Introduction
Among the various homeostatic mechanisms, thermogenesis is the most vital. It plays a very significant role in the survival of an organism, especially during episodes of malignant hyperthermia (Rowland et al. 1279). During this time, the skeletal muscle tissues serve as a source of heat for the body. Research indicates that the core body temperature rises due to the following factors; muscle contractures, organ metabolism increases, and the inability of the body to remove heat through peripheral tissues (Iaizzo 1134).
Organelle Storing Calcium in Muscles Cells
The storage, dissipation, and re-uptake of calcium in the muscle cells are regulated by the sarcoplasmic reticulum (SP) (Dirksen 389). This is a crucial aspect of the skeletal muscle because ATP from the mitochondria powers its contractile mechanism, and the calcium ions released from the SR.
The Events That Must Occur in the Muscle Cell Before Calcium Is Released From the SR
The function of the mitochondria and the SR are interdependent in the muscle (Dirksen 389). The process of oxidative phosphorylation and the production of mitochondrial ATP is stimulated by the increased production of ATP resulting from the intake of calcium by the mitochondria (Szent-Gyorgyi 707). As a result, the oxygen and nitrogen, reactive species, produced stimulate the release of calcium by the SR.
Calcium Functioning to Cause Contraction of a Skeletal Muscle Cell
The flow of events following the contraction of an individual skeletal muscle cell begins with a signal delivered by the neurotransmitter of that particular cell from the motor neuron of its local fibre (Irnich 2013). The local membrane of the fibre depolarizes as positively charged sodium ions (Na+) enter. This action stimulates the spread of the action potential to the rest of the membrane, depolarizing it. As a result, the SR is triggered to release calcium ions (Ca++), which then initiates the contraction of the muscle, an action sustained by ATP (Lam 2542).
Metabolic pathways that function to synthesize ATP for skeletal muscle contraction. Which of these pathways produces carbon dioxide as a by-product?
The following pathways serve as sources of ATP during skeletal muscle contraction, the citric acid cycle, glycolysis, and oxidative phosphorylation. Both the citric acid cycle and glycolysis produce carbon dioxide as a by-product (Lai 273).
The Role of ATP in Cross-Bridge Cycling
ATP plays a critical role in the binding of myosin as well as its rejuvenation during muscle contractions. ATP binds to myosin, promoting it to high energy state (Tewari 11). Myosin is activated to attach to an actin active site and then to ATP later after the power stroke which restarts the cross-bridge cycle.
The Role of ATP in Generating a Resting Membrane Potential
ATP provides the energy required by the sodium/calcium pump that maintains a positive charge outside the membrane and a positive one inside the membrane, preventing an influx of either charge(Tewari 11).
The Role of ATP in Maintaining Calcium Concentration Gradients
Since a lot of calcium is produced during a case of malignant hyperthermia, ATP maintains its concentration gradient through the hydrolysis of one molecule of ATP for every two molecules of Ca+ transported to the SR (Jeremy Pinnell 85).
The Dantrolene Inhibition of Calcium Channels and How It Helps to Terminate Skeletal Muscle Contraction
Malignant hyperthermia causes increases cell metabolism, which produces a lot of calcium ions. These ions are then transported to the SR for storage, which causes muscle relaxation. Dantrolene inhibits the release of these ions by the SR to cause muscle contraction (Krause 368). Reduced muscle contractions would lower David's body temperature.
Works Cited
Dirksen, Robert T. "Sarcoplasmic reticulum-mitochondrial through-space coupling in skeletal muscle." Applied physiology, nutrition, and metabolism = Physiologie applique, nutrition et metabolism vol. 34,3 (2009): 389-95. doi:10.1139/H09-044
Iaizzo, Paul A., and Daniel I. Sessler. "Skeletal Muscle Is Responsible for Heat Production in Porcine Malignant Hyperthermia." Anesthesia & Analgesia 83.5 (1996): 1134.
Irnich, Dominik. Myofascial trigger points: comprehensive diagnosis and treatment. Elsevier Health Sciences, 2013.
Jeremy Pinnell, Simon Turner, Simon Howell, Cardiac muscle physiology, Continuing Education in Anaesthesia Critical Care & Pain, Volume 7, Issue 3, June 2007, Pages 85-88, doi:10.1093/bjaceaccp/mkm013
Krause, Th, et al. "Dantrolene-a review of its pharmacology, therapeutic use and new developments." Anaesthesia 59.4 (2004): 364-373.
Lai, Nicola et al. "Models of muscle contraction and energetics." Drug discovery today. Disease models vol. 5,4 (2008): 273-288. doi:10.1016/j.ddmod.2009.07.001
Lam, Andy KM, and Antony Galione. "The endoplasmic reticulum and junctional membrane communication during calcium signalling." Biochimica et Biophysica Acta (BBA)-Molecular Cell Research 1833.11 (2013): 2542-2559.
Rowland, Leslie A et al. "The role of skeletal-muscle-based thermogenic mechanisms in vertebrate endothermy." Biological reviews of the Cambridge Philosophical Society vol. 90,4 (2015): 1279-97. doi:10.1111/brv.12157
Szent-Gyorgyi, A G. "Calcium regulation of muscle contraction." Biophysical Journal vol. 15,7 (1975): 707-23. doi:10.1016/S0006-3495(75)85849-8
Tewari, Shivendra G et al. "Dynamics of cross-bridge cycling, ATP hydrolysis, force generation, and deformation in cardiac muscle." Journal of molecular and cellular cardiology vol. 96 (2016): 11-25. doi:10.1016/j.yjmcc.2015.02.006
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