• Energy Research

Some tendons, such as the human Achilles and equine superficial digital flexor tendon (SDFT), act as energy stores, stretching and recoiling to increase efficiency during locomotion. Our previous observations of rotation in response to applied strain in SDFT fascicles suggest a helical structure, which may provide energy-storing tendons with a greater ability to extend and recoil efficiently. Despite this specialization, energy-storing tendons are prone to age-related tendinopathy. The aim of this study was to assess the effect of cyclic fatigue loading (FL) on the microstructural strain response of SDFT fascicles from young and old horses. The data demonstrate two independent age-related mechanisms of fatigue failure; in young horses, FL caused low levels of matrix damage and decreased rotation. This suggests that loading causes alterations to the helix substructure, which may reduce their ability to recoil and recover. By contrast, fascicles from old horses, in which the helix is already compromised, showed greater evidence of matrix damage and suffer increased fibre sliding after FL, which may partially explain the age-related increase in tendinopathy. Elucidation of helix structure and the precise alterations occurring owing to both ageing and FL will help to develop appropriate preventative and repair strategies for tendinopathy.

The predominant function of tendons is to position the limb during locomotion. Specific tendons also act as energy stores. Energy-storing (ES) tendons are prone to injury, the incidence of which increases with age. This is likely related to their function; ES tendons are exposed to higher strains and require a greater ability to recoil than positional tendons. The specialized properties of ES tendons are thought to be achieved through structural and compositional differences. However, little is known about structure-function relationships in tendons. This study uses fascicles from the equine superficial digital flexor (SDFT) and common digital extensor (CDET) as examples of ES and positional tendons. We hypothesized that extension and recoil behaviour at the micro-level would differ between tendon types, and would alter with age in the injury-prone SDFT. Supporting this, the results show that extension in the CDET is dominated by fibre sliding. By contrast, greater rotation was observed in the SDFT, suggesting a helical component to fascicles in this tendon. This was accompanied by greater recovery and less hysteresis loss in SDFT samples. In samples from aged SDFTs, the amount of rotation and the ability to recover decreased, while hysteresis loss increased. These findings indicate that fascicles in the ES SDFT may have a helical structure, enabling the more efficient recoil observed. Further, the helix structure appears to alter with ageing; this coincides with a reduction in the ability of SDFT fascicles to recoil. This may affect tendon fatigue resistance and predispose aged tendons to injury.

Extracorporeal shock wave therapy (ESWT) is a non-invasive treatment for chronic tendinopathies, however little is known about the in-vivo biological mechanisms of ESWT. Using microdialysis, we examined the real-time biological response of healthy and pathological tendons to ESWT. A single session of ESWT was administered to the mid-portion of the Achilles tendon in thirteen healthy individuals (aged 25.7 ± 7.0 years) and patellar or Achilles tendon of six patients with tendinopathies (aged 39.0 ± 14.9 years). Dialysate samples from the surrounding peri-tendon were collected before and immediately after ESWT. Interleukins (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70, IL-17A, vascular endothelial growth factor and interferon-γ were quantified using a cytometric bead array while gelatinase activity (MMP-2 and -9) was examined using zymography. There were no statistical differences between the biological tissue response to ESWT in healthy and pathological tendons. IL-1β, IL-2, IL-6 and IL-8 were the cytokines predominantly detected in the tendon dialysate. IL-1β and IL-2 did not change significantly with ESWT. IL-6 and IL-8 concentrations were elevated immediately after ESWT and remained significantly elevated for four hours post-ESWT (p < 0.001). Pro-forms of MMP-2 and -9 also increased after ESWT (p < 0.003), whereas there were no significant changes in active MMP forms. In addition, the biological response to ESWT treatment could be differentiated between possible responders and non-responders based on a minimum 5-fold increase in any inflammatory marker or MMP from pre- to post-ESWT. Our findings provide novel evidence of the biological mechanisms underpinning ESWT in humans in vivo. They suggest that the mechanical stimulus provided by ESWT might aid tendon remodelling in tendinopathy by promoting the inflammatory and catabolic processes that are associated with removing damaged matrix constituents. The non-response of some individuals may help to explain why ESWT does not improve symptoms in all patients and provides a potential focus for future research.