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Aortic and Arterial Mechanics
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
A unique feature of many soft tissues is their ability to contract via actin–myosin interactions within specialized cells called myocytes. Examples include the cardiac muscle of the heart, the skeletal muscle of the arms and legs, and the smooth muscle, which is found in many tissues, including the airways, arteries, and uterus. A famous equation in muscle mechanics was postulated in 1938 by A.V. Hill to describe the force–velocity relationship. This relationship, like many subsequent ones, focuses on one-dimensional (1D) behavior of the myocyte or muscle along its axis; data typically come from tests on muscle fibers or strips or, in some cases, rings taken from arteries or airways. Although much has been learned, much remains to be discovered, particularly with respect to the multiaxial behavior. The interested reader is referred to Fung [17].
Electrical stimulation of cells derived from muscle
Published in Ze Zhang, Mahmoud Rouabhia, Simon E. Moulton, Conductive Polymers, 2018
Anita F. Quigley, Justin L. Bourke, Robert M. I. Kapsa
Cardiac and skeletal muscle tissues comprise a number of cellular types, including mature myofibers or cardiomyocytes, progenitor cells (myoblasts in skeletal muscle or myocytes in cardiac muscle), and the cells of associated vasculature and interstitial tissues. Whilst electrical stimulation has the potential to influence the majority of the cell types present in muscles through ion flux (including myoblasts, myocytes, and vasculature), the immediate effect of electrical stimulation in skeletal muscle is seen macroscopically in the muscle fibers or mature cardiac muscle through induced contraction. In rat skeletal muscle, chronic electrical stimulation can induce changes in the status of muscle fiber type profile, changing fast-type muscle fibers to slow-type muscle fibers (Windisch et al. 1998; Putman et al. 2001); however, fiber type changes have been reported to be related to the frequency of the stimulation, with higher-frequency stimulation showing a slow to fast transition (Boonyarom et al. 2009; Radisic et al. 2005). This effect has also been observed in rabbits (Kubis et al. 2002). Studies in humans have also demonstrated an effect of electrical stimulation predominantly on type II fast muscle fibers (Cabric et al. 1988). Although electrical stimulation has been reported to increase the metabolism and maximal force of muscles in humans, the associated fiber type changes can be somewhat variable, suggesting that there are other factors influencing changes in fiber type, other than contractile activity alone (Minetto et al. 2013; Rochester et al. 1995; Dal Corso et al. 2007). Despite some variation in the effects of electrical stimulation in human fiber type changes in the literature, electrical stimulation has been used to reduce muscle wasting in immobile patients (Dirks et al. 2015), as well to help maintain muscle function in denervated and aging muscles (Elzinga et al. 2015; Zealear et al. 2014; Dow et al. 2005).
Sternocleidomastoid Muscle and Head Position: How to Minimize Muscle Tension
Published in IISE Transactions on Occupational Ergonomics and Human Factors, 2022
Simona Rubine-Gatina, Nadina Rimere, Zane Zundane, Alise Gulajeva, Jelena Reste
Considering that the SCM muscle is among the largest and main muscles maintaining head posture, we aimed to objectively evaluate its tension and other biomechanical aspects. During the methodology development process, we were unable to find a sufficient number of studies of the SCM muscle. Thus, we aimed to objectively measure SCM muscle tension with participants using different head positions. A MyotonPRO myotonometer was used since it measures the following biomechanical parameters:Oscillation frequency (in Hertz), the intrinsic tension of the muscle in its passive state;Dynamic stiffness (in Newtons per meter), the resistance to deformation;Logarithmic decrement, a parameter that reflects muscle elasticity, that is, a muscle’s ability to reduce tension after work. The more elastic a muscle is, the faster myocyte relaxation occurs, which provides a better blood supply;Mechanical stress relaxation time (in milliseconds), the time it takes the muscle to restore its shape from deformation; andCreep (in Deborah numbers), the gradual elongation of the muscle over time when placed under constant tensile stress (Davidson et al., 2017).
The influence of carbohydrate ingestion on peripheral and central fatigue during exercise in hypoxia: A narrative review
Published in European Journal of Sport Science, 2021
Hunter L. Paris, Erin C. Sinai, Ren-Jay Shei, Alexandra M. Keller, Timothy D. Mickleborough
Peripheral fatigue originates from mechanisms that occur at, or distal to, the neuromuscular junction (Gandevia, 2001). Causative factors of fatigue within the muscle vary, though research primarily indicates metabolic inhibition of contractile function. Factors such as elevations in H+, , and Pi concentrations, alteration of Na+-K+ pump function, impaired regulation of Ca2+ within the myocyte, buildup of K+ in the transverse-tubular system, exercise-induced muscle damage, and glycogen depletion can all disrupt cross-bridge function in the skeletal muscle (Kent-Braun et al., 2012). These factors do not represent an exhaustive list of metabolites and processes contributing to peripheral fatigue and for further understanding we refer the reader to the review from Kent-Braun, Fitts, and Christie (Kent-Braun et al., 2012).
Adverse cardiovascular effects of exposure to cadmium and mercury alone and in combination on the cardiac tissue and aorta of Sprague–Dawley rats
Published in Journal of Environmental Science and Health, Part A, 2021
Sandra Arbi, Megan Jean Bester, Liselle Pretorius, Hester Magdalena Oberholzer
In contrast, a decrease in collagen degradation also has a profibrotic effect. Collagen degradation is mediated by MMPs which are regulated by hormones, various growth factors and cytokines as well as mechanical strain on the tissue.[1] Although MMPs are involved in collagen degradation, activation can further promote the synthesis of additional collagen in tissues, and therefore, creating a positive feedback mechanism for fibrosis.[51,52] The degradation pathways also often favor the degradation of healthy, intrinsic collagen over newly formed collagen, which in fibrosis is oxidized and highly cross-linked and this results in the accumulation of stiffer collagen.[4,5] In disease levels of myofibroblasts are increased and this causes an increase in the procollagen synthesis and secretion into the pericellular space, where it forms collagen fibrils that assemble into fibers. Functionally, any changes to the ECM components and MMP activity of the myocardium affects the contractile function of myocytes.[3–5] The presence of collagen in smooth muscle has been shown to affect contractility, myocyte mediated signal transduction between cells, as well as growth factor release, the most important of which is TGF – β1.[23,25]