Abstract

Introduction: Several conditions such as training, aging, estrogen deficiency and drugs could affect the biological and anatomo-physiological characteristics of the tendon. Additionally, recent preclinical and clinical studies examined the effect of detraining on tendon, showing alterations in its structure and morphology and in tenocyte mechanobiology. However, few data evaluated the importance that cessation of training might have on tendon. Basically, we do not fully understand how tendons react to a phase of training followed by sudden detraining. Therefore, within this review, we summarize the studies where tendon detraining was examined.Materials and Methods: A descriptive systematic literature review was carried out by searching three databases (PubMed, Scopus and Web of Knowledge) on tendon detraining. Original articles in English from 2000 to 2015 were included. In addition, the search was extended to the reference lists of the selected articles. A public reference manager (www.mendeley.com) was adopted to remove duplicate articles.Results: An initial literature search yielded 134 references (www.pubmed.org: 53; www.scopus.com: 11; www.webofknowledge.com: 70). Fifteen publications were extracted based on the title for further analysis by two independent reviewers. s and complete articles were after that reviewed to evaluate if they met inclusion criteria.Conclusions: The revised literature comprised four clinical studies and an in vitro and three in vivo reports. Overall, the results showed that tendon structure and properties after detraining are compromised, with an alteration in the tissue structural organization and mechanical properties. Clinical studies usually showed a lesser extent of tendon alterations, probably because preclinical studies permit an in-depth evaluation of tendon modifications, which is hard to perform in human subjects. In conclusion, after a period of sudden detraining (e.g., after an injury), physical activity should be taken with caution, following a targeted rehabilitation program. However, further research should be performed to fully understand the effect of sudden detraining on tendons.

Highlights

  • Several conditions such as training, aging, estrogen deficiency and drugs could affect the biological and anatomo-physiological characteristics of the tendon

  • While physiologic loads are required to maintain tendon homeostasis, (Galloway et al, 2013) unusual loading could direct to tendon injury, either through an acute traumatic injury or chronic, degenerative process resulting from an increase of microdamages and an altered cell/matrix response (Arnoczky et al, 2007; Magnusson et al, 2010)

  • Despite previous studies showed complete histological and biochemical characteristics of tendons rupture and some of these have been included into the clinical scenario, little is known concerning the mechanical response of muscles to tendon injury (Jamali et al, 2000; Derwin et al, 2006; Sandri, 2008; Charvet et al, 2012; Zhang et al, 2013)

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Summary

Introduction

Several conditions such as training, aging, estrogen deficiency and drugs could affect the biological and anatomo-physiological characteristics of the tendon. Tendons are a specialized tissues that join muscle to bone and are composed by extracellular collagen fibers arranged in regular arrays (Aslan et al, 2008) This mechanosensitive tissue shows detailed mechanical properties that allow it to adapt and respond to loading transmitted by muscles (Fang and Lake, 2015). This load transfer provide the principal mechanical stimulus for tendon cells (Kondratko-Mittnacht et al, 2015). Muscle atrophy subsequent to tendon rupture is a frequent complication found by physicians and orthopedic surgeons This condition proves significantly weaker musculature resulting in unfavorable functional consequences, with a consequent reduction in muscle force generation (Sandri, 2008; Zhang et al, 2013). Recently Zhang et al (2013) demonstrated that tendon rupture has a supplementary influence on muscle biomechanics in comparison to disuse

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