Tendon neuroplastic training: changing the way we think about tendon rehabilitation: a narrative review

Tendinopathy can be resistant to treatment and often recurs, implying that current treatment approaches are suboptimal. Rehabilitation programmes that have been successful in terms of pain reduction and return to sport outcomes usually include strength training. Muscle activation can induce analgesia, improving self-efficacy associated with reducing one's own pain. Furthermore, strength training is beneficial for tendon matrix structure, muscle properties and limb biomechanics. However, current tendon rehabilitation may not adequately address the corticospinal control of the muscle, which may result in altered control of muscle recruitment and the consequent tendon load, and this may contribute to recalcitrance or symptom recurrence. Outcomes of interest include the effect of strength training on tendon pain, corticospinal excitability and short interval cortical inhibition. The aims of this concept paper are to: (1) review what is known about changes to the primary motor cortex and motor control in tendinopathy, (2) identify the parameters shown to induce neuroplasticity in strength training and (3) align these principles with tendon rehabilitation loading protocols to introduce a combination approach termed as tendon neuroplastic training. Strength training is a powerful modulator of the central nervous system. In particular, corticospinal inputs are essential for motor unit recruitment and activation; however, specific strength training parameters are important for neuroplasticity. Strength training that is externally paced and akin to a skilled movement task has been shown to not only reduce tendon pain, but modulate excitatory and inhibitory control of the muscle and therefore, potentially tendon load. An improved understanding of the methods that maximise the opportunity for neuroplasticity may be an important progression in how we prescribe exercise-based rehabilitation in tendinopathy for pain modulation and potentially restoration of the corticospinal control of the muscle-tendon complex

MATERIALS IN RESTORATIVE DENTISTRY

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73465/1/j.1749-6632.1968.tb20274.x.pd

2016 Research & Innovation Day Program

A one day showcase of applied research, social innovation, scholarship projects and activities.https://first.fanshawec.ca/cri_cripublications/1003/thumbnail.jp

Relationship between compressive loading and ECM changes in tendons

Tendons are designed to absorb and transfer large amounts of tensile load. The well organised, strong yet flexible, extracellular matrix allows for this function. Many tendons are also subject to compressive loads, such as at the entheses, as the tendon wraps around bony protuberances or from internal compression during tensile loading or twisting. Tendinopathy, the clinical syndrome of pain and dysfunction in a tendon is usually the result of overload. However, it is not only the tensile overload that should be considered, as it has been shown that compressive loads change tendon structure and that combination loads can induce tendon pathology. This review summarises how load is detected by the tenocytes, how they respond to compressive load and the resulting extracellular matrix changes that occur. Understanding the effect of compression on tendon structure and function may provide directions for future matrix based intervention

The continuum of tendon pathology : Current view and clinical implications

Cook and Purdam first proposed the Continuum model in 2009, with the aim of improving the understanding of the complexity of tendon pathologies. The Continuum is based on three states of tendon structure: reactive tendon, tendon disrepair and degenerative tendon. In contrast to other proposals, the Continuum model describes continuous changes in tendon structure. Each state of tendon structure represents a particular clinical presentation and requires a particular type of management. Evidence seen in histopathological studies, imaging and clinical studies all support the Continuum model for the analysis of tendon pathologies. © 2017 Consell Català de l'Esport. Generalitat de Cataluny

hCINAP is an atypical mammalian nuclear adenylate kinase with an ATPase motif:Structural and functional studies

Human coilin interacting nuclear ATPase protein (hCINAP) directly interacts with coilin, a marker protein of Cajal Bodies (CBs), nuclear organelles involved in the maturation of small nuclear ribonucleoproteins UsnRNPs and snoRNPs. hCINAP has previously been designated as an adenylate kinase (AK6), but is very atypical as it exhibits unusually broad substrate specificity, structural features characteristic of ATPase/GTPase proteins (Walker motifs A and B) and also intrinsic ATPase activity. Despite its intriguing structure, unique properties and cellular localization, the enzymatic mechanism and biological function of hCINAP have remained poorly characterized. Here, we offer the first high-resolution structure of hCINAP in complex with the substrate ADP (and dADP), the structure of hCINAP with a sulfate ion bound at the AMP binding site, and the structure of the ternary complex hCINAP-Mg 2+ADP-Pi. Induced fit docking calculations are used to predict the structure of the hCINAP-Mg 2+ATP-AMP ternary complex. Structural analysis suggested a functional role for His79 in the Walker B motif. Kinetic analysis of mutant hCINAP-H79G indicates that His79 affects both AK and ATPase catalytic efficiency and induces homodimer formation. Finally, we show that in vivo expression of hCINAP-H79G in human cells is toxic and drastically deregulates the number and appearance of CBs in the cell nucleus. Our findings suggest that hCINAP may not simply regulate nucleotide homeostasis, but may have broader functionality, including control of CB assembly and disassembly in the nucleus of human cells