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bibliography * The PainScience Bibliography contains plain language summaries of thousands of scientific papers and others sources, like a specialized blog. This page is about a single scientific paper in the bibliography, Andersson 2011.

How rabbit tendons respond to overuse

updated
Andersson G, Forsgren S, Scott A, Gaida JE, Stjernfeldt JE, Lorentzon R, Alfredson H, Backman C, Danielson P. Tenocyte hypercellularity and vascular proliferation in a rabbit model of tendinopathy: contralateral effects suggest the involvement of central neuronal mechanisms. Br J Sports Med. 2011 Apr;45(5):399–406. PubMed #20605910.
Tags: tendinosis, counter-intuitive, etiology, neat, chronic pain, neurology, pain problems, overuse injury, injury, pro

PainSci summary of Andersson 2011?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided at the bottom of the page, as often as possible. ★★★☆☆?3-star ratings are for typical studies with no more (or less) than the usual common problems. Ratings are a highly subjective opinion, and subject to revision at any time. If you think this paper has been incorrectly rated, please let me know.

Andersson et al. studied how rabbit tendons responded to exercise over a period of weeks (a relatively harmless experiment for the rabbits, as these things go). The “exercise” was electrically stimulated contraction of the triceps surae muscle, as well as a bunch of passive movement (basically just moving a rabbit’s foot over and over again, like that robot chair-stresser at Ikea). Three groups of rabbits were subjected to variations on this regimen, while a fourth group was left unmolested, for comparison purposes.

There was no difference after just a week, but the exercised rabbits showed more tendon cells and blood vessels after three weeks… and signs of damage after six. The results show the difference between exercise (a good thing) and over-exercise (too much of a good thing).

That’s all lovely and all, but there was one really neato discovery in this study: only one side was artificially exercised, but both sides reacted after three weeks. Changes in the tendons were therefore obviously neurologically regulated, like a slow-motion reflex reaction on sides, reacting to the stimulus on one side. That is extremely interesting.

~ Paul Ingraham

original abstract

OBJECTIVE: To determine whether there are objective findings of tendinosis in a rabbit tendinopathy model on exercised and contralateral (non-exercised) Achilles tendons.

DESIGN: Four groups of six New Zealand white rabbits per group were used. The animals of one (control) group were not subjected to exercise/stimulation.

INTERVENTIONS: Animals were subjected to a protocol of electrical stimulation and passive flexion-extension of the right triceps surae muscle every second day for 1, 3 or 6 weeks.

MAIN OUTCOME MEASURES: Tenocyte number and vascular density were calculated. Morphological evaluations were also performed as well as in-situ hybridisation for vascular endothelial growth factor (VEGF) messenger RNA.

RESULTS: There was a significant increase in the tenocyte number after 3 and 6 weeks of exercise, but not after 1 week, in comparison with the control group. This was seen in the Achilles tendons of both legs in experimental animals, including the unexercised limb. The pattern of vascularity showed an increase in the number of tendon blood vessels in rabbits that had exercised for 3 weeks or more, compared with those who had exercised for 1 week or not at all. VEGF-mRNA was detected in the investigated tissue, with the reactions being more clearly detected in the tendon tissue with tendinosis-like changes (6-week rabbits) than in the normal tendon tissue (control rabbits).

CONCLUSIONS: There were bilateral tendinosis-like changes in the Achilles tendons of rabbits in the current model after 3 weeks of training, suggesting that central neuronal mechanisms may be involved and that the contralateral side is not appropriate as a control.

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