagen subtype expression changes, and degradative enzymes such as MMPs and ADAMTS increase [3,4]. Alterations in inflammatory mediators and nociceptive neuropeptides also emerge, with patterns that vary across different stages of tendon pathology [5,6]. As these biochemical changes accumulate, disruptions in the surrounding matrix likely impair integrin‑mediated mechanotransduction, weakening the physical and biochemical coupling between the ECM, integrins, and the cytoskeleton that normally governs load‑responsive signaling [7]. These cellular and pericellular disturbances alter how load is sensed and transmitted at the microscale, setting the stage for the fibrillar and interfascicular changes observed next.

Microstructure Remodeling

At the microscale, altered loading signals coincide with consistent shifts in the composition and organization of the extracellular matrix. Hydrophilic molecules such as proteoglycans and glycosaminoglycans (GAGs) are often increased or redistributed, contributing to higher tissue hydration and altered local compliance [6]. These changes modify how shear and compressive forces are transmitted through the matrix, potentially altering microscale strain behavior even when gross collagen alignment appears relatively intact [8,9].

Both collagen organization and the relation between fascicles shift in predictable ways, reflecting the downstream consequences of impaired mechanotransduction and altered matrix maintenance. Pathological tissue shows more disorganized, crimped, and thinned fibers, with increased type III and V collagen [6,3]. The interfascicular matrix (IFM) between these immature collagen structures displays reduced sliding capacity, which is associated with increased microdamage and region‑specific pathology [10–12].

Opportunistic Ingrowth as a Consequence of Matrix Disruption

Within this altered matrix environment, vascular and neural elements begin to invade regions they normally cannot access [6]. As the ECM becomes more disorganized, hydrated, and permeable, the tightly packed collagen architecture that normally excludes vessels and nerves becomes loosened [6]. This physical opening is accompanied by molecular signals that further facilitate invasion [13].

Matrix degradation, altered molecular composition, and regulatory enzymatic imbalance trigger angiogenic cues, creating a microenvironment that favors pathological angiogenesis [13]. Proteolytic activity disrupts collagen integrity and releases bound growth factors, increasing tissue permeability and supporting endothelial and neural migration. GAGs and proteoglycans bind and regulate pro‑angiogenic and pro‑inflammatory mediators, amplifying these signals within the disorganized matrix [6].

Neural elements appear to follow similar pathways. Chronic tendinopathy shows upregulation of nociceptive neuropeptides and neural markers within the paratenon and interfascicular regions, suggesting that neoinnervation accompanies and potentially exploits the same structural vulnerabilities that permit vascular ingrowth [5].

This ingrowth is not merely a byproduct of pathology; it may further disrupt local mechanics by altering stress distribution, increasing metabolic demand, and perpetuating inflammatory signaling. 

Together, these findings support a sequential logic: matrix disorganization creates opportunity, biochemical dysregulation provides invitation, and vascular–neural ingrowth reinforces the pathological loop.

Macro‑Level Alterations

These microscale disturbances accumulate into tissue‑level changes that become visible at the macroscopic scale. Imaging commonly reveals tendon thickening, focal hypoechoic regions, and heterogeneous collagen alignment in symptomatic populations [1,14]. These structural changes coincide with meaningful alterations in mechanical behavior. Symptomatic tendons consistently demonstrate reduced stiffness, altered compliance, and impaired material properties [15,16]. These mechanical deficits align with observed reductions in plantarflexor output, diminished heel‑rise endurance, and modified neuromotor strategies during tasks requiring rapid force development [17,18].

These changes have clear implications for athletic performance. A tendon that stores and returns less energy, or that deforms more under load, can drastically alter movement outcomes. To compensate, athletes may consciously or unconsciously adjust joint excursion, redistribute work to other tissues, or modify body orientation to manage force transmission. These adjustments can influence sprint acceleration, change of direction, jump height, and repeated high‑force tasks, particularly in environments where rapid force transmission and efficient elastic recoil are essential.

Recursive Dysregulation: How Microstructural Disturbance Disrupts Load Sensing and Reinforces Pathology

Clinical evidence shows that tendinopathy often follows a prolonged and variable course. Symptoms may persist for many months, and a substantial proportion of individuals continue to experience pain or functional limitations despite structured rehabilitation [19,20]. Long‑term follow‑up frequently reveals incomplete resolution, and many individuals do not return to their pre‑injury level of function even after extended periods of modified loading [21].

These observations raise an important question: why does this condition remain so resistant to change, even when loading is adjusted and symptoms are addressed?

Once pathological changes are present, the regulatory mechanisms that maintain tendon integrity become disrupted. This disruption follows a recognizable sequence:

• Higher strain exposure accelerates micromorphological deterioration

• Micromorphological deterioration impairs mechanotransduction

• Impaired mechanotransduction alters collagen synthesis and organization

• Altered collagen organization increases compliance

• Increased compliance raises strain exposure during normal contractions

(Supported by strain‑exposure, mechanotransduction, and microstructural evidence [22–29].)

Individuals who reach higher tendon strain magnitudes, or who reach high strain more frequently during maximal efforts, demonstrate greater micromorphological deterioration over time [22,23,24]. This pattern reflects a reduction in the tendon’s ability to interpret and respond to mechanical demand.

As discussed in Part 2 of our Foundational Science series, load is the language tendons speak. When that communication becomes inconsistent, we see adjustments across domains.

For mechanical load to guide tendon adaptation, it must be transmitted from the extracellular environment to the tendon cells through integrin‑mediated mechanotransduction. As the matrix becomes more disorganized, this transmission becomes less reliable, and the signals that normally regulate collagen synthesis and alignment become increasingly noisy and inconsistent.

Neural and vascular ingrowth, described earlier, may further disrupt local mechanics, alter stress distribution, and increase metabolic demand, reinforcing the destabilizing cycle.

As compliance increases and mechanotransduction becomes less reliable, the tendon enters a progressively destabilizing loop. Each step reinforces the next, which makes the pathological state increasingly difficult to reverse. 

Yet symptoms often behave in ways that structure and mechanics alone cannot account for.

The Structural-Symptom Disconnect in Tendinopathy

Although the structural and mechanical features of established tendinopathy are increasingly well described, they do not fully explain how the condition develops, behaves, or is experienced. Early cellular and microstructural disturbances fall below imaging thresholds [14], and structural changes can precede or outlast symptoms [27–29]. These observations make clear that tendinopathy cannot be understood through structural or mechanobiological findings alone.

To capture the variability seen in clinical practice, we must consider additional domains that meaningfully shape symptom behavior, load tolerance, and recovery. Over the past two decades, several such domains have emerged as essential contributors to how tendinopathy develops, behaves, and is experienced [30–32]. These domains do not represent competing explanations. Instead, they highlight the many interacting influences that shape tendon health and symptom behavior. The following sections outline these domains and the specific ways they contribute to clinical variability.

Structural and Temporal Contributors

Structural changes can precede symptoms, persist after symptoms resolve, or remain entirely asymptomatic [27–29]. These observations show that structure alone cannot account for symptom onset, irritability, or recovery trajectory. They also reflect the slow and regionally heterogeneous nature of tendon remodeling, which complicates attempts to link structural findings to clinical state.

Mechanical Contributors

Mechanical behavior varies widely between individuals performing the same task. Internal tendon strain depends on tendon stiffness, muscle force, and muscle–tendon interaction, all of which differ substantially across people. As discussed earlier, these individual differences influence how frequently a tendon reaches higher strain magnitudes during normal loading [22,23]. Dysregulated load transfer and altered viscoelastic behavior may affect performance or tolerance, yet these mechanical features do not map cleanly onto pain or disability [3,32]. Mechanical capacity therefore must be assessed directly rather than inferred from structure or diagnosis.

Neuromotor Contributors

Pain alters motor unit behavior, force steadiness, and movement strategies, but these adaptations vary widely across individuals and often persist independently of structural change [18,37]. These neuromotor adjustments can meaningfully influence how load is distributed across the lower limb. For example, reduced dorsiflexion, altered timing, or preferential reliance on proximal musculature may shift work away from the symptomatic tendon during athletic tasks or routine daily movements. Such compensations can mask or amplify symptoms without reflecting tissue state, adding another layer of variability to tendon presentation.

Sensory and Neurovascular Contributors

Neoinnervation and vascular changes in the paratenon have been proposed as contributors to symptom persistence [5]. Pathological tendons frequently demonstrate increased vascularity on Doppler imaging [6,13]. When compared to healthy tendons, pathological tissues also show increased nociceptive neuropeptides and changes in local inflammatory mediators [29,28].

Despite these measurable differences, the specific roles that sensory and neurovascular alterations play in pain, function, and disability remain uncertain. Current evidence is preliminary, and relationships between vascularity, sensory changes, symptoms, and functional capacity remain inconsistent across studies [30].

Even with these uncertainties, such changes may contribute to why some individuals report disproportionate sensitivity during routine loading despite similar structural findings [5,6,13,27–30].

Psychological and Contextual Contributors

Psychological and contextual factors can shape pain intensity, participation, and functional tolerance, yet they do not reliably predict long‑term outcome [30,31]. Recent evidence shows that people with persistent tendinopathy demonstrate higher pain catastrophizing and modest elevations in depression and anxiety compared with nontendinopathy controls, particularly in lower‑limb presentations where pain is difficult to avoid during daily activities [33]. These differences are small and inconsistent across studies, and many psychological constructs such as kinesiophobia, self‑efficacy, and personality traits show no clear group differences [33].

Pain is a complex phenomenon that adds a challenging interpretive filter to the evaluation and management of tendinopathy. Psychological and contextual influences shape how symptoms are perceived, interpreted, and tolerated. While directionality is difficult to determine, broader pain‑science literature shows that factors such as stress, sleep disruption, and daily demands can shape symptom behavior independent of tissue state [41,42]. This combined evidence underscores the futility of separating morphological and mechanical features of the condition from the lived experience of the individuals we work with.

What These Domains Reveal

Together, these domains illustrate why tendinopathy cannot be understood through a single lens. Structure, mechanics, neuromotor behavior, sensory processing, and contextual factors each contribute meaningful information, yet none reliably dominates across individuals or time. This growing body of evidence supports a more inclusive conceptualization of tendinopathy, one that acknowledges the interaction of multiple domains rather than privileging any single one.

Unifying Concept: Tendinopathy as a Multidomain Condition

Across decades of tendon research, one message has become increasingly clear: tendinopathy cannot be reduced to a single mechanism, a single tissue property, or a single explanatory level. The accumulated evidence shows a condition shaped by interacting biological, mechanical, and behavioral processes, none of which reliably dominate across individuals or time.

Structural changes may be present without symptoms [27,28], and symptoms may fluctuate independently of structure [29]. Mechanical behavior varies widely between people performing the same task [22,23]. Neuromotor adaptations can mask or amplify symptoms without reflecting tissue state [18]. Psychological and contextual factors influence pain and participation but do not dictate recovery [30,31]. Even symptom duration fails to meaningfully stratify severity or prognosis [17,36].

These findings show that tendinopathy does not behave like a linear progression or a tidy causal chain. It behaves like a multidimensional clinical presentation, a pattern emerging from the interaction of multiple domains, each capable of amplifying or dampening the others.

Tendinopathy is a multidomain condition in which structure, mechanics, symptoms, neuromotor behavior, and psychosocial factors interact in complex and often non‑linear ways.

- No single domain explains the condition.

- No single domain predicts recovery.

- No single domain should dominate evaluation.

This multidomain perspective clarifies why traditional evaluation falls short and why a structured multidomain framework is required.

Clinical Practice Guidelines

The multidomain nature of tendinopathy demands an evaluative process that can organize diverse clinical findings into a coherent picture. Ruth Chimenti’s clinical practice guideline offers that structure. Her hierarchical decision tree provides a clear, disciplined way to integrate medical screening, differential evaluation, irritability, outcome measures, and intervention planning into a single reasoning framework. What follows is a focused look at the five components of her model, highlighting how each contributes to a comprehensive and clinically grounded approach to tendon evaluation. Each component builds on the one before it, creating a stepwise process that moves from exclusion to classification to interpretation to action.

Component 1: Medical Screening

Screening for non‑musculoskeletal concerns is firmly cemented as the initial consideration in any encounter. This is taught as the primary step for every patient‑facing clinician, and these CPGs make no exception. Medical screening remains the first safeguard in Chimenti’s hierarchical framework.

This exclusionary process clarifies whether the presentation fits the expected pattern of a load‑related tendon disorder or whether it reflects a masquerading pathology such as infection, systemic disease, or neuropathic involvement. Once this is established, the clinician can proceed confidently into the musculoskeletal domain, where structure, mechanics, and symptom behavior must be interpreted together rather than in isolation.

Component 2: Classifying the Condition Through Differential Evaluation (ICF + ICD)

After screening, the next task is classification. Classification organizes clinical presentations into meaningful patterns that guide decision making. Chimenti’s framework integrates ICD diagnosis with ICF-based functional profiling to distinguish tendinopathy from other sources of pain and dysfunction. The goal is not to label the tendon but to clarify the dominant features shaping the presentation while recognizing the multiple factors that contribute to it.

A central part of this process is determining how symptoms behave under load. Movement evoked pain (as conceptualized in recent pain science frameworks [43]) is especially informative because it reflects the interaction of task demand, neuromotor strategy, and contextual influences rather than tendon structure alone. Identifying whether movement evoked pain is the primary complaint helps differentiate tendon dominant presentations from those driven by adjacent structures or broader contributors.

A clear classification anchors expectations and ensures that management targets the features most responsible for the individual’s current limitations.

Component 3: Determining Irritability

Irritability describes how easily symptoms are provoked, how intense they become, and how long they take to settle. It is a functional measure of system sensitivity rather than a surrogate for tissue damage. System sensitivity reflects the combined influence of mechanical load, neuromotor behavior, symptom history, and contextual and psychological factors. Each of these domains can shape how symptoms respond to a given task, and none map cleanly onto structural state [30-33, 37].

Irritability must therefore be understood within the multidomain reasoning structure Chimenti emphasizes.

A holistic perspective, however, does not imply that all variables carry equal weight. Precision becomes essential. Several familiar clinical assumptions do not align with the evidence. Symptom duration does not predict irritability or recovery potential [17,36], kinesiophobia shows an inconsistent relationship with outcomes [34], and anxiety and fear of rupture, rather than fear of movement, show the strongest links to pain and stiffness [32]. These findings clarify that irritability cannot be inferred from intuitive predictors and must instead be interpreted through a disciplined, evidence‑guided multidomain framework.

In this context, Chimenti’s model provides a structured way to integrate multiple domains without treating them as interchangeable. It reflects the evidence that some commonly assumed predictors have limited relevance and that clinical reasoning must be guided by observed patterns rather than by intuition alone.

Irritability guides which tasks are appropriate to assess, how aggressively to progress, and how to interpret symptom responses. By anchoring decisions to a composite finding like symptom responsiveness rather than structural assumptions, irritability provides a practical guide for individualized loading and day‑to‑day decision making.

Component 4: Selecting Outcome Measures

This component asks a simple but essential question: given what we have identified, how will we know if this person is improving? Outcome measures serve as the feedback loop for the entire framework, allowing clinicians to monitor progress across domains, detect mismatches between symptoms and capacity, and adjust evaluation or intervention accordingly. Chimenti emphasizes selecting measures that reflect the comprehensive nature of tendinopathy and that are sensitive to change in the domains most relevant to the individual.

The 2024 guideline endorses a Core Outcome Set for Achilles tendinopathy that includes the VISA‑A, single‑leg heel‑rise endurance, and movement‑evoked pain with tendon‑loading activities [30]. These measures provide a minimum standard for monitoring symptom severity, functional capacity, and pain during load. The guideline also notes recent concerns regarding VISA‑A validity and describes the development of newer instruments, such as the TENDINS‑A and VISA‑A sedentary, which may be particularly useful for nonathletes [30].

Beyond this minimum set, outcome selection should reflect the broader tendon health model:

• Symptoms: VISA‑A or alternatives, pain with loading tasks, morning stiffness, movement‑evoked pain

• Lower extremity function: heel‑rise endurance, hopping tests, jump performance, Silbernagel battery

• Psychological factors: kinesiophobia, pain interference, anxiety, fear of rupture

• Participation: daily activities, work demands, sport involvement

• Patient‑related factors: BMI, activity level, injury history

• Tendon structure and mechanics: cross‑sectional area, thickening, shear modulus, viscosity

The goal is not to collect measures from every domain but to select those that best capture the individual’s key limitations and the domains most likely to change with intervention. This ensures that outcome tracking remains targeted, interpretable, and aligned with the multidomain reasoning structure established earlier in the framework.

Component 5: Intervention Strategies Informed by the Prior Components

Intervention planning integrates all prior components of the decision tree. Once irritability, functional demands, symptom behavior, and contextual factors are understood, the goal is to select interventions that address the full multidimensional nature of tendinopathy rather than focusing on any single impairment or mechanism. The 2024 guideline reinforces that tendon loading exercise is the foundational intervention across irritability levels, with multiple loading strategies demonstrating benefit and no single approach showing clear superiority [30]. Loading is therefore scaled to the individual’s tolerance and progressed according to symptoms and functional capacity.

Beyond loading, interventions should be selected to address the broader mechanical, functional, psychological, behavioral, and symptomatic contributors identified in earlier components. This may include strategies to improve movement capacity, support self‑efficacy and adherence, modify symptoms to enable participation in loading, or address contextual factors influencing recovery. Adjunctive or second‑line options may be considered when progress stalls, but they do not replace loading as the primary driver of improvement.

Framed in this way, intervention strategies become the action arm of the multidomain model. They translate the findings from screening, classification, irritability assessment, and outcome measures into a coherent plan that reduces symptoms, restores capacity, and supports participation in meaningful activities.

Closing Synthesis

Tendinopathy reflects changes that unfold across the entire organizational hierarchy of the tendon. Cellular activity, matrix behavior, tissue mechanics, neuromotor control, and whole‑limb function each contribute to a process that can evolve into a persistent and self‑perpetuating problem.

These biological changes do not occur in isolation. They interact with the demands placed on the limb, the individual’s movement strategies, their responses to pain, and the broader psychological and contextual environment in which symptoms develop.

This complexity makes reductionist thinking inadequate. Effective clinical reasoning requires attention to how these elements influence one another and shape the presentation over time. A structured evaluative system provides the means to do this in a way that is both nuanced and actionable. It organizes the interacting features of tendon health into a coherent process that supports clear interpretation, pattern recognition, and individualized decision making. This is the rationale for the framework presented in this installment and the foundation for successful management.

Looking Ahead

Newsletter 5 will shift from conceptual understanding to applied reasoning. We will take the same hierarchical evaluation structure and deconstruct specific elements for clarity. Informed by contemporary clinical perspectives (including recent work from Seth O’Neill) we will walk through a tendinopathy case to illustrate how a structured, comprehensive evaluation guides clinical decision making. This example will show how the framework adapts across presentations that differ in acuity, irritability, and structural findings. In doing so, we will demonstrate that the framework is not specific to any single tendon disorder, but is a general approach to tendon evaluation more broadly.

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

*If you plan to attend the Summit, but haven't yet registered, we recommend doing so soon—we're limited to 40 attendees.

Miss a previous edition? Find our archive here.

Reference List 

[1] Cook JL, Feller JA, Bonar SF, Khan KM. Abnormal tenocyte morphology is more prevalent than collagen disruption in asymptomatic athletes' patellar tendons. J Orthop Res. 2004;22(2):334‑338.

[2] Jaworski Ł, Zabrzyńska M, Klimaszewska‑Wiśniewska A, Zielińska W, Grzanka D, Gagat M. Advances in microscopic studies of tendinopathy. J Clin Med. 2022;11(6):1572.

[3] Klatte‑Schulz F, Minkwitz S, Schmock A, et al. Different Achilles tendon pathologies show distinct histological and molecular characteristics. Int J Mol Sci. 2018;19(1):E203.

[4] Minkwitz S, Schmock A, Kurtoglu A, et al. Time‑dependent alterations of MMPs, TIMPs and tendon structure after acute rupture. Int J Mol Sci. 2017;18(10):2199.

[5] Palee S, Jarusriwanna A, Lee D, et al. Chronic tendinopathy driven by neoinnervation. Pain Physician. 2025;28(4):287‑297.

[6] Steinmann S, Pfeifer CG, Brochhausen C, Docheva D. Spectrum of tendon pathologies: triggers, trails and end‑state. Int J Mol Sci. 2020;21(3):844.

[7] Li Z, Lee H, Zhu C. Molecular mechanisms of mechanotransduction in integrin‑mediated cell‑matrix adhesion. Exp Cell Res. 2016;349(1):85‑94.

[8] Muljadi PM, Andarawis‑Puri N. Glycosaminoglycans modulate microscale mechanics and viscoelasticity in fatigue‑injured tendons. J Biomech. 2023;152:111584.

[9] Blank JL, Eekhoff JD, Soslowsky LJ. Glycosaminoglycans influence regional mechanics in young but not old Achilles tendons. J Physiol. 2025;603(23):7589‑7601.

[10] Thorpe CT, Chaudhry S, Lei II, et al. Tendon overload results in alterations in cell shape and increased markers of inflammation and matrix degradation. Scand J Med Sci Sports. 2015;25(4):e381‑e391.

[11] Thorpe C, Peffers M, Simpson D, et al. Anatomical heterogeneity of tendon. Sci Rep. 2016;6:20455.

[12] Thorpe CT, Riley GP, Birch HL, Clegg PD, Screen HRC. Fascicles and the interfascicular matrix show adaptation for fatigue resistance in energy‑storing tendons. Acta Biomater. 2016;42:308‑315.

[13] Gehwolf R, Tempfer H, Cesur NP, et al. Tendinopathy: the interplay between mechanical stress, inflammation, and vascularity. Adv Sci. 2025;12(36):e06440.

[14] Docking SI, Rosengarten SD, Daffy J, Cook J. Structural integrity is decreased in both Achilles tendons in people with unilateral Achilles tendinopathy. J Sci Med Sport. 2015;18(4):383‑387.

[15] Arya S, Kulig K. Tendinopathy alters mechanical and material properties of the Achilles tendon. J Appl Physiol. 2010;108(3):670‑675.

[16] Wiesinger HP, Seynnes OR, Kösters A, Müller E, Rieder F. Mechanical and material tendon properties in patients with proximal patellar tendinopathy. Front Physiol. 2020;11:704.

[17] Hanlon SL, Scattone Silva R, Honick BJ, Silbernagel KG. Effect of symptom duration on injury severity and recovery in patients with Achilles tendinopathy. Orthop J Sports Med. 2023;11(5):23259671231164956.

[18] Arvanitidis M, Falla D, Sanderson A, Martinez‑Valdes E. Does pain influence control of muscle force. Eur J Pain. 2025;29(2):e4716.

[19] Magnusson SP, Langberg H, Kjaer M. The pathogenesis of tendinopathy. Nat Rev Rheumatol. 2010;6(5):262‑268.

[20] Thorpe CT, Riley GP, Birch HL, Clegg PD, Screen HRC. Fascicles and the interfascicular matrix show decreased fatigue life with ageing. Acta Biomater. 2017;56:58‑64.

[21] Couppé C, Svensson RB, Skovlund SV, et al. Habitual side‑specific loading leads to structural, mechanical, and compositional changes in the patellar tendon. J Appl Physiol. 2021;131(4):1187‑1199.

[22] Mersmann F, Pentidis N, Tsai MS, et al. Patellar tendon strain associates to tendon structural abnormalities in adolescent athletes. Front Physiol. 2019;10:963.

[23] Domroes T, Weidlich K, Bohm S, Mersmann F, Arampatzis A. Personalized tendon loading reduces muscle‑tendon imbalances in male adolescent elite athletes. Scand J Med Sci Sports. 2024;34(1):e14555.

[24] Mersmann F, Bohm S, Arampatzis A, Karamanidis K, Seynnes O. Editorial: muscle and tendon plasticity. Front Physiol. 2021;12:678801.

[25] Matsushima T, Hiroshi A. Molecular mechanisms of mechanosensing and plasticity of tendons and ligaments. J Biochem. 2024;176(4):263‑269.

[26] Stańczak M, Kacprzak B, Gawda P. Tendon cell biology: effect of mechanical loading. Cell Physiol Biochem. 2024;58(6):677‑701.

[27] Hullfish TJ, Hagan KL, Casey E, Baxter JR. Achilles tendon structure differs between competitive distance runners and nonrunners. J Appl Physiol. 2018;125(2):453‑458.

[28] Radovanovic G, Bohm S, Arampatzis A, Legerlotz K. Symptomatic and asymptomatic tendon differences. J Clin Med. 2023;12(3):1102.

[29] Murphy MC, Bright F, White G, et al. Reduced Achilles tendinopathy symptoms relate to perceived resolution. Res Sports Med. 2025;33(5):578‑589.

[30] Chimenti RL, Neville C, Houck J, et al. Achilles pain, stiffness, and muscle power deficits. J Orthop Sports Phys Ther. 2024;54(12):CPG1‑CPG32.

[31] Hasani F, Haines TP, Munteanu SE, Vicenzino B, Malliaras P. LOADIT trial protocol. Pilot Feasibility Stud. 2020;6:99.

[32] Sancho I, Malliaras P, Barton C, Willy RW, Morrissey D. Biomechanical alterations in Achilles tendinopathy. Gait Posture. 2019;73:189‑201.

[33] Mest J, Flood A, Toufexis C, Waddington G, Malliaras P, Fearon AM. Differences in psychological factors between people with persistent tendinopathy and those without tendinopathy: a systematic review with meta‑analysis. J Orthop Sports Phys Ther. 2025;55(12):1‑18. doi:10.2519/jospt.2025.13307.

[34] Smitheman HP, Hanlon SL, Lundberg M, Pohlig RT, Silbernagel KG. Comparison of short term recovery in patients with midportion Achilles tendinopathy with varying degrees of kinesiophobia treated with the Silbernagel protocol: a prospective single cohort analysis. Phys Ther Sport. 2024;70:101‑109. doi:10.1016/j.ptsp.2024.10.004.

[35] Hanlon SL, Scattone Silva R, Honick BJ, Silbernagel KG. Effect of symptom duration on injury severity and recovery in patients with Achilles tendinopathy. Orthop J Sports Med. 2023;11(5):23259671231164956.

[36] Potter M, Rio E, Gravare Silbernagel K, et al. Patient‑reported improvement thresholds for Achilles tendinopathy: establishing minimal clinically important differences. J Orthop Sports Phys Ther. 2025;55(8):1‑12. doi:10.2519/jospt.2025.13288.

[37] Andringa‑Bate J, Almusallam M, Coventry M, et al. Neuromotor function following lower‑limb muscle or tendon injury: systematic review and meta‑analysis. Sports Med Health Sci. 2025; doi:10.1016/j.smhs.2025.07.012.

[38] Chimenti RL, Neville C, Houck J, et al. Achilles pain, stiffness, and muscle power deficits: Achilles tendinopathy clinical practice guideline. J Orthop Sports Phys Ther. 2024;54(12):CPG1‑CPG32.

[39] Hasani F, Haines TP, Munteanu SE, Vicenzino B, Malliaras P. Efficacy of different load intensity and time‑under‑tension calf loading protocols for Achilles tendinopathy (the LOADIT trial): protocol for a randomised pilot study. Pilot Feasibility Stud. 2020;6:99.

[40] Sancho I, Malliaras P, Barton C, Willy RW, Morrissey D. Biomechanical alterations in individuals with Achilles tendinopathy during running and hopping: a systematic review with meta‑analysis. Gait Posture. 2019;73:189‑201.

[41] Vinstrup J, Jakobsen MD, Calatayud J, Jay K, Andersen LL. Association of Stress and Musculoskeletal Pain With Poor Sleep: Cross-Sectional Study Among 3,600 Hospital Workers. Front Neurol. 2018 Nov 21;9:968. doi: 10.3389/fneur.2018.00968. PMID: 30519210; PMCID: PMC6258880.

[42] Aboushaar N, Serrano N. The mutually reinforcing dynamics between pain and stress: mechanisms, impacts and management strategies. Front Pain Res (Lausanne). 2024 Nov 18;5:1445280. doi: 10.3389/fpain.2024.1445280. PMID: 39624230; PMCID: PMC11609167.

[43] Butera KA, Chimenti RL, Alsouhibani AM, et al. Through the lens of movement-evoked pain: a theoretical framework of the “Pain-Movement Interface.” J Pain. 2024;25(7):104486. doi:10.1016/j.jpain.2024.01.351.