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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 othe...
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
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