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• CONSIDER HYPOXIA NOT OVERLOAD
  Jennifer M Robinson
  Published on: 11 October 2022

• Published on: 11 October 2022

  CONSIDER HYPOXIA NOT OVERLOAD

  • Jennifer M Robinson, doctor

  I read with appreciation Cook and Purdam's article, as this continuum model is probably quite helpful in determining treatment choices. Where the article falls short though is the unproved presumption that the key initiating factor is over load. In perpetuating this oft quoted presumption the article fails to acknowledge the large population who develop tendon pain without overload/ overuse.

  I suggest that othe...

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  I read with appreciation Cook and Purdam's article, as this continuum model is probably quite helpful in determining treatment choices. Where the article falls short though is the unproved presumption that the key initiating factor is over load. In perpetuating this oft quoted presumption the article fails to acknowledge the large population who develop tendon pain without overload/ overuse.

  I suggest that other factors are far more important precipitants of the pathological changes in this continuum, and propose that hypoxia is a far better fit as to a key initiating factor.

  Hypoxia explains a number of key features of tendinopathy that are inexplicable from an overload model. Examples include:

  - The location of pathology in the athlete appears primarily in the stress shield area of the tendon: the area subject to compression with use. There is no doubt the blood flow will be interrupted by this compression. If the frequency of compression is sufficient to prevent adequate blood flow restoration a relative hypoxic status even temporarily may initiate the onset of what Cook and Purdam term reactive tendinopathy.

  - Hypoxia certainly explains the neovascularisation that is one of the primary pathological findings, likely through an upregulation of VEGF in the hypoxic state.

  - Microvascular disease may explain the prevalence of tendon pathology in those with diabetes

  - The success of sclerosing treatment may have more to do with the short term increase in vascularity after treatment, the eventual sclerosis an unfavourable side effect.

  - The success of Glyceryl trinitrate may simply be due to a local vasodilatory effect of the drug.

  - That surgery is less successful in non athletic individuals compared with athletes may be explained by a lack of collateral circulation in the non athlete, where the remaining tendon remains under a relative hypoxia, compared with the improved collateral circulation and oxygenation via collateral arterial supply in the remaining tendon that likely occurs in the athletic population.

  - That exercise therapy remains a mainstay of treatment, may be one factor that increases blood flow, improves circulation to the tendon in general and hence reduces the hypoxic effect.

  - Pain, may simply be due to ischaemia.

  I suggest Cook and Purdam's paper makes more sense if the word "hypoxia" is substituted for "overload" then there is no difficulty explaining why exercise is the prime prescription for tendinopathies, and why rest is not helpful as a therapeutic model.

  In future publications about tendon pathology, I would like to see less thoughtless presumption that overload is a primary initiating factor, as this oversimplifies what is no doubt a multi-factorial condition. Cook and Purdam acknowledged intrinsic factors such as genetics, sex, body composition; but neglected to mention circulatory disturbance, and attrition age related, disuse or arthritic. Factors proposed as early as 1966 in "The Standard Nomenclature of Athletic Injuries, 1966". While a hypoxic model may not be perfect, I propose that a biochemical model deserves consideration as the overload model has out lived it's usefulness.

  In summary, I challenge the prevailing presumption of overload as a primarily initiating factor for development of tendon pathology and suggest in fact the exact opposite. I challenge that despite the rare excessive compressive loads experienced in a high level athlete, by far the majority of tendon pathology is due to under use, not overuse; due to inadequate exercise not overload; due to inadequate tissue oxygenation not hypervascularity.

  Conflict of Interest:

  None declared

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  Conflict of Interest:
  None declared.

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