Changes in muscle coactivation during running: a comparison between two techniques, forefoot vs rearfoot

Introduction: According to the literature, eccentric exercise has been considered a precursor of neuromuscular changes generated by post-exercise damage, mainly causing an alteration in the muscle cell membrane. Muscle fiber conduction velocity (MFCV) has been one of the physiological variables that have allowed to quantify this alteration. Some investigations have shown a decrease in the MFCV after eccentric exercise protocols; however, few studies have confirmed these findings. This review aimed to describe the recent scientific evidence that reports changes in the MFCV after eccentric exercise protocols. Material and method: From 265 articles, 6 articles were selected from EBSCO and MEDLINE platforms with a temporal filter of 10 years (between 2010 and April 2020), using inclusion/exclusion criteria predetermined. Firstly, the information from eccentric exercise effect on MFCV, and exercise protocols were described. Secondly, the techniques used to record electromyographic signals and some criteria to determine the MFCV were reported. Results: Modifications of MFCV can be observed after eccentric exercise in almost all selected articles. At the same time, a decrease of this variable was observed in four studies, associated with the biceps brachii and two portions of the quadriceps muscles. However, one article describes an increase of the MFCV in the vastus lateralis quadriceps. Conclusion: The articles suggest that eccentric contractions could modify the MFCV behavior of some muscles. However, evidence is still lacking to describe the real cause of these changes.

Structure based analysis of KATP channel with a DEND syndrome mutation in murine skeletal muscle

Developmental delay, epilepsy, and neonatal diabetes (DEND) syndrome, the most severe end of neonatal diabetes mellitus, is caused by mutation in the ATP-sensitive potassium (KATP) channel. In addition to diabetes, DEND patients present muscle weakness as one of the symptoms, and although the muscle weakness is considered to originate in the brain, the pathological effects of mutated KATP channels in skeletal muscle remain elusive. Here, we describe the local effects of the KATP channel on muscle by expressing the mutation present in the KATP channels of the DEND syndrome in the murine skeletal muscle cell line C2C12 in combination with computer simulation. The present study revealed that the DEND mutation can lead to a hyperpolarized state of the muscle cell membrane, and molecular dynamics simulations based on a recently reported high-resolution structure provide an explanation as to why the mutation reduces ATP sensitivity and reveal the changes in the local interactions between ATP molecules and the channel.

Is GLUT4 translocation the answer to exercise stimulated muscle glucose uptake?

Exercise increases muscle glucose uptake up to 100 fold compared to rest. The magnitude of increase depends on exercise intensity and duration. While KO of GLUT4 convincingly has shown that GLUT4 is necessary for exercise to increase muscle glucose uptake, studies only show an approximate 2-fold increase in GLUT4 translocation to the muscle cell membrane when transitioning from rest to exercise. Therefore, there is a big discrepancy between the increase in glucose uptake and GLUT4 translocation. It is suggested that either the methods for measurements of GLUT4 translocation in muscle grossly underestimate the real translocation of GLUT4 or alternatively that GLUT4 intrinsic activity increases in muscle during exercise, perhaps due to increased muscle temperature and/or mechanical effects during contraction/relaxation cycles.

Annexin A2 Mediates Dysferlin Accumulation and Muscle Cell Membrane Repair

Muscle cell plasma membrane is frequently damaged by mechanical activity, and its repair requires the membrane protein dysferlin. We previously identified that, similar to dysferlin deficit, lack of annexin A2 (AnxA2) also impairs repair of skeletal myofibers. Here, we have studied the mechanism of AnxA2-mediated muscle cell membrane repair in cultured muscle cells. We find that injury-triggered increase in cytosolic calcium causes AnxA2 to bind dysferlin and accumulate on dysferlin-containing vesicles as well as with dysferlin at the site of membrane injury. AnxA2 accumulates on the injured plasma membrane in cholesterol-rich lipid microdomains and requires Src kinase activity and the presence of cholesterol. Lack of AnxA2 and its failure to translocate to the plasma membrane, both prevent calcium-triggered dysferlin translocation to the plasma membrane and compromise repair of the injured plasma membrane. Our studies identify that Anx2 senses calcium increase and injury-triggered change in plasma membrane cholesterol to facilitate dysferlin delivery and repair of the injured plasma membrane.

Integrin degradation during postmortem cold storage and the level of drip loss in pork

Integrins are a family of transmembrane adhesion proteins. An integrin molecule is composed of two subunits called α and β, each of which has a large extracellular domain, a transmembrane fragment, and a short cytoplasmic sequence. The main function of integrin is to bind extracellular matrix proteins and the skeletal muscle cell membrane. In addition, integrin as a membrane receptor is involved in signal transduction and cell response to microenvironmental signals, by relaying information about the structure and composition of the cell environment. Postmortem integrin degradation has been the subject of several studies, mainly in pork, where the mechanisms of postmortem integrin degradation are not completely understood. Therefore, the aim of the study was to present current knowledge on the role of integrin in postmortem drip loss in pork. Research to date has shown that postmortem integrin degradation could contribute to the formation of drip channels between the cell body and cell membrane of muscle fibers, which increases the drip loss from pork.