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Purpose:To understand the mechanisms for the effects of resistance training on functional parameters, and to assess the injury risk of the involved tissues, it is necessary to examine the underlying morphological and structural changes of the respective tissues.Methods:The presented information on physiological adaptations have been deduced from cross-sectional studies comparing youth athletes with controls and children with adults as well as from longitudinal studies examining the effects of resistance training in untrained children and adolescents and in youth athletes.Results:The evidence indicates, that training induced changes in motor performance rely partly on enhanced neuromuscular control, and partly on morphological adaptation of muscles and tendons, such as changes in muscle, muscle fiber and tendon cross-sectional area, muscle composition, and tendon material properties, with the bone also adapting by increasing bone mineral content and cortical area.Conclusion:Although the training induced adaptations of the investigated tissues follows similar principles in children as in adults, the magnitude of the adaptive response appears to be more subtle. As studies investigating physiological adaptation in youth athletes are sparse, more research in this area is warranted to elucidate the specific physiological stimulus-response relationship necessary for effective training programs and injury prevention.

It is believed that hormonal changes during pregnancy lead to an increased compliance in ligaments and tendons, increasing the risk to suffer from connective tissue injuries particularly during exercise. While the laxity of the pelvic ligaments may increase to facilitate childbirth, to our knowledge no study has ever investigated the mechanical properties of human tendons in different stages of pregnancy. Thus, the purpose of our longitudinal study was to investigate the mechanical properties of the patellar tendon in different stages of pregnancy and postpartum. Nineteen pregnant women (30 ± 4 years) and 11 non-pregnant controls (28 ± 3 years) performed maximum isometric knee extension contractions on a dynamometer. Muscle strength and mechanical properties of the patellar tendon were determined integrating ultrasound, kinematic, and electromyographic measurements. In pregnant women, measurements were performed in the 16 ± 4th week of pregnancy (EP), the 29 ± 4th week of pregnancy (LP) and 32 ± 9th weeks postpartum (PP). On average, muscle strength as well as patellar tendon stiffness, force, and relative strain did not change during pregnancy and did not differ from non-pregnant controls. Tendon length measured at 90° knee flexion continuously increased during and after pregnancy (tendon length PP>EP; PP>controls). Our results indicate that patellar tendon stiffness is not universally affected by pregnancy. We found no evidence to support the often stated assumption that tendons would become more compliant during pregnancy. However, variability between individuals as well as the progressive increase in tendon rest length during and after pregnancy and its implications on injury risk need to be further examined.

The different methods used to assess patellar tendon elongation in vivo may partly explain the large variation of mechanical properties reported in the literature. The present study investigated the effects of tracking landmark position and tibial point of resistive force application during leg extensions in a dynamometer. Nineteen adults performed isometric contractions with a proximal and distal dynamometer shank pad position. Knee joint moments were calculated employing an inverse dynamics approach. Tendon elongation was measured using the patellar apex and either the tibial tuberosity (T) or plateau (P) as tracking landmark. Using P for tracking introduced a bias towards greater values of tendon elongation at all force levels from 100 N to maximum tendon force (TFmax; p

The black-and-white patterning of tendon fascicles when visualized by light microscopy, also known as crimp, is a well-known feature of fiber-forming collagens. However, not much is known about its development, function and response to strain. The objective of this study is to investigate the interaction of tenocyte and crimp morphology as well as their changes with increasing age and acute strain. In contrast to previous studies, which used indirect measures, such as polarized light, to investigate the crimp structure, this study visualizes internal crimp structure in three dimensions without freezing, sectioning, staining or fixing the tissue, via two-photon imaging of green fluorescent protein expressing cells within mouse tail tendon fascicles. This technique further allows straining of the live tissue while visualizing changes in crimp morphology and cell shape with increasing specimen length. Combining this novel microscopy technique with computational image and data analysis revealed a complex relationship between tenocytes and the extracellular matrix that evolves with increasing age. While the reduction of crimping with strain was observed as expected, most of the crimps were gone at 0–1% strain already. Even relatively low strains of 3% led to pronounced changes in the crimp structure after relaxation, particularly in the young animals, which could not be seen with bright-field imaging. Cell length and gap width increased with strain. However, while the cells were able to return to their original length even after high strains of 6%, the gaps between the cells widened, which may imply modified cell–cell communication after overstretching.

Tendinopathies are a range of diseases characterised by degeneration and chronic tendon pain and represent a significant cause of morbidity. Relatively little is known about the underlying mechanisms; however onset is often associated with physical activity. A number of molecular changes have been documented in tendinopathy such as a decrease in overall collagen content, increased extracellular matrix turnover and protease activity. Metalloproteinases are involved in the homeostasis of the extracellular matrix and expression is regulated by mechanical strain. The aims of this study were to determine the effects of strain upon matrix turnover by measuring metalloproteinase and matrix gene expression and to elucidate the mechanism of action. Primary Human Achilles tenocytes were seeded in type I rat tail collagen gels in a Flexcell™ tissue train system and subjected to 5% cyclic uniaxial strain at 1 Hz for 48 h. TGFβ1 and TGFβRI inhibitor were added to selected cultures. RNA was measured using qRT-PCR and TGFβ protein levels were determined using a cell based luciferase assay. We observed that mechanical strain regulated the mRNA levels of multiple protease and matrix genes anabolically, and this regulation mirrored that seen with TGFβ stimulation alone. We have also demonstrated that the inhibition of the TGFβ signalling pathway abrogated the strain induced changes in mRNA and that TGFβ activation, rather than gene expression, was increased with mechanical strain. We concluded that TGFβ activation plays an important role in mechanotransduction. Targeting this pathway may have its place in the treatment of tendinopathy., Highlights • Mechanical strain regulates multiple protease and matrix genes at the mRNA level. • Changes in mRNA level are analogous to those induced by TGFβ stimulation. • The inhibition of the TGFβ signalling pathway abrogated the strain-induced changes. • A SMAD activatory soluble factor is increased in activity in response to mechanical load.

Cyclic and static loading regimes are commonly used to study tenocyte metabolism in vitro and to improve our understanding of exercise-associated tendon pathologies. The aims of our study were to investigate if cyclic and static stress relaxation affected the mechanical properties of tendon fascicles differently, if this effect was reversible after a recovery period, and if the removal of glycosaminoglycans (GAGs) affected sample recovery. Tendon fascicles were dissected frombovine-foot extensors and subjected to 14% cyclic (1Hz) or static tensile strain for 30min. Additional fascicles were incubated overnight in buffer with 0.5U chondroitinase ABC or in buffer alone prior to the static stress-relaxation regime. To assess the effect of different stress-relaxation regimes, a quasi-static test to failure was carried out, either directly post loading or after a 2h recovery period, and compared with unloaded control fascicles. Both stress-relaxation regimes led to a significant reduction in fascicle failure stress and strain, but this was more pronounced in the cyclically loaded specimens. Removal of GAGs led to more stress relaxation and greater reductions in failure stress after static loading compared to controls. The reduction in mechanical properties was partially reversible in all samples, given a recovery period of 2h. This has implications for mechanical testing protocols, as a time delay between fatiguing specimens and characterization of mechanical properties will affect the results. GAGs appear to protect tendon fascicles from fatigue effects, possibly by enabling sample hydration.

Tendinopathies, chronic tendon disorders characterized by pain and functional impairment, are a common problem particularly in elite and recreational athletes. There is a high prevalence of Achilles tendinopathy in runners, while patellar tendinopathies, also referred to as jumpers knee, are very common amongst volleyball and basketball players. However, tendinopathies also occur in the sedentary population. The syndrome is associated with a variety of morphological, histopathological, biochemical and molecular changes, such as an increase in tendon cross sectional area, loss of fibre organization and infiltration of blood vessels. It has been shown that exercise or mechanical loading plays a role, which is why overuse is suspected to initiate tendinopathies. The exact mechanisms are still poorly understood, which makes the treatment problematic. A variety of treatment options are available, ranging from non-invasive procedures such as exercise treatment, topical nitroglycerin patches or shock wave therapy, over injections of various substances, such as corticosteroids, platelet-rich plasma or sclerosing agents, to surgical debridement. However, most of the treatment options focus solely on symptom relief, and the evidence for their effectiveness is often poor. The effectiveness of a treatment is furthermore likely to depend on the stage of the tendinapathy. In contrast to many therapies, exercise treatment has been relatively well investigated, has been shown to work in the majority of cases and is considered the gold standard.

Repetitive strain or 'overuse' is thought to be a major factor contributing to the development of tendinopathy. The aims of our study were to develop a novel cyclic loading system, and use it to investigate the effect of defined loading conditions on the mechanical properties and gene expression of isolated tendon fascicles. Tendon fascicles were dissected from bovine-foot extensors and subjected to cyclic tensile strain (1 Hz) at 30% or 60% of the strain at failure, for 0 h (control), 15 min, 30 min, 1 h, or 5 h. Post loading, a quasi-static test to failure assessed damage. Gene expression at a selected loading regime (1 h at 30% failure strain) was analyzed 6 h post loading by quantitative real-time polymerase chain reaction. Compared with unloaded controls, loading at 30% failure strain took 5 h to lead to a significant decrease in failure stress, whereas loading to 60% led to a significant reduction after 15 min. Loading for 1 h at 30% failure strain did not create significant structural damage, but increased Collagen-1-alpha-chain-1 and interleukin-6 (IL6) expression, suggesting a role of IL6 in tendon adaptation to exercise. Correlating failure properties with fatigue damage provides a method by which changes in gene expression can be associated with different degrees of fatigue damage.

Compared with muscle or bone, there is a lack of information about the relationship between tendon adaptation and the applied loading characteristic. The purpose of the present study was to analyze the effect of different exercise modes characterized by very distinct loading patterns on the mechanical, morphological, and biochemical properties of the Achilles tendon. Sixty-four female Sprague-Dawley rats were divided into five groups: nonactive age-matched control (AMC; n = 20), voluntary wheel running (RT; n = 20), vibration strength-trained (LVST; n = 12), high-vibration strength-trained (HVST; n = 6), and high strength-trained (HST; n = 6) group. After a 12-wk-long experimental period, the Achilles tendon was tested mechanically and the cross-sectional area, the soleus and gastrocnemius muscle mass, and mRNA concentration of collagen I, collagen III, tissue inhibitor of metalloproteinase-1 (TIMP-1), transforming growth factor-β, connective tissue growth factor, and matrix metalloproteinase-2 was determined. Neither in the LVST nor in the HVST group could any adaptation of the Achilles tendon be detected, although the training had an effect on the gastrocnemius muscle mass in the LVST group ( P < 0.05). In the HST group, the highest creep was found, but the effect was more pronounced compared with the LVST group ( P < 0.05) than with the AMC group. That indicates that this was rather induced by the low muscle mass rather than by training. However, the RT group had a higher TIMP-1 mRNA concentration in the Achilles tendon in contrast to AMC group ( P < 0.05), which suggests that this exercise mode may have an influence on tendon adaptation.

Most overuse tendinopathies are thought to be associated with repeated microstrain below the failure threshold, analogous to the fatigue failure that affects materials placed under repetitive loading. Investigating the progression of fatigue damage within tendons is therefore of critical importance. There are obvious challenges associated with the sourcing of human tendon samples for in vitro analysis so animal models are regularly adopted. However, data indicates that fatigue life varies significantly between tendons of different species and with different stresses in life. Positional tendons such as rat tail tendon or the bovine digital extensor are commonly applied in in vitro studies of tendon overuse, but there is no evidence to suggest their behaviour is indicative of the types of human tendon particularly prone to overuse injuries. In this study, the fatigue response of the largely positional digital extensor and the more energy storing deep digital flexor tendon of the bovine hoof were compared to the semitendinosus tendon of the human hamstring. Fascicles from each tendon type were subjected to either stress or strain controlled fatigue loading (cyclic creep or cyclic stress relaxation respectively). Gross fascicle mechanics were monitored after cyclic stress relaxation and the mean number of cycles to failure investigated with creep loading. Bovine extensor fascicles demonstrated the poorest fatigue response, while the energy storing human semitendinosus was the most fatigue resistant. Despite the superior fatigue response of the energy storing tendons, confocal imaging suggested a similar degree of damage in all three tendon types; it appears the more energy storing tendons are better able to withstand damage without detriment to mechanics.

Overuse tendinopathies are often considered to be the result of repeated microstrain below the failure threshold, analogous to the fatigue failure of materials under repeated loading [1, 2]. Investigation of tendon overuse in vitro is thus of potential benefit towards characterizing the progression of damage.

Objectives. Histological examination of pathological tendon generally does not reveal signs of inflammation. However, the inflammatory cytokine IL-6 has been shown to be expressed in ruptured rotator cuff tendon. The aim of this study was to investigate the expression of IL-6 family members in painful posterior tibialis tendon (PTT) and in painful and ruptured Achilles tendon (AT) compared with normal tendon. Methods. AT samples were obtained from cadavers (normal) or from patients undergoing surgical procedures to treat chronic painful tendinopathy or ruptured tendon. PTT samples were obtained from patients undergoing surgery for other reasons (normal) and from patients with PTT dysfunction (painful). Total RNA was extracted and mRNA expression was analysed by quantitative real-time PCR. Results. Collagen type I α-chain I (COL1A1) expression was increased in both painful PTT and AT compared with normal. Ciliary neurotrophic factor levels were increased in painful PTT only. In the painful AT, cyclooxygenase-2 (COX2) and IL-6 expression increased compared with normal. In the ruptured AT, levels of VEGF A, COX2, oncostatin-M, leukaemia inhibitory factor and IL-6 expression were higher compared with both normal and painful AT. IL-6R expression decreased in both painful and ruptured AT compared with normal. Conclusion. Painful AT and PTT show different expression patterns, indicating a substantial difference between those two tendinopathies. Inflammatory markers are up-regulated in painful and particularly in ruptured AT, pointing towards a role of inflammation not only in rupture healing, but also in Achilles tendinopathy.

Stress, strain and modulus are regularly used to characterize material properties of tissue samples. However, when comparing results from different studies it is evident the reported material properties, particularly failure strains, vary hugely. The aim of our study was to characterize how and why specimen length and cross-sectional area (CSA) appear to influence failure stress, strain and modulus in fascicles from two functionally different tendons. Fascicles were dissected from five rat tails and five bovine foot extensors, their diameters determined by a laser micrometer, and loaded to failure at a range of grip-to-grip lengths. Strain to failure significantly decreased with increasing in specimen length in both rat and bovine fascicles, while modulus increased. Specimen length did not influence failure stress in rat tail fascicles, although in bovine fascicles it was significantly lower in the longer 40mm specimens compared to 5 and 10mm specimens. The variations in failure strain and modulus with sample length could be predominantly explained by end-effects. However, it was also evident that strain fields along the sample length were highly variable and notably larger towards the ends of the sample than the mid-section even at distances in excess of 5mm from the gripping points. Failure strain, stress and modulus correlated significantly with CSA at certain specimen lengths. Our findings have implications for the mechanical testing of tendon tissue: while it is not always possible to control for fascicle length and/or CSA, these parameters have to be taken into account when comparing samples of different dimensions.

Background Tendon ruptures have been linked to anabolic steroid usage, suggesting pathological changes in tendon structure due to steroid intake. Anecdotal reports from athletes suggest a protective effect of GH on tendon, especially in those who use anabolic steroids. Aim To investigate how administration of insulin-like growth factor 1 (IGF-1), anabolic steroid and combination of the two affect the expression of genes involved in collagen metabolism. Methods Fascicles were harvested from bovine extensor tendons: n=4 to calculate optimal loading and n=8 to assess hormone plus optimal loading effect on eight genes involved in collagen metabolism. Total RNA was extracted and mRNA expression analysed by quantitative real-time reverse transcription-PCR, normalised to GAPDH and 18S ribosomal RNA±control (Con). Results Maximal collagen expression occurred at 6 h of light exercise, following 1 h of heavy loading. One tendon failed to have RNA extracted and was therefore removed from the study (n=7). IL-6 expression was significantly higher than control when exercised fascicles were exposed to: (1) anabolic steroid (normalised to: 18S; GAPDH; 18S & Con and GAPDH & Con); (2) IGF-1 (normalised to: GAPDH; 18S & Con and GAPDH & Con); (3) Dulbecco’s modified Eagle’s medium & PenStrep (normalised to: 18S & Con and GAPDH & Con) and (4) anabolic steroid & IGF-1 (normalised to: 18S & Con and GAPDH & Con). Conclusion The results of this study suggest that tendon is an IL-6 producing region during exercise which may also contribute to IL-6 increases in plasma during exercise.