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How physical exercise changes rat myotendinous junctions: an ultrastructural study

TLDR
It was demonstrated that the myotendinous junctions is able to adapt to an increase in tensile force by enlarging the muscle-tendon contact area and, consequently, mechanical resistance.
Abstract
Myotendinous junctions can be easily injured by overloading or trauma, and exercise training may be a way of increasing their resistance to mechanical stress. To this end, we examined herein the morphological changes induced by moderate exercise training in the myotendinous junctions of extensor digitorum longus and gastrocnemius muscles in rats. Twelve Sprague-Dawley rats were used in this investigation. Six of them were trained to run on a treadmill for 1 h/day, 3 days/week over 10 weeks in order for them to achieve a running rate of 25 m/min at the end of the training period. Six age-matched sedentary rats were used as controls. The rats were sacrificed 24 h after the final training session, and the extensor digitorum longum (EDL) and the gastrocnemium were excised; the myotendinous junctions (MTJ) were then prepared and observed with electron microscopy. Digitation branching was evaluated by counting the bifurcations in the MTJ protrusions. Our observations indicate that exercise does indeed induce changes in MTJ morphology. In both muscles the number of bifurcated interdigitations increased significantly, as well as, in gastrocnemius, the branching of the finger-like processes. It was demonstrated that the MTJ is able to adapt to an increase in tensile force by enlarging the muscle-tendon contact area and, consequently, mechanical resistance.

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Mechanisms of acute adductor longus injuries in male football players: a systematic visual video analysis

TL;DR: A rapid muscle activation during a rapid muscle lengthening appears to be the fundamental injury mechanism for acute adductor longus injuries in football.
Journal ArticleDOI

The human myotendinous junction: An ultrastructural and 3D analysis study

TL;DR: The 3D reconstruction revealed that tendon made ridge‐like protrusions, which interdigitiated with groove‐like indentations in the muscle cell, which revealed the ultrastructure of the human MTJ and render 3D reconstructions.
Journal ArticleDOI

Remodeling of muscle fibers approaching the human myotendinous junction.

TL;DR: The immunohistochemical findings suggest that the rate of remodeling of muscle fibers near the MTJ is very high, and the finding that there was no increased number of satellite cells and fibroblasts could be explained as a dynamic phenomenon.
Journal ArticleDOI

Skeletal muscle features in myotonic dystrophy and sarcopenia: do similar nuclear mechanisms lead to skeletal muscle wasting?

TL;DR: Interestingly, the accumulation of pre-mRNA processing factors in the myonuclei of DM1 and DM2 patients is reminiscent of the nuclear alterations typical of sarcopenia, i.e., the loss of muscle mass and function which physiologically occurs during ageing.
Journal ArticleDOI

Growth hormone plus resistance exercise attenuate structural changes in rat myotendinous junctions resulting from chronic unloading.

TL;DR: Findings indicate that the interaction between exercise and GH treatments attenuates the changes in MTJ structure that result from chronic unloading and thus can be used as a countermeasure to these adaptations.
References
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Journal ArticleDOI

Absence of integrin alpha 7 causes a novel form of muscular dystrophy.

TL;DR: Findings demonstrate that αβ1 integrin represents an indispensable linkage between the muscle fibre and the extracellular matrix that is independent of the dystrophin–dystroglycan complex–mediated interaction of the cytoskeleton with the muscle basement membrane.
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Mutations in the integrin alpha7 gene cause congenital myopathy.

TL;DR: The results demonstrate that mutations in ITGA7 are involved in a form of congenital myopathy, and α7 protein expression in muscle biopsies from 117 patients with unclassified congenitals myopathy and congenital muscular dystrophy is determined by immunocytochemistry.
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C2C12 murine myoblasts as a model of skeletal muscle development: morpho-functional characterization.

TL;DR: The differentiation of C2C12 cells, a primary line of murine myoblasts, was investigated by a multiple technical approach, and M-cadherin, an adhesion molecule characteristic of satellite cells, also seems to be involved in their assembling.
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β1 Integrins Regulate Myoblast Fusion and Sarcomere Assembly

TL;DR: It is shown that extracellular matrix (ECM) receptors of the beta1 integrin family regulate myoblast fusion, providing evidence that different ECM receptors have nonredundant functions in skeletal muscle fibers.
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