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Tendinopathy is the most common disorder in sports medicine. Multiple hypotheses have been proposed for the aetiopathogenesis, but many aspects still remain elusive. Microdialysis studies have shown high levels of lactate within tendinosis, even at resting tendons,1 suggesting that hypoxia persists in tendinopathy. The presence of necrotic tenocytes, blocked arteries and anaerobic enzymes within tendinopathy lesions lend further support to the role of hypoxia in the aetiopathogenesis.2 Finally, ‘tendinosis’, the pathognomonic histopathological finding in tendinopathy, is composed of hypoxic, mucoid, hyaline and fibrinoid tissue.2 These tissue types are known to be hypoxia induced.
Tendons are generally poorly vascularised, while certain regions—those most prone to injury—are almost avascular. This can be considered an evolutionary ‘design failure’ that makes tendons susceptible to chronic and acute injuries. As a consequence, healthy tendons have a virtually non-existent tissue turnover throughout adulthood.3 However, somewhat paradoxically, tissue turnover is increased in tendinopathic tendons.3 Given the persisting hypoxia and subsequent anaerobic metabolism,1 2 it comes as no surprise that the enhanced tissue turnover leads to production of poorly organised tissue—tendinosis—in tendinopathy.2
The fundamental survival mechanism of any cell under hypoxia is the activation of hypoxia-inducible factor-1α (HIF-1α),4 a transcription factor that turns …
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