How physical exercise changes rat myotendinous junctions: an ultrastructural study

Abstract

Myotendinous junctions (MTJ) 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 MTJ of extensor digitorum longus (EDL) 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 EDL and the gastrocnemium were excised; the 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.

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

“…In addition, it is thought that the meshwork formed by the branching and subsequent joining of the processes is important for regulating tension. 8,41 …”

“…A moderate treadmill-running regimen applied to rats increased the percentage of the branched tendon interdigitations at the MTJ and the number of bifurcations of the digit-like processes. 8 …”

Histochemistry as an irreplaceable approach for investigating functional cytology and histology

“…66-72 Here too, the unusual localization or translocation of specific proteins was considered as an important evidence, 72 all the more so as it occurs under pathological conditions ( e.g ., in myotonic dystrophy) or in sarcopenia, i.e ., the loss of muscle mass and function physiologically occurring in the aging process. 67,76,77 As demonstrated by ultrastructural immunocytochemistry, the dystrophic phenotype would depend on a general alteration in the post-transcriptional maturation of pre-mRNAs. Interestingly, the accumulation of pre-mRNA processing factors in the myonuclei of dystrophic patients is reminiscent of the nuclear alterations found in age-related sarcopenia.…”

“…The effect of physical exercise on the structural features of skeletal muscle cells (both myocytes and satellite cells) has repeatedly been investigated, 75,76 but so far much less attention has been paid to the consequence of exercise on the myotendineous junction: 77,78 Molecular and ultrastructural analyses demonstrated that the myotendineous junction is able to adapt to increased tensile forces by enlarging the muscle-tendon contact area, thus increasing mechanical resistance.…”

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

“…The mechanisms underlying age-related skeletal muscle wasting and weakness are probably manifold and still remain to be fully elucidated; 30 however, although no specific therapy is presently available to counteract its onset or progress, studies performed on humans and other mammals have stressed the importance of physical exercise as an effective, although still debated, approach to prevent or limit the age-related muscle mass loss. 32–36 …”