Achilles tendinopathy is a painful overuse injury that is extremely common in athletes, especially those who participate in running and jumping sports. In addition to pain, Achilles tendinopathy is accompanied by alterations in the tendon's structure and mechanical properties, altered lower extremity function, and fear of movement. Cumulatively, these impairments limit sport participation and performance. A thorough evaluation and comprehensive treatment plan, centered on progressive tendon loading, is required to ensure full recovery of tendon health and to minimize the risk of reinjury. In this review, we will provide an update on the evidence-based evaluation, outcome assessment, treatment, and return-to-sport planning for Achilles tendinopathy. Furthermore, we will provide the strength of evidence for these recommendations using the Strength of Recommendation Taxonomy system.

Athletic performance relies on tendons, which enable movement by transferring forces from muscles to the skeleton. Yet how load-bearing structures in tendon sense and adapt to physical demands is not understood. Here, by performing calcium (Ca 2+ ) imaging in mechanically loaded tendon explants from rats and in primary tendon cells from rats and humans, we show that tenocytes detect mechanical forces via the mechanosensitive ion channel PIEZO1, which senses shear stresses induced by collagen-fibre sliding. Via tenocyte-targeted loss-of-function and gain-of-function experiments in rodents, we show that reduced PIEZO1 activity decreased tendon stiffness and that elevated PIEZO1 mechanosignalling increased tendon stiffness and strength, seemingly through upregulated collagen crosslinking. We also show that humans carrying the PIEZO1 E756del gain-of-function mutation display a 13.2% average increase in normalized jumping height, presumably owing to a higher rate of force generation or to the release of a larger amount of stored elastic energy. Further understanding of the PIEZO1-mediated mechanoregulation of tendon stiffness should aid research on musculoskeletal medicine and on sports performance.

Background Nine core domains for tendinopathy have been identified. For Achilles tendinopathy there is large variation in outcome measures used, and how these fit into the core domains has not been investigated. Objective To identify all available outcome measures outcome measures used to assess the clinical phenotype of Achilles tendinopathy in prospective studies and to map the outcomes measures into predefined health-related core domains. Design Systematic review. Data Sources Embase, MEDLINE (Ovid), Web of Science, CINAHL, The Cochrane Library, SPORTDiscus and Google Scholar. Eligibility Criteria for Selecting Studies Clinical diagnosis of Achilles tendinopathy, sample size ≥ ten participants, age ≥ 16 years, and the study design was a randomized or non-randomized clinical trial, observational cohort, single-arm intervention, or case series. Results 9376 studies were initially screened and 307 studies were finally included, totaling 13,248 participants. There were 233 (177 core domain) different outcome measures identified across all domains. For each core domain outcome measures were identified, with a range between 8 and 35 unique outcome measures utilized for each domain. The proportion of studies that included outcomes for predefined core domains ranged from 4% for the psychological factors domain to 72% for the disability domain. Conclusion 233 unique outcome measures for Achilles tendinopathy were identified. Most frequently, outcome measures were used within the disability domain. Outcome measures assessing psychological factors were scarcely used. The next step in developing a core outcome set for Achilles tendinopathy is to engage patients, clinicians and researchers to reach consensus on key outcomes measures. Prospero Registration CRD42020156763.

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Tendons enable movement by transferring muscle forces to the skeleton, and athletic performances critically rely on mechanically-optimized tendons. How load-bearing structures of tendon sense and adapt to physical demands is an open question of central importance to musculoskeletal medicine and human sports performance. Here, with calcium imaging in tendon explants and primary tendon cells we characterized how tenocytes detect mechanical forces and determined collagen fiber-sliding-induced shear stress as a key stimulus. CRISPR/Cas9 screening in human and rat tenocytes identified PIEZO1 as the crucial shear sensor. In rodents, elevated mechano-signaling increased tendon stiffness and strength both in vitro by pharmacological channel activation and in vivo by a Piezo1 gain-of-function mutation. Strikingly, humans carrying the PIEZO1 gain-of-function E756del mutation revealed a 16% average increase in normalized jumping height, with more effective storage of potential energy released during dynamic jumping maneuvers. We propose that PIEZO1-mediated mechano-signaling regulates tendon stiffness and impacts human athletic performance.