How do tendons adapt? Going beyond tissue responses to understand positive adaptation and pathology development: A narrative review

Sean I Docking, Jill Cook, Sean I Docking, Jill Cook

Abstract

Understanding how tendons adapt to load is crucial to understanding how training can improve performance, minimise the risk of injury and aid rehabilitation. Adaptation is the positive response of an organism or tissue to benefit its function. In tendons, numerous tissue responses to load have been identified in vivo. Changes in tendon dimensions, structure on imaging, mechanical properties, and blood flow have been reported in response to mechanical stimuli. However, research has focused on tissue level changes with little understanding of how changes at the tissue level affect the person, their athletic performance or injury risk. Tendons can have a paradoxical response to load, load can induce positive adaptation, however it is also a major factor in the development of tendon pathology and pain. Tendon pathology is a risk factor for developing symptoms, yet the high rate of asymptomatic pathology suggests that the pathological tendon must adapt to be able to tolerate load. Similarly, there is mounting evidence to suggest that tendon remodelling or repair is not necessary for a positive clinical outcome following rehabilitation, suggesting that the tendon must adapt via other mechanisms. This narrative review synthesises evidence of how normal and pathological tendons adapts to load, and how this relates to adaptation of load capacity and function of the individual.

Keywords: Adaptation; Injury; Pathology; Rehabilitation; Tendon.

Conflict of interest statement

The authors have no conflict of interest.

Figures

Figure 1
Figure 1
Schematic representation of the ‘mechanostat point’ for tendons. Mechanical stimulus within a certain level maintains homeostasis and potential adaptation of the tendon. Mechanical stimulus below this level (ie no strain, 1% cyclic strain) produces a maladaptive response due to increases in digestive enzymes. Conversely, large cyclic strains (ie 9% and over) produces increase in inflammatory cytokines and markers of apoptosis consistent with maladaptation. Figure adapted from[3,13,14,99].
Figure 2
Figure 2
Schematic representation of re-calibration of the ‘mechanostat point’ following stress deprivation or overload. Maladaptation results in a shift of the ‘mechanostat point’, where stress deprivation now results in an adaptive/homeostatic process. Adaptation results an increase in load capacity and the ‘mechanostat point’. Where overload once triggered a maladaptive response, the change in ‘mechanostat point’ now results in an adaptive process.
Figure 3
Figure 3
Defining adaptation based on contribution of tissue-level response to person-level changes.

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