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Skeletal Muscle
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The cell membrane of the muscle fiber is the sarcolemma and has the ionic properties characteristic of excitable cells, manifested as a resting membrane voltage of about –90 mV and the ability to generate and propagate a muscle action potential. The sarcolemma is coated on the outside by a basement membrane formed largely of glycoproteins, and each muscle fiber is surrounded by a delicate layer of connective tissue, the endomysium (Figure 9.1). Groups of about 10 to more than 100 muscle fibers are bundled together into fascicles, the number of muscle fibers in a fascicle being larger in muscles that produce greater force, with less fineness of control. Fascicles are surrounded, in turn, by another layer of connective tissue, the perimysium. The whole muscle is ensheathed by a dense layer of irregular connective tissue, the epimysium.
Force Generation Mechanism of Skeletal Muscle Contraction
Published in Yuehong Yin, Biomechanical Principles on Force Generation and Control of Skeletal Muscle and their Applications in Robotic Exoskeleton, 2020
T-tubule transfers excitation from sarcolemma to the deeper part of muscle fiber through the connecting point of T-tubule and SR. The T-tubule with the SR (longitudinal tubule) on its two sides is called the thribble structure. The T-tubule connects with SR terminal cisterna through the coupling structure of dihydropyridine (DHPR) and ryanodine receptor (RyR) (tetramer) [19]. Tetramer is actually an electrically and mechanically coupled L-type Ca2+ channel. When the AP on T-tubule reaches the terminal cisterna, DHPR will take conformational change when the potential rise is detected. Then it drives RyR to move from SR to open the channel so that the high-concentration Ca2+ in SR could be released to cytoplasm. It can be seen that the tetramer channel acts like a molecular stopper. The motion of the stopper is controlled by the potential of T-tubule. The structure of tetramer is illustrated in Figure 1.12b. Each group of RyR is arranged like a parallelogram, corresponding to the four DHPRs, respectively. Through the electrically and mechanically coupled L-type Ca2+ channel, the AP spreading on sarcolemma is able to control [Ca2+] in sarcoplasm to activate muscle contraction.
Techniques to Evaluate Damage and Pain on Injection
Published in Sandeep Nema, John D. Ludwig, Parenteral Medications, 2019
Srinidi Mohan, Gayle A. Brazeau, Pramod Gupta
Consultation with toxicologists can provide important insight into identifying the potential mechanisms responsible for tissue damage at the injection site. For example, in skeletal muscle, there are several mechanisms that can be initially considered when evaluating formulations for their potential to cause tissue damage. These potential mechanisms by which a molecule could cause muscle damage include (i) a disruption of the sarcolemma (the muscle membrane), which could disrupt intracellular homeostasis; (ii) a disruption or alteration in the mechanisms responsible for maintaining intracellular calcium homeostasis as this is essential to muscle functioning and increased cytosolic calcium is associated with tissue damage; (iii) an interference in mitochondrial functioning, thus disrupting homeostatic processes; (iv) increased oxidative stress leading to the formulation of reactive molecules, thus disrupting cellular functioning; and (v) dramatic changes in intracellular or extracellular pH or tonicity, which can result in cellular distress [9–16].
Exertional rhabdomyolysis and acute kidney injury in endurance sports: A systematic review
Published in European Journal of Sport Science, 2021
Daniel Rojas-Valverde, Braulio Sánchez-Ureña, Jennifer Crowe, Rafael Timón, Guillermo J. Olcina
More commonly reported physiological symptoms and biomarkers indicators for ER and AKI were S-Cr and S-CK (74.42%). ER is the result of muscle damage induced by exercise. This damage is represented in myocyte damage and energy depletion at the cellular level (Hernández-Contreras et al., 2015; Stella & Shariff, 2012). During rest, ion channels (Na+ / K+ pump and Na+ / Ca+ exchange) located in the plasma membrane (sarcolemma) of muscle cells, maintain low intracellular concentrations of Na+ and Ca+ and high concentrations of K+. Muscular depolarization causes Ca+ release from the reserves located in the sarcoplasmic reticulum to the cytoplasm or sarcoplasm, causing actin–myosin binding. These changes are the result of insufficient energy in the form of ATP. Any adverse event that causes injury to the ion channels or availability of ATP, would cause an imbalance in the electrolyte concentration. In the case of myocyte injury and ATP depletion, an intracellular increase in Na+, causes a flow of water into the intracellular space, and an intracellular increase of Ca+, which causes sustained myofibrillary contractions. This leads to a decrease in ATP (Al-Ismaili, Piccioni, & Zappitelli, 2011) and mitochondrial dysfunction resulting in the production of oxygen radicals and increasing cell damage (Patel, Gyamfi, & Torres, 2009).
Greater decrements in neuromuscular function following interval compared to continuous eccentric cycling
Published in European Journal of Sport Science, 2022
David James Green, Kevin Thomas, Glyn Howatson
Total work done during the sessions and all baseline neuromuscular variables (Table I) were similar between the INT and CONT exercise groups, demonstrating effective matching. Furthermore, levels of voluntary activation pre-exercise were consistent with previous research using the same twitch technique which indicates that participants arrived in a rested state (Brownstein et al., 2017; Thomas et al., 2015). In agreement with previous studies, eccentric exercise elicited reductions in MVC, peripheral muscle contractility, and VA (Goodall et al., 2017; Prasartwuth, Allen, Butler, Gandevia, & Taylor, 2006; Prasartwuth, Taylor, & Gandevia, 2005). The overall decrease in knee extensor MVC immediately post exercise (17%) is consistent with that observed after a similar eccentric cycling protocol (∼19%) (Peñailillo et al., 2013). Our data indicated that reductions in muscle contractility might partially result from changes in sarcolemma excitability as demonstrated by a reduction in Mmax. Proske and Allen (2005) suggest that sarcolemma disruption can occur following eccentric exercise due to an accumulation of mechanically damaged sarcomeres and loss of calcium mediated homeostasis leading to lipolysis and proteolysis. However, M-wave was depressed only immediately post-exercise whereas muscle function remained suppressed at 24 h. Therefore, whilst decreased sarcolemma excitability might contribute to the reductions in twitch force observed immediately following eccentric exercise it is unlikely to be the primary mediator of prolonged muscle function impairment (Sayers et al., 2003). It is likely that the changes in muscle contractility observed in the current study stem from sarcomere disruption (Lauritzen, Paulsen, Raastad, Bergersen, & Owe, 2009; Proske & Morgan, 2001) or non-sarcolemma related impairment of the excitation-coupling process (Corona et al., 2010; Warren et al. 2001) such as sarcoplasmic reticulum dysfunction (Hill, Thompson, Ruell, Thom, & White, 2001).