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Neuromuscular Physiology
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Muscle fibers, unlike other cells, often have specialized names for structures. The sarcolemma (plasmalemma) surrounds the fiber and contains sarcoplasm (cytoplasm). The sarcolemma is an asymmetrical fluid mosaic, approximately 7.5 nm thick, largely made of lipids and proteins. As with other cell membranes, the sarcolemma has two major functions: (i) enclosing the cell contents and (ii) regulation of entry and exit of various substances into and out of the fiber. Analyses of the biochemistry and ultrastructure of the sarcolemma indicate it is largely composed of a bilayer of phospholipids arranged perpendicularly to the longitudinal axis of the fiber (Figure 1.6). Hydrophilic lipid heads create most of the inner and outer surface of membrane, with their hydrophobic tails forming the inside of the membrane. The hydrophilic heads are primarily composed of choline, phosphate, and glycerol; the tails consist of fatty acid chains (125, 127). Structural stability and stiffness are added to the membrane as a result of cholesterol bridges between the phospholipid molecules. Additionally, periodic invaginations of the sarcolemma forming tunnels, gives rise to the transverse tubules (TT). The TT is a network for sensing depolarization through dihydropyridine receptors (DHP). The depolarization of this sensing receptor results in a calcium flux caused by the subsequent activation of ryanodine receptors (RYR).
Initial Approach in Muscle Biopsy
Published in Maher Kurdi, Neuromuscular Pathology Made Easy, 2021
Dystrophy is a type of myopathic feature but with structural defect in any sarcolemmal protein. It is due to partial degeneration with compensation on different types of muscle fibers. That is the reason why we see hypertrophic and atrophic fibers embedded in a fibrotic background in dystrophy cases (Figure 10.4). Because of the perimysial and endomysial fibrosis, the spaces between muscle fibers become widened. Moreover, multiple splitting fibers and internal nuclei are easily seen. A few necrotic fibers can also be found.
Ultrastructure of The Myometrium and The role of Gap Junctions in Myometrial Function
Published in Gabor Huszar, The Physiology and Biochemistry of the Uterus in Pregnancy and Labor, 2020
Arie Verhoeff, Robert E. Garfield
The plasma membrane of uterine smooth muscle cells, the sarcolemma, is a trilaminar structure of approximately 8 nm in thickness, as in other cells,28 and is thought to be composed of phospholipids and proteins. Intramembranous protein particles about 9 nm in diameter are seen in freeze-fracture replicates of the plasma membrane. These particles are more numerous on the P-face (protoplasmic) than on the E-face (external) of the membrane,11 as in other types of smooth muscle.29,30
Propofol versus insulin cardioplegia in valvular heart surgeries assessed by myocardial histopathology and troponin I
Published in Egyptian Journal of Anaesthesia, 2022
Omyma Shehata Mohamed, Shady Eid Al-Elwany, Mina Maher Raouf, Heba Mohamed Tawfik, Ibrahim Abbas Youssef
Although the usefulness of cardioplegia solution to arrest the heart during cardiac surgery with cardiopulmonary bypass (CPB), different degrees of myocardial damage and dysfunction can occur as a result of ischemia and disruption of metabolic and ionic homeostasis [1]. During ischemia, anaerobic metabolism leads to formation and accumulation of lactic acid (intracellular acidosis), which consequently elevate the concentration of intracellular sodium. The later can cause osmotic swelling and damage of sarcolemma of the cells. Moreover, prolonged ischemia can also lead to uncontrolled cellular calcium mobilization and formation of reactive oxygen species (ROS). Persistent elevation of intracellular calcium and the generation of ROS can destruct the integrity of mitochondrial cell membrane [2], disturb the electrical properties and contractility and eventually mitochondrial disruption with death of cardiomyocyte [3].
The ultrastructure of muscle fibers and satellite cells in experimental autoimmune encephalomyelitis after treatment with transcranial magnetic stimulation
Published in Ultrastructural Pathology, 2022
María Angeles Peña-Toledo, Evelio Luque, Manuel LaTorre, Ignacio Jimena, Fernando Leiva-Cepas, Ignacio Ruz-Caracuel, Eduardo Agüera, J. Peña-Amaro, Isaac Tunez
Since EAE induces neurogenic injury in the skeletal muscle,8,18 it is likely that an apoptosis process occurs in this model. Borisov and Carlson2 showed that the ultrastructural characteristics of apoptosis in denervated muscle are very similar if not identical to those considered to be the nuclear and cytoplasmic markers of apoptosis. Indeed, denervated muscle fibers exhibit immunoreactivity against proteins and apoptotic factors.27 However, it has recently been pointed out that the traditional tools used to detect apoptosis lack the resolution required to properly determine which side of the sarcolemma dying cells reside.28 Electron microscopy is therefore a very useful tool for evaluating these changes. This technique allowed us to confirm that, although some apoptotic nuclei were observed in the interstitium and some normal nuclei were found, most changes corresponded to the myonuclei. Thus, apoptotic, necrotic, and normal myonuclei can coincide in the same muscle fiber.29
Androgen receptor gene microsatellite polymorphism is associated with muscle mass and strength in bodybuilders and power athlete status
Published in Annals of Human Biology, 2021
João Paulo L. F. Guilherme, Yulia V. Shikhova, Rimma R. Dondukovskaya, Alexandra A. Topanova, Ekaterina A. Semenova, Irina V. Astratenkova, Ildus I. Ahmetov
In the absence of ligands, the AR is confined to sarcoplasm in a multi-heteromeric inactive complex with accessory heat shock proteins (Georget et al. 2002). The steroidal nature of androgens allows them to cross the lipid bilayer of the sarcolemma to form a complex with the ARs and ultimately enhance gene transcription (Beato and Klug 2000). The molecular interaction with androgens induces the dissociation of the AR from the accessory proteins and its dimerisation and translocation to the nucleus, where it binds to androgen response elements (AREs) at specific DNA sites, stimulating the transcription of target genes (Palazzolo et al. 2008). This mechanism represents the classical genomic pathway for the action of androgens in skeletal muscle, but the androgen–AR complex can also interfere with other signalling pathways via non-genomic actions. While the genomic pathway encodes muscle-specific transcription factors, enzymes and structural proteins, non-genomic actions are faster and can translate signals on muscle through activating specific kinases (Dubois et al. 2012) and trigger an increase in intracellular calcium (Ca2+) levels (Estrada et al. 2003). Collectively, these mechanisms have the potential to influence muscle biology.