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Screening and Pharmacological Management of Neuropathic Pain
Published in Suvardhan Kanchi, Rajasekhar Chokkareddy, Mashallah Rezakazemi, Smart Nanodevices for Point-of-Care Applications, 2022
Manu Sharma, Ranju Soni, Kakarla Raghava Reddy, Veera Sadhu, Raghavendra V. Kulkarni
Meprobamate, an anxiolytic drug, exhibits affinity to bind GABA receptors to pepper the neuronal transmission in the spinal cord. This symptomatically lessens pain sensation and produces sedation. Similarly, methocarbamol, a central muscle relaxant, is used to treat skeletal muscle spasms caused by musculoskeletal disorders, tetanus, and injury [42]. The GABA-derivative drug, baclofen, is mainly effective in managing muscle spasticity associated with spinal cord injury. Metaxalone is extensively used to relax muscle during strains, sprains, and other musculoskeletal conditions, although its mechanism of action is unclear [43]. Dantrolene is a hydantoin derivative. It produces muscle relaxation by dissociating excitation-contraction coupling possibly by restricting secretion of Ca+2 from sarcoplasmic reticulum by binding to ryanodine receptor1. It has been found suitable for the treatment of fulminant hypermetabolism of skeletal muscles [44].
Muscle Physiology and Electromyography
Published in Verna Wright, Eric L. Radin, Mechanics of Human Joints, 2020
The action potential sweeping over the surface of the muscle causes a response in the contractile system by the process of excitation-contraction coupling. Between the myofibrils are sacs of sarcoplasmic reticulum, and the surface of thesarcolemma frequently invaginates, giving rise to ‘T tubules,” so called because they traverse the muscle fibers (see Fig. 9). A T tubule and its surrounding sarcoplasmic reticulum are collectively termed a triad, but although they are closely associated with the sarcoplasmic reticulum, the T tubules are not connected to it. In human muscle, the triads are located at the boundary of the A and I bands of the sarcomeres (10). As the action potential sweeps over the surface of the muscle, the depolarization spreads down the T tubules. In response to the action potential, the sarcoplasmic reticulum releases calcium ions into the myoplasm. The free calcium initiates the mechanical events of a contraction, and the contraction is subsequently turned off when the calcium is removed from the binding sites. Although in the process of a contraction some calcium ions may become bound to other myoplasmic proteins, they are all eventually returned to the internal compartment of the sarcoplasmic reticulum by a calcium ATPase resident in the membrane of the sarcoplasmic reticulum, to arm the system for the next contraction (11).
Medium Design for Cell Culture Processing
Published in Wei-Shou Hu, Cell Culture Bioprocess Engineering, 2020
Phosphate makes up part of the nucleic acids and nucleotides of cell biomass. It is also present as various phosphorylated metabolic intermediates and as inorganic phosphate. A high level of phosphate in the medium is necessary for carrying out the stoichiometric need to synthesize new biomass. Magnesium plays key metabolic roles in energy metabolism and is conjugated to many metabolites. The intracellular level of Mg2+ is high, but free Mg2+ is only at about ~.25–1 mM, as the majority is complexed to ATP and other organic acids. Phosphate, K+, and Mg2+ are thus three inorganic components that appear at higher concentrations intracellularly than in the medium. Calcium is essential for signaling in some differentiated cells, and is present in high concentrations in the endoplasmic reticulum (ER) and the sarcoplasmic reticulum in muscle cells. The concentrations of the most abundant bulk ions (Na+, Cl−, and K+) in commonly used media spans a small range. In contrast, HCO32+ spans a much wider range.
The effects of taurine ingestion on anaerobic and physiological performance in female rugby players
Published in Research in Sports Medicine, 2023
Azize Bingöl Diedhiou, Zoran Milanović, Mustafa Can Eser, Fatma Neşe Şahin, Michael Hamlin, Ulaş Can Yıldırım
Dietary supplements, such as energy drinks, often consist of different ingredients that are thought to increase athletic performance (Astorino et al., 2009; Stellingwerff & Cox, 2014). However, the combination of various performance-enhancing stimulants and substances in energy drinks makes it difficult to understand the real effects of some of them on athletes’ performance (Milioni et al., 2016). An example, taurine, a sulphur-containing non-essential amino acid, is one of the main ingredients in many popular energy drinks (Warnock et al., 2017) and regulates intracellular Ca2+ utilization in skeletal muscle fibres and Ca2+ sensitivity of myofibrils (Hamilton et al., 2006). However, the ergogenic effect of taurine on athletic performance remains uncertain (Buzdaglı et al., 2022) despite the fact that many athletes take taurine in sports drinks. It is thought that taurine-depleted muscle fibres fatigue faster than muscle fibres with adequate taurine due to the change in Ca2+ utilization in the sarcoplasmic reticulum (Hamilton et al., 2006).
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).
The acute angiogenic signalling response to low-load resistance exercise with blood flow restriction
Published in European Journal of Sport Science, 2018
Richard A. Ferguson, Julie E. A. Hunt, Mark P. Lewis, Neil R. W. Martin, Darren J. Player, Carolin Stangier, Conor W. Taylor, Mark C. Turner
The greater phosphorylation of p38MAPK is perhaps not surprising given it is considered to be a stress-activated kinase and has been repeatedly shown to be activated in response to various exercise modalities including resistance training (Camera, Hawley, & Coffey, 2015). p38MAPK lies downstream of the calcium/calmodulin-dependent protein kinase (CAMK) which is activated by cytosolic increases in Ca2+, that ultimately leads to increased PGC-1α expression (Wright et al., 2007). The key physiological stimulus causing the release of Ca2+ from the sarcoplasmic reticulum is depolarisation of the muscle surface membrane in the form of an action potential (Endo, 1977). Thus, an increase in motor unit activity (i.e. EMG activity) which has been reported during BFR resistance exercise (Fatela, Reis, Mendonca, Avela, & Mil-Homens, 2016) likely explains the greater phosphorylation of p38MAPK. Moreover, ROS generated in response to ischaemia-reperfusion and muscle contraction can also activate MAPK and PGC-1α signalling pathways (Kang et al., 2009) and may contribute to the phosphorylation of p38MAPK following BFR resistance exercise. However, ROS production during BFR resistance exercise may be minor given that levels of oxidative stress markers are unaltered post-exercise (Nielsen et al., 2017). It is, however, surprising that AMPK was not similarly activated given the additional metabolic stimulus BFR has been purported to provide (Krustrup et al., 2009; Suga et al., 2009). This may be reflected by the specific protocol used in the present study (1 × 30 reps, 2 × 15 reps, 1× reps to fatigue, with 30 s recovery between sets) which may not have been as metabolically challenging as expected.