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Both over and under use may cause harm tendons

updated

Tags: anatomy, etiology, exercise, biology, treatment, tendinosis, pro, self-treatment, pain problems, overuse injury, injury

Three articles on PainSci cite Arampatzis 2007: (1) The Trouble with Chairs(2) The Complete Guide to Patellofemoral Pain Syndrome(3) What Can a Runner With Knee Pain Do at the Gym?

PainSci notes on Arampatzis 2007:

The importance of tissue health is well known in tendinopathy. Biomechanics is still considered important — but in terms of tissue loading and adaptation rather than gross structural abnormalities. For instance, this study demonstrated that both over and under use of tendons can lead to pathology. Tenocytes (tendon cells) adapt to the forces imparted on them, creating a tissue tolerance “set point” depending on your activity level. This set point can decrease with disuse, and increase with exercise — as long as there’s enough rest. Activity that is too frequent or intense might damage cells without giving them a chance to adapt. Not only is this biological proof of “use it or lose it”, but perhaps: “use it or lose it, but not too much!” Therein lies the problem of reducing health information to sound bites.

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

Tendons are able to remodel their mechanical and morphological properties in response to mechanical loading. However, there is little information about the effects of controlled modulation in cyclic strain magnitude applied to the tendon on the adaptation of tendon's properties in vivo. The present study investigated whether the magnitude of the mechanical load induced as cyclic strain applied to the Achilles tendon may have a threshold in order to trigger adaptation effects on tendon mechanical and morphological properties. Twenty-one adults (experimental group, N=11; control group, N=10) participated in the study. The participants of the experimental group exercised one leg at low-magnitude tendon strain (2.85+/-0.99%) and the other leg at high-magnitude tendon strain (4.55+/-1.38%) of similar frequency and volume. After 14 weeks of exercise intervention we found a decrease in strain at a given tendon force, an increase in tendon-aponeurosis stiffness and tendon elastic modulus and a region-specific hypertrophy of the Achilles tendon only in the leg exercised at high strain magnitude. These findings provide evidence of the existence of a threshold or set-point at the applied strain magnitude at which the transduction of the mechanical stimulus may influence the tensional homeostasis of the tendons. The results further show that the mechanical load exerted on the Achilles tendon during the low-strain-magnitude exercise is not a sufficient stimulus for triggering further adaptation effects on the Achilles tendon than the stimulus provided by the mechanical load applied during daily activities.

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