Altered Triceps Surae Muscle-Tendon Unit Properties after 6 Months of Static Stretching.

INTRODUCTION: This study examined the effects of 24 wk of daily static stretching of the plantarflexors (unilateral 4 × 60-s stretching, whereas the contralateral leg served as a control; n = 26) on joint range of motion (ROM), muscle-tendon unit morphological and mechanical properties, neural activation, and contractile function. METHODS: Torque-angle/velocity was obtained in passive and active conditions using isokinetic dynamometry, whereas muscle-tendon morphology and mechanical properties were examined using ultrasonography. RESULTS: After the intervention, ROM increased (stretching, +11° ± 7°; control, 4° ± 8°), and passive torque (stretching, -10 ± 11 N·m; control, -7 ± 10 N·m) and normalized EMG amplitude (stretching, -3% ± 6%; control, -3% ± 4%) at a standardized dorsiflexion angle decreased. Increases were seen in passive tendon elongation at a standardized force (stretching, +1.3 ± 1.6 mm; control, +1.4 ± 2.1 mm) and in maximal passive muscle and tendon elongation. Angle of peak torque shifted toward dorsiflexion. No changes were seen in tendon stiffness, resting tendon length, or gastrocnemius medialis fascicle length. Conformable changes in ROM, passive dorsiflexion variables, tendon elongation, and angle of peak torque were observed in the nonstretched leg. CONCLUSIONS: The present findings indicate that habitual stretching increases ROM and decreases passive torque, altering muscle-tendon behavior with the potential to modify contractile function.

An advanced glycation endproduct (AGE)-rich diet promotes accumulation of AGEs in Achilles tendon.

Advanced Glycation Endproducts (AGEs) accumulate in long-lived tissue proteins like collagen in bone and tendon causing modification of the biomechanical properties. This has been hypothesized to raise the risk of orthopedic injury such as bone fractures and tendon ruptures. We evaluated the relationship between AGE content in the diet and accumulation of AGEs in weight-bearing animal Achilles tendon. Two groups of mice (C57BL/6Ntac) were fed with either high-fat diet low in AGEs high-fat diet (HFD) (n = 14) or normal diet high in AGEs (ND) (n = 11). AGE content in ND was six to 50-fold higher than HFD The mice were sacrificed at week 40 and Achilles and tail tendons were carefully excised to compare weight and nonweight-bearing tendons. The amount of the AGEs carboxymethyllysine (CML), methylglyoxal-derived hydroimidazolone (MG-H1) and carboxyethyllysine (CEL) in Achilles and tail tendon was measured using ultraperformance liquid chromatography tandem mass spectrometry (UPLC-MS/MS) and pentosidine with high-pressure liquid chromatography (HPLC) with fluorescent detection. AGEs in Achilles tendon were higher than in tail tendon for CML (P < 0.0001), CEL (P < 0.0001), MG-H1 and pentosidine (for both ND and HFD) (P < 0.0001). The AGE-rich diet (ND) resulted in an increase in CML (P < 0.0001), MG-H1 (P < 0.001) and pentosidine (P < 0.0001) but not CEL, in Achilles and tail tendon. This is the first study to provide evidence for AGE accumulation in injury-prone, weight-bearing Achilles tendon associated with intake of an AGE-rich diet. This indicates that food-derived AGEs may alter tendon properties and the development of tendon injuries.

Tensile force transmission in human patellar tendon fascicles is not mediated by glycosaminoglycans.

Correct mechanical function of tendons is essential to human physiology and therefore the mechanical properties of tendon have been a subject of research for many decades now. However, one of the most fundamental questions remains unanswered: How is load transmitted through the tendon? It has been suggested that the proteoglycan-associated glycosaminoglycans (GAGs) found on the surface of the collagen fibrils may be an important transmitter of load, but existing results are ambiguous and have not investigated human tendons. We have used a small-scale mechanical testing system to measure the mechanical properties of fascicles from human patellar tendon at two different deformation rates before and after removal of GAGs by treatment with chondroitinase ABC. Efficiency of enzyme treatment was quantified using dimethylmethylene blue assay. Removal of at least 79% of the GAGs did not significantly change the tendon modulus, relative energy dissipation, peak stress, or peak strain. The effect of deformation rate was not modulated by the treatment either, indicating no effect on viscosity. These results suggest that GAGs cannot be considered mediators of tensile force transmission in the human patellar tendon, and as such, force transmission must either take place through other matrix components or the fibrils must be mechanically continuous at least to the tested length of 7 mm.