Background: In rehabilitation, immobilization of skeletal muscles in the elongated position is performed as a countermeasure in order to reverse the effects of severe muscle shortening and postoperative events. The return to normal functional activities is believed to stimulate mechanotransducers capable of reorganizing the normal muscle cytoarchitecture, but few data describing the histopathological changes relating to these procedures are available in the literature.
Objectives: To assess and quantify histological abnormalities induced by immobilization of the extensor digitorum longus (EDL) muscle in elongation and to compare them with free movement of the animal after this procedure.
Methods: Eighteen female Wistar rats were used, divided into the following groups: Control; Immobilized in plantar flexion (EDL in an elongated position) for 14 days (GI); Immobilized for 14 days and released for 10 days (GIL). EDL fragments were frozen, sectioned and processed through immunohistochemical reactions for collagens I and III and histochemical methods for myofibrillar adenosine triphosphatase using hematoxylin-eosin.
Results: GI animals presented slight increases in collagen I and fiber expression in a degenerative/necrotic process, and reductions in the proportion of FT2A fibers and in the diameters of all fiber types, compared with the controls. In GIL, the quantity of collagen I returned to control conditions; the proportion of FT2D decreased; the number of centralized nuclei increased; and the fiber diameter was smaller than in GI. However, FT2B and FT2D expression did not reach the reference values.
Conclusions: The data presented show that the recovery of function over a 10-day period was partially efficient with regard to recuperation of the characteristics of the EDL muscle after the period of immobilization. If the data are extrapolated to physiotherapeutic clinical practice, use of procedures directed towards primary dysfunctions of the muscle may favor a morphofunctional response in the segment and its full recovery.
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Int J Mol Sci
January 2025
Myology Laboratory, Institute of Biomedical Problems (IBP), RAS, 123007 Moscow, Russia.
During skeletal muscle unloading, phosphoinositide 3-kinase (PI3K), and especially PI3K gamma (PI3Kγ), can be activated by changes in membrane potential. Activated IP3 can increase the ability of Ca to enter the nucleus through IP3 receptors. This may contribute to the activation of transcription factors that initiate muscle atrophy processes.
View Article and Find Full Text PDFBMC Musculoskelet Disord
January 2025
Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
Background: Ankle sprains often result in muscle atrophy and reduced range of motion, which can cause long-term ankle instabilities. Understanding the changes to muscle-such as atrophy-and concomitant changes to deep fascia-which may thicken alongside muscle loss-after ankle sprain injury is important to understanding structural changes about the joint and how they might contribute to longer-term impairments. Here, we employ advanced MRI to investigate skeletal muscle and fascial structural changes during the recovery period of one patient undergoing immobilization after ankle sprains.
View Article and Find Full Text PDFCalcif Tissue Int
January 2025
Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy.
Rett syndrome (RS) is a rare neurodevelopmental disorder primarily caused by mutations in the X-linked methyl-CpG binding protein 2 (MECP2) gene, responsible for encoding MECP2 which plays a pivotal role in regulating gene expression. The neurological and non-neurological manifestations of RS vary widely in severity depending on the specific mutation type. Bone complications, mostly scoliosis but also osteoporosis, hip displacement, and a high rate of fractures, are among the most prevalent non-neurological comorbidities observed in girls with RS.
View Article and Find Full Text PDFIn Vivo
December 2024
Laboratory of Physiology, School of Health Sciences, Toyohashi SOZO University, Toyohashi, Japan;
Background/aim: Lactate is a physiologically active substance secreted by skeletal muscle that has been suggested to stimulate muscle mass gain. However, the molecular mechanism for lactate-associated muscle hypertrophy remains unclear. The purpose of the present study was to investigate whether oral administration of lactate increases muscle mass under different loading conditions.
View Article and Find Full Text PDFMar Drugs
December 2024
Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Republic of Korea.
The objective of this study was to examine whether fucosterol, a phytosterol of marine algae, could ameliorate skeletal muscle atrophy in tumor necrosis factor-alpha (TNF-α)-treated C2C12 myotubes and in immobilization-induced C57BL/6J mice. Male C57BL6J mice were immobilized for 1 week to induce skeletal muscle atrophy. Following immobilization, the mice were administrated orally with saline or fucosterol (10 or 30 mg/kg/day) for 1 week.
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