A novel application of the principles of linear elastic fracture mechanics (LEFM) to the fatigue behavior of tendon tissue

BACKGROUND: Experiments on the fatigue of tendons have shown that cyclic loading induces failure at stresses lower than the ultimate tensile strength (UTS) of the tendons. The number of cycles to failure (Nf) has been shown to be dependent upon the magnitude of the applied cyclic stress. METHOD OF APPROACH: Utilizing data collected by Schechtman (1995), we demonstrate that the principles of Linear Elastic Fracture Mechanics (LEFM) can be used to predict the fatigue behavior of tendons under cyclic loading for maximum stress levels that are higher than 10% of the ultimate tensile strength (UTS) of the tendon (the experimental results at 10% UTS did not fit with our equations). CONCLUSIONS: LEFM and other FM approaches may prove to be very valuable in advancing our understanding of damage accumulation in soft connective tissues.     

Mechanical damage to the intervertebral disc annulus fibrosus subjected to tensile loading

Damage of the annulus fibrosus is implicated in common spinal pathologies. The objective of this study was to obtain a quantitative relationship between both the number of cycles and the magnitude of tensile strain resulting in damage to the annulus fibrosus. Four rectangular tensile specimens oriented in the circumferential direction were harvested from the outer annulus of 8 bovine caudal discs (n = 32) and subjected to one of four tensile testing protocols: (i) ultimate tensile strain (UTS) test; (ii) baseline cyclic test with 4 series of 400 cycles of baseline cyclic loading (peak strain = 20% UTS); (iii & iv) acute and fatigue damage cyclic tests consisting of 4 x 400 cycles of baseline cyclic loading with intermittent loading to 1 and 100 cycles, respectively, with peak tensile strain of 40%, 60%, and 80% UTS. Normalized peak stress for all mechanically loaded specimens was reduced from 0.89 to 0.11 of the baseline control levels, and depended on the magnitude of damaging strain and number of cycles at that damaging strain. Baseline, acute, and fatigue protocols resulted in permanent deformation of 3.5%, 6.7% and 9.6% elongation, respectively. Damage to the laminate structure of the annulus in the absence of biochemical activity in this study was assessed using histology, transmission electron microscopy, and biochemical measurements and was most likely a result of separation of annulus layers (i.e., delamination). Permanent elongation and stress reduction in the annulus may manifest in the motion segment as sub-catastrophic damage including increased neutral zone, disc bulging, and loss of nucleus pulposus pressure. The preparation of rectangular tensile strip specimens required cutting of collagen fibers and may influence absolute values of results, however, it is not expected to affect the comparisons between loading groups or dose-response reported.     

Biomechanical and structural response of healing Achilles tendon to fatigue loading following acute injury

Achilles tendon injuries affect both athletes and the general population, and their incidence is rising. In particular, the Achilles tendon is subject to dynamic loading at or near failure loads during activity, and fatigue induced damage is likely a contributing factor to ultimate tendon failure. Unfortunately, little is known about how injured Achilles tendons respond mechanically and structurally to fatigue loading during healing. Knowledge of these properties remains critical to best evaluate tendon damage induction and the ability of the tendon to maintain mechanical properties with repeated loading. Thus, this study investigated the mechanical and structural changes in healing mouse Achilles tendons during fatigue loading. Twenty four mice received bilateral full thickness, partial width excisional injuries to their Achilles tendons (IACUC approved) and twelve tendons from six uninjured mice were used as controls. Tendons were fatigue loaded to assess mechanical and structural properties simultaneously after 0, 1, 3, and 6 weeks of healing using an integrated polarized light system. Results showed that the number of cycles to failure decreased dramatically (37-fold, p<0.005) due to injury, but increased throughout healing, ultimately recovering after 6 weeks. The tangent stiffness, hysteresis, and dynamic modulus did not improve with healing (p<0.005). Linear regression analysis was used to determine relationships between mechanical and structural properties. Of tendon structural properties, the apparent birefringence was able to best predict dynamic modulus (R²=0.88–0.92) throughout healing and fatigue life. This study reinforces the concept that fatigue loading is a sensitive metric to assess tendon healing and demonstrates potential structural metrics to predict mechanical properties.     

Continuum damage mechanics (CDM) modelling demonstrates that ligament fatigue damage accumulates by different mechanisms than creep damage

Ligaments can be subjected to creep and fatigue damage when loaded to higher than normal stresses due to injury of a complementary joint restraint. Continuum damage mechanics (CDM) assumes that diffuse damage accumulates in a material, thereby reducing the effective cross-sectional area and leading to eventual rupture. The objective of this study was to apply CDM modelling to ligament creep and fatigue to reveal mechanisms of damage. Fatigue was modelled by cyclically varying the stress in the creep model. A few novel approaches were used. First, area reduction was not assumed equal to modulus reduction; thus, allowing damaged fibres to potentially contribute to load-bearing through the extracellular matrix. Modulus ratio was related to area reduction using residual strength. Second, damage rate was not assumed constant but rather was determined directly from the modulus ratio change with respect to time. Third, modulus ratio was normalized to maximum modulus to avoid artificial calculation of negative damage. With this approach, the creep time-to-rupture was predicted with -4% error at 60% UTS and -13% error at 30% UTS. At 15% UTS, no test was undertaken experimentally for a duration as long as the 24 days predicted theoretically. Oscillating the time-dependent damage in the creep model could not completely explain the fatigue behaviour because the fatigue time-to-rupture was predicted with over 1300% error at all stresses. These results suggest that a cycle-dependent damage mechanism, in addition to a time-dependent one, was responsible for fatigue rupture. Cycle-dependent damage may be an important consideration for rehabilitation activities following injury of a complementary ligament restraint.     

Mechanical characteristics of biological soft tissue]

In a detailed study mechanical properties of tendons, muscles, nerves, blood-vessels and skin of just slaughtered pigs have been investigated in nearly stationary stress tests. Tensile tests have produced tensile strength, ultimate stress and their appropriate strains, Young's modulus and the work up to fatigue of samples. In hysteresis tests the deformation work has been determined as a function of numbers of stress cycles. The hysteresis decrease with the number of stress cycles and approaches asymptotically to cero. By preconditioning of tendons, nerves and blood-vessels to steady state significant differences of strain at tensile strength and of Young's modulus have been established. Moreover for nerves the tests have revealed significant deviations of tensile strength. Bruise tests have been carried out with muscle tissue. For the described setup the limit force can be specified, at which pathological changes appear. Subsequently conducted histological investigations have demonstrated this. In dynamical bruise tests there appeared no pathological changes in muscle tissue in spite of higher transmitted energy.     

The effect of cement creep and cement fatigue damage on the micromechanics of the cement–bone interface

The cement–bone interface provides fixation for the cement mantle within the bone. The cement–bone interface is affected by fatigue loading in terms of fatigue damage or microcracks and creep, both mostly in the cement. This study investigates how fatigue damage and cement creep separately affect the mechanical response of the cement–bone interface at various load levels in terms of plastic displacement and crack formation. Two FEA models were created, which were based on micro-computed tomography data of two physical cement–bone interface specimens. These models were subjected to tensile fatigue loads with four different magnitudes. Three deformation modes of the cement were considered: ‘only creep’, ‘only damage’ or ‘creep and damage’. The interfacial plastic deformation, the crack reduction as a result of creep and the interfacial stresses in the bone were monitored. The results demonstrate that, although some models failed early, the majority of plastic displacement was caused by fatigue damage, rather than cement creep. However, cement creep does decrease the crack formation in the cement up to 20%. Finally, while cement creep hardly influences the stress levels in the bone, fatigue damage of the cement considerably increases the stress levels in the bone. We conclude that at low load levels the plastic displacement is mainly caused by creep. At moderate to high load levels, however, the plastic displacement is dominated by fatigue damage and is hardly affected by creep, although creep reduced the number of cracks in moderate to high load region.     

Early response to tendon fatigue damage accumulation in a novel in vivo model

This study describes the development and application of a novel rat patellar tendon model of mechanical fatigue for investigating the early in vivo response to tendon subfailure injury. Patellar tendons of adult female Sprague-Dawley rats were fatigue loaded between 1–35 N using a custom-designed loading apparatus. Patellar tendons were subjected to Low-, Moderate- or High-level fatigue damage, defined by grip-to-grip strain measurement. Molecular response was compared with that of a laceration-repair injury. Histological analyses showed that progression of tendon fatigue involves formation of localized kinked fiber deformations at Low damage, which increased in density with presence of fiber delaminations at Moderate damage, and fiber angulation and discontinuities at High damage levels. RT-PCR analysis performed at 1- and 3-day post-fatigue showed variable changes in type I, III and V collagen mRNA expression at Low and Moderate damage levels, consistent with clinical findings of tendon pathology and were modest compared with those observed at High damage levels, in which expression of all collagens evaluated were increased markedly. In contrast, only type I collagen expression was elevated at the same time points post-laceration. Findings suggest that cumulative fatigue in tendon invokes a different molecular response than laceration. Further, structural repair may not be initiated until reaching end-stage fatigue life, where the repair response may unable to restore the damaged tendon to its pre-fatigue architecture.     

The dynamics of collagen uncrimping and lateral contraction in tendon and the effect of ionic concentration

Under tensile loading, tendon undergoes a number of unique structural changes that govern its mechanical response. For example, stretching a tendon is known to induce both the progressive “uncrimping” of wavy collagen fibrils and extensive lateral contraction mediated by fluid flow out of the tissue. However, it is not known whether these processes are interdependent. Moreover, the rate-dependence of collagen uncrimping and its contribution to tendon's viscoelastic mechanical properties are unknown. Therefore, the objective of this study was to (a) develop a methodology allowing for simultaneous measurement of crimp, stress, axial strain and lateral contraction in tendon under dynamic loading; (b) determine the interdependence of collagen uncrimping and lateral contraction by testing tendons in different swelling conditions; and (c) assess how the process of collagen uncrimping depends on loading rate. Murine flexor carpi ulnaris (FCU) tendons in varying ionic environments were dynamically stretched to a set strain level and imaged through a plane polariscope with the polarizer and analyzer at a fixed angle. Analysis of the resulting images allowed for direct measurement of the crimp frequency and indirect measurement of the tendon thickness. Our findings demonstrate that collagen uncrimping and lateral contraction can occur independently and interstitial fluid impacts tendon mechanics directly. Furthermore, tensile stress, transverse contraction and degree of collagen uncrimping were all rate-dependent, suggesting that collagen uncrimping plays a role in tendon's dynamic mechanical response. This study is the first to characterize the time-dependence of collagen uncrimping in tendon, and establishes structure–function relationships for healthy tendons that can be used to better understand and assess changes in tendon mechanics after disease or injury.     

Isolated fibrillar damage in tendons stimulates local collagenase mRNA expression and protein synthesis

The etiology of repetitive stress injuries in tendons has not been clearly identified. While minor trauma has been implicated as an inciting factor, the precise magnitude and structural level of tissue injury that initiates this degenerative cascade has not been determined. The purpose of this study was to determine if isolated tendon fibril damage could initiate an upregulation of interstitial collagenase (MMP13) mRNA and protein in tendon cells associated with the injured fibril(s). Rat tail tendon fascicles were subjected to in vitro tensile loading until isolated fibrillar damage was documented. Once fibrillar damage occurred, the tendons were immediately unloaded to 100g and maintained at that displacement for 24h under tissue culture conditions. In addition, non-injured tendon fascicles were maintained under unloaded (stress-deprived) conditions in culture for 24h to act as positive controls. In situ hybridization or immunohistochemistry was then performed to localize collagenase mRNA expression or protein synthesis, respectively. Fibrillar damage occurred at a similar stress (41.13+/-5.94MPa) and strain (13.24+/-1.94%) in the experimental tendons. In situ hybridization and immunohistochemistry demonstrated an upregulation of interstitial collagenase mRNA and protein, respectively, in only those cells associated with the damaged fibril(s). In the control (stress-deprived) specimens, collagenase mRNA expression and protein synthesis were observed throughout the fascicle. The results suggest that isolated fibrillar damage and the resultant upregulation of collagenase mRNA and protein in this damaged area occurs through a mechanobiological understimulation of tendon cells. This collagenase production may weaken the tendon and put more of the extracellular matrix at risk for further damage during subsequent loading.     

Mechanical effects of load speed on the human colon

The aim of this study was to examine the mechanical behavior of the colon using tensile tests under different loading speeds.Specimens were taken from different locations of the colonic frame from refrigerated cadavers. The specimens were submitted to uniaxial tensile tests after preconditioning using a dynamic load (1 m/s), intermediate load (10 cm/s), and quasi-static load (1 cm/s).A total of 336 specimens taken from 28 colons were tested. The stress-strain analysis for longitudinal specimens indicated a Young’s modulus of 3.17 ± 2.05 MPa under dynamic loading (1 m/s), 1.74 ± 1.15 MPa under intermediate loading (10 cm/s), and 1.76 ± 1.21 MPa under quasi-static loading (1 cm/s) with p < 0.001. For the circumferential specimen, the stress-strain curves indicated a Young’s modulus of 3.15 ± 1.73 MPa under dynamic loading (1 m/s), 2.14 ± 1.3 MPa under intermediate loading (10 cm/s), and 0.63 ± 1.25 MPa under quasi-static loading (1 cm/s) with p < 0.001. The curves reveal two types of behaviors of the colon: fast break behavior at high speed traction (1 m/s) and a lower break behavior for lower speeds (10 cm/s and 1 cm/s). The circumferential orientation required greater levels of stress and strain to obtain lesions than the longitudinal orientation. The presence of taeniae coli changed the mechanical response during low-speed loading.Colonic mechanical behavior varies with loading speeds with two different types of mechanical behavior: more fragile behavior under dynamic load and more elastic behavior for quasi-static load.     

True stress and Poisson's ratio of tendons during loading

Excessive axial tension is very likely involved in the aetiology of tendon lesions, and the most appropriate indicator of tendon stress state is the true stress, the ratio of instantaneous load to instantaneous cross-sectional area (CSA). Difficulties to measure tendon CSA during tension often led to approximate true stress by assuming that CSA is constant during loading (i.e. by the engineering stress) or that tendon is incompressible, implying a Poisson's ratio of 0.5, although these hypotheses have never been tested. The objective of this study was to measure tendon CSA variation during quasi-static tensile loading, in order to assess the true stress to which the tendon is subjected and its Poisson's ratio. Eight equine superficial digital flexor tendons (SDFT, about 30cm long) were tested in tension until failure while the CSA of each tendon was measured in its metacarpal part by means of a linear laser scanner. Axial elongation and load were synchronously recorded during the test. CSA was found to linearly decrease with strain, with a mean decrease at failure of -10.7±2.8% (mean±standard deviation). True stress at failure was 7.1-13.6% higher than engineering stress, while stress estimation under the hypothesis of incompressibility differed from true stress of -6.6 to 2.3%. Average Poisson's ratio was 0.55±0.12 and did not significantly vary with load. From these results on equine SDFT it was demonstrated that tendon in axial quasi-static tension can be considered, at first approximation, as an incompressible material.     

Collagen fibril diameter distribution does not reflect changes in the mechanical properties of in vitro stress-deprived tendons

The purpose of this study was to determine if an association exists between the tensile properties and the collagen fibril diameter distribution in in vitro stress-deprived rat tail tendons. Rat tail tendons were paired into two groups of 21 day stress-deprived and 0 time controls and compared using transmission electron microscopy (n = 6) to measure collagen fibril diameter distribution and density, and mechanical testing (n =6) to determine ultimate stress and tensile modulus. There was a statistically significant decrease in both ultimate tensile strength (control: 17.95+/-3.99 MPa, stress-deprived: 6.79+/-3.91 MPa) and tensile modulus (control: 312.8+/-89.5 MPa, stress-deprived: 176.0+/-52.7 MPa) in the in vitro stress-deprived tendons compared to controls. However, there was no significant difference between control and stress-deprived tendons in the number of fibrils per tendon counted, mean fibril diameter, mean fibril density, or fibril size distribution. The results of this study demonstrate that the decrease in mechanical properties observed in in vitro stress-deprived rat tail tendons is not correlated with the collagen fibril diameter distribution and, therefore, the collagen fibril diameter distribution does not, by itself, dictate the decrease in mechanical properties observed in in vitro stress-deprived rat tail tendons.     

An experimental and numerical study on the transverse deformations in tensile test of tendons

The transverse deformations of tendons assessed in tensile tests seems to constitute a controversial issue in literature. On the one hand, large positive variations of the Poisson’s ratio have been reported, indicating volume reduction under tensile states. On the other hand, negative values were also observed, pointing out an auxetic material response. Based on these experimental observations, the following question is raised: Are these large and discrepant transverse deformations intrinsically related to the constitutive response of tendons or they result from artifacts of the mechanical test setup? In order to provide further insights to this question, an experimental and numerical study on the transverse kinematics of tendons was carried out. Tensile experiments were performed in branches of deep digital flexor tendons of domestic porcine, where the transverse displacements were measured by two high-speed, high-accuracy optical digital micrometers placed transversely to one another. Aiming at a better understanding of the effects of the mechanical test setup in the transverse measurements, a three-dimensional finite element model is proposed to resemble the tensile experiment. The main achieved results strongly support the following hypotheses regarding tensile tests of tendons: the clamping region considerably affects the kinematics of the specimen even at a large distance from the clamps; the transverse deformations are mainly ruled by stiff fibers embedded in a soft matrix; the generalization of the Poisson’s ratio to draw conclusions about changes in volume of tendons may lead to misinterpretations.     

Effects of elastase on the mechanical and failure properties of engineered elastin-rich matrices.

Pulmonary emphysema and vessel wall aneurysms are diseases characterized by elastolytic damage to elastin fibers that leads to mechanical failure. To model this, neonatal rat aortic smooth muscle cells were cultured, accumulating an extracellular matrix rich in elastin, and mechanical measurements were made before and during enzymatic digestion of elastin. Specifically, the cells in the cultures were killed with sodium azide, the cultures were lifted from the flask, cut into small strips, and fixed to a computer-controlled lever arm and a force transducer. The strips were subjected to a broadband displacement signal to study the dynamic mechanical properties of the samples. Also, quasi-static stress-strain curves were measured. The dynamic data were fit to a linear viscoelastic model to estimate the tissues' loss (G) and storage (H) modulus coefficients, which were evaluated before and during 30 min of elastase treatment, at which point a failure test was performed. G and H decreased significantly to 30% of their baseline values after 30 min. The failure stress of control samples was approximately 15 times higher than that of the digested samples. Understanding the structure-function relationship of elastin networks and the effects of elastolytic injury on their mechanical properties can lead to the elucidation of the mechanism of elastin fiber failure and evaluation of possible treatments to enhance repair in diseases involving elastolytic injury.     

The implications of the adaptable fatigue quality of tendons for their construction,repair and function

Different tendons are (i) subject to very different stresses from their muscles and (ii) differ in their susceptibility to fatigue damage. The fatigue quality of each tendon is matched to the stress it experiences, so that, in life, all tendons are similarly prone to damage. On-going damage must be routinely repaired to maintain homeostasis and prevent damage from becoming symptomatic. The discovery of major differences in fatigue quality among tendons, which had previously seemed fairly similar in their mechanical properties, raises a wide range of new questions. (A) What structural and chemical differences underlie the variations in fatigue quality? (B) What molecular structure in the tendon is damaged and how is repair organised? (C) Is fatigue quality adaptable and if so what is the trigger for adaptation? Putting these questions into context leads to an integrated review of tendon, including structure and chemistry, the turnover of proteins, the cross-linking of collagen and the response of tenocytes to load on the tendon.     

Zonal and directional variations in tensile properties of bovine articular cartilage with special reference to strain rate variation

THE AIMS of this study were: (i) to investigate the variation in the tensile properties of articular cartilage with depth through cartilage thickness and fibre orientation; (ii) to determine the effect of strain rate on tensile properties of articular cartilage. MATERIALS AND METHOD: All experimental work was performed on cartilage specimens taken from two bovine knee joints. Osteochondral plugs 12 mm in diameter were harvested with a special reamer from the femur and the tibial plateaux of each knee. Slices (0.2 mm thick), of articular cartilage were cut from the plug with a microtome. The predominant orientation of the collagen fibres on the cartilage surface was determined using the pinpricking technique. Each specimen used for the tensile test was cut, so as to produce a dumbbell shape, with a gauge length of 6 mm. Uniaxial tensile tests were performed on each specimen in order to determine the tensile Young's modulus, and ultimate tensile strength (UTS). In this investigation, these tensile tests were carried out at different strain rate: 1, 20, 50 and 70%/sec. RESULTS: As regards the zonal properties, it was found that tensile stiffness was greater in the superficial layer than in deep layer. However, a few specimens from the deep layer displayed similar or greater stiffness compared to the superficial layer. With respect to the directional properties, the specimens oriented parallel to the predominant alignment of collagen, were stiffer than those, which were perpendicular to it in each layer. However, only the results regarding the deep layer can be considered statistically significant. In regard to the variation of modulus with the strain-rate, the results showed that there is no significant increase of the modulus with increasing strain rate from 20 to 50% per second. However, at 70% per second, articular cartilage stiffness considerably increased by up to one order of magnitude greater than that determined at lower strain rates in both the superficial and deep layer. Moreover, the UTS of cartilage specimens tested at 70% per second showed a significant rise, reaching values of four to five times that of those measured at 1, 20 or 50% per second. CONCLUSION: The steep increases in both the stiffness and ultimate tensile strength of cartilage at high strain rates point to the existence in cartilage of a mechanism for its protection from damage by stresses arising in trauma, which are usually applied at high rates. This mechanism needs to be elucidated. The reduced anisotropy found in the present study pointed out that collagen is likely to be less organized in bovine cartilage than in the human and therefore, a study of its ultra-structure would be appropriate.     

The relationships between cyclic fatigue loading, changes in initial mechanical properties, and the in vivo temporal mechanical response of the rat patellar tendon

Damage accumulation underlies tendinopathy. Animal models of overuse injuries do not typically control loads applied to the tendon. Our in vivo model in the rat patellar tendon allows direct control of the loading applied to the tendon. Despite this advantage, natural variation among tendons results in different amounts of damage induced by the same loading protocol. Our objectives were to (1) assess changes in the initial mechanical parameters (hysteresis, stiffness of the loading and unloading load-displacement curves, and elongation) after fatigue loading to identify parameters that are indicative of the induced damage, and (2) evaluate the relationships between these identified initial damage indices with the stiffness 7 day after loading. Left patellar tendons of adult, female retired breeder, Sprague-Dawley rats (n = 68) were fatigue loaded per our previously published in vivo fatigue loading protocol. To induce a range of damage, fatigue loading consisted of either 5, 100, 500 or 7200 cycles that ranged from 1 N to 40 N. Diagnostic tests were applied before and immediately after fatigue loading, and after 45 min of recovery to deduce recoverable and non-recoverable changes in initial damage indices. Relationships between these initial damage indices and the 7-day stiffness (at sacrifice) were determined. Day-0 hysteresis, loading and unloading stiffness exhibited cycle-dependent changes. Initial hysteresis loss correlated with the 7-day stiffness. k-means cluster analysis demonstrated a relationship between 7-day stiffness and day-0 hysteresis and unloading stiffness. This analysis also separated samples that exhibited low from high damage in response to both high or low number of cycles; a key delineation for interpretation of the biological response in future studies. Identifying initial parameters that reflect the induced damage is critical since the ability of the tendon to repair depends on the damage induced and the number of applied loading cycles.     

Mechanical properties of collagen fascicles from the rabbit patellar tendon

Tensile and viscoelastic properties of collagen fascicles of approximately 300 microns in diameter, which were obtained from rabbit patellar tendons, were studied using a newly designed micro-tensile tester. Their cross-sectional areas were determined with a video dimension analyzer combined with a CCD camera and a low magnification microscope. There were no statistically significant differences in tensile properties among the fascicles obtained from six medial-to-lateral locations of the patellar tendon. Tangent modulus, tensile strength, and strain at failure of the fascicles determined at about 1.5 percent/s strain rate were 216 +/- 68 MPa, 17.2 +/- 4.1 MPa, and 10.9 +/- 1.6 percent (mean +/- S.D.), respectively. These properties were much different from those of bulk patellar tendons; for example, the tensile strength and strain at failure of these fascicles were 42 percent and 179 percent of those of bulk tendons, respectively. Tangent modulus and tensile strength of collagen fascicles determined at 1 percent/s strain rate were 35 percent larger than those at 0.01 percent/s. The strain at failure was independent of strain rate. Relaxation tests showed that the reduction of stress was approximately 25 percent at 300 seconds. These stress relaxation behavior and strain rate effects of collagen fascicles differed greatly from those of bulk tendons. The differences in tensile and viscoelastic properties between fascicles and bulk tendons may be attributable to ground substances, mechanical interaction between fascicles, and the difference of crimp structure of collagen fibrils.     

Repetitive static muscle contractions in humans —a trigger of metabolic and oxidative stress?

Repetitive static exercise (RSE) is a repetitive condition of partial ischaemia/reperfusion and may therefore be connected to the formation of oxygen-derived free radicals and tissue damage. Seven subjects performed two-legged intermittent knee extension exercise repeating at 10 s on and 10 s off at a target force corresponding to about 30% of the maximal voluntary contraction force. The RSE was continued for 80 min (n = 4) or to fatigue (n = 3). Four of the subjects also performed submaximal dynamic exercise (DE) at an intensity of about 60% maximal oxygen uptake (VO2max) for the same period. Whole body oxygen uptake (VO2) increased gradually with time during RSE (P less than 0.05), indicating a decreased mechanical efficiency. This was further supported by a slow increase in leg blood flow (P less than 0.05) and leg oxygen utilization (n.s.) during RSE. In contrast, prolonged RSE had no effect on VO2 during submaximal cycling. Maximal force (measured in six additional subjects) declined gradually during RSE and was not completely restored after 60 min of recovery. After 20 and 80 min (or at fatigue) RSE phosphocreatine (PC) dropped to 74% and 60% of the initial value, respectively. A similar decrease in PC occurred during DE. Muscle and arterial lactate concentrations remained low during both RSE and DE. The three subjects who were unable to continue RSE for 80 min showed no signs of a more severe energy imbalance than the other subjects. A continuous release of K+ occurred during both RSE and DE.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of a hydrogel-fiber composite for ACL tissue engineering

The anterior cruciate ligament (ACL) is necessary for normal knee stability and movement. Unfortunately the ACL is also the most frequently injured ligament of the knee with severe disruptions requiring surgical intervention. In response to this, tissue engineering has emerged as an option for ACL replacement and repair. In this study we present a novel hydrogel-fibrous scaffold as a potential option for ACL replacement. The scaffold was composed of PLLA fibers, in a previously evaluated braid-twist structure, combined with a polyethylene glycol diacrylate (PEGDA) hydrogel to improve viscoelastic properties. Both hydrogel concentration (10%, 15%, and 20%) and amount of hydrogel (soaking the fibrous scaffold in hydrogel solution or encasing the scaffold in a block of hydrogel) were evaluated. It was found that the braid-twist scaffold had a greater porosity and larger number of pores above 100 μm than braided scaffolds with the same braiding angle. After testing for their effects on swelling, fiber degradation, and protein release, as well as viscoelastic and tensile testing (when combined with fibrous scaffolds), it was found that the composite scaffold soaked in 10% hydrogel had the best chemical release and mechanical properties. The optimized structure behaved similarly to natural ligament in tension with the addition of the hydrogel decreasing the ultimate tensile stress (UTS), but the UTS was still comparable to natural ACL. In addition, cellular studies showed that the hydrogel-PLLA fiber composite supported fibroblast growth.