The Role of Detraining in Tendon Mechanobiology

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. Abstracts 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.

Acute tendon changes in intense CrossFit workout: an observational cohort study

“…In our study, participants were asked to finish the workout at hand in the shortest amount of time possible, leading to a much higher velocity in all repetitions, and probably less attention to technique. (Frizziero et al, 2016) also found that physical activity such as training after an injury, or other sudden detraining scenarios, should be performed cautiously and by following targeted rehabilitation programs to get the desirable effect on the affected tendon.…”

Detraining and Anabolic-Androgenic Steroid Discontinuation Change Calcaneal Tendon Morphology

“…This adaptation consisted of weight lifting sessions (50% body weight load), once a day, five days per week, in water at 30 ± 2 • C. The training was induced by the instinctive reactions of rats submitted to a jump exercise protocol in a plastic tube (25 cm diameter and 40 cm length) with water at 30 ± 2 • C. The overload was attached to the animal's chest by means of a vest fitted to its body. The numbers of sets [2][3][4] and repetitions [5][6][7][8][9][10] were adjusted daily and increased gradually. All sessions were performed in the afternoon after 4 p.m. Vertical jump protocol: After the adaptation week, the animals were submitted to the experimental jump protocol, which consisted in the first training week of: 4 sets of 10 jumps with a 30 s rest period between sets and overload of 50% of body weight.…”

“…It is generally presumed that the increased secretion of these growth factors and enzymes is responsible for the development of exercise-induced adaptations, which include an increased tendon cross-sectional area, tendon stiffness, and collagen crosslinking [2,8,9]. Thus, it is clear that physiological loads influence tendon cells, producing cellular signals that lead to positive adaptations to the tissue.On the other hand, a systematic review investigated the effects of training interruption on tendon mechanobiology, indicating that detraining (four weeks of no exercise in animals) causes rearrangement in the collagen fiber, increasing collagen type III and reducing collagen type I, causing a loss of resistance to tension, increasing rigidity and the risk of rupture in the entheses [10]. In addition, detraining leads to a reduction in collagen type I and III synthesis and tenocyte activity, despite the matrix metalloproteinases (MMPs) synthesized during the training phase remaining active, assisting tissue remodeling [10,11].Moreover, in sports, particularly in competitive athletes, the use of anabolic-androgenic steroids (AAS) has already become a chronic practice due to the continuous search for better performance [12].…”

“…Thus, it is clear that physiological loads influence tendon cells, producing cellular signals that lead to positive adaptations to the tissue.On the other hand, a systematic review investigated the effects of training interruption on tendon mechanobiology, indicating that detraining (four weeks of no exercise in animals) causes rearrangement in the collagen fiber, increasing collagen type III and reducing collagen type I, causing a loss of resistance to tension, increasing rigidity and the risk of rupture in the entheses [10]. In addition, detraining leads to a reduction in collagen type I and III synthesis and tenocyte activity, despite the matrix metalloproteinases (MMPs) synthesized during the training phase remaining active, assisting tissue remodeling [10,11].Moreover, in sports, particularly in competitive athletes, the use of anabolic-androgenic steroids (AAS) has already become a chronic practice due to the continuous search for better performance [12]. AAS can cause various adverse effects, such as an elevated risk of tendon rupture [13,14], likely due to degenerative changes in the tendon, and disorganized collagen fibers, including dysplastic fibrils with a clear disruption of the fibril interface [15].A number of harmful side effects of AAS administration associated with training in rats are reported in the biomechanical properties of the CT, superficial flexor tendon (SFT), and deep flexor tendon (DFT), characterized by a less flexible and weaker tendon [16].…”

Efficacy and safety of hyaluronic acid (500-730kDa) Ultrasound-guided injections on painful tendinopathies: a prospective, open label, clinical study

“…Even mechanical overloading is considered as the main risk factor, other intrinsic and extrinsic factors may contribute to the pathogenesis 2,3 . In particular, poor vascularity, underload, age, gender, as well as genetic, endocrine and metabolic factors may play a central role [4][5][6] . Over the last decade, various models have been proposed to explain the intrinsic pathogenic mechanism of tendinopathies, which determine the failed healing response.…”