To see the other types of publications on this topic, follow the link: Muscle activation.
Books on the topic 'Muscle activation'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 46 books for your research on the topic 'Muscle activation.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse books on a wide variety of disciplines and organise your bibliography correctly.
1
Rüegg, Johann Caspar. Calcium in Muscle Activation. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-96981-2.
Full text
2
Calcium in muscle activation: A comparative approach. Berlin: Springer-Verlag, 1986.
Find full text
3
Calcium in muscle activation: A comparative approach. 2nd ed. Berlin: Springer-Verlag, 1988.
Find full text
4
Rüegg, Johann Caspar. Calcium in muscle activation: A comparative approach. Berlin: Springer-Verlag, 1986.
Find full text
5
Rüegg, Johann Caspar. Calcium in Muscle Activation: A Comparative Approach. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986.
Find full text
6
Burns, Jennifer. Calcineurin activation is implicated in skeletal muscle hypertrophy. Sudbury, Ont: Laurentian University, 1999.
Find full text
7
Stein, Wendy Karen. a-Adrenoceptors and calcium activation mechanisms in vascular muscle. Birmingham: Aston University. Department of Pharmaceutical Sciences, 1987.
Find full text
8
Drechsler, Wendy Isobel. Quadriceps femoris muscle activation: Evaluation after major knee injury. London: University of East London, 2002.
Find full text
9
McAdams, Richard Philip. Factors modifying activation of alpha-adrenoceptors in smooth muscle. Uxbridge: Brunel University, 1986.
Find full text
10
O'Brien, Lee. Expression of c-fos mRNA within rat skeletal muscle in response to nerve-mediated activation. Sudbury, Ont: Laurentian University, 1998.
Find full text
11
KAMARU, Alex. Muscle Activation Exercise: A Complete Guide on the Practices and Benefits of Performing Muscle Activation Exercise Prior to Strength Training. Independently Published, 2022.
Find full text
12
Shankar, Hariharan, and Karan Johar. Piriformis Muscle, Psoas Muscle, and Quadratus Lumborum Muscle Injections: Ultrasound. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199908004.003.0047.
Full textAbstract:
This chapter describes the anatomy, technique, available evidence, and complications of piriformis, psoas, and quadratus lumborum muscle injections. Traditionally landmark-based injections of the piriformis muscle were performed using the posterior inferior iliac spine and the greater trochanter as bony landmarks. Subsequently, fluoroscopy, electromyography, and CT were used to facilitate the injection. Activation of myofascial trigger points within the iliopsoas muscle can cause referred pain to the groin and anterior thigh. Landmark-based injections and CT-guided iliopsoas injections have been described. But they carry the risk of radiation, bowel injury, intravascular injection, and nerve injury. Ultrasound-guided injection into the psoas muscle may be performed at two different locations, the iliopsoas muscle and the iliopsoas tendon. The quadratus lumborum is a common cause of low back pain, and ultrasound-guided injection of local anesthetic into quadratus lumborum muscle may be performed.
13
Kuo, Huey-ju. Factors affecting the activation of rabbit muscle phosphofructokinase by actin. 1986.
Find full text
14
Ruegg, J. C. Calcium in Muscle Activation: A Comparative Approach (Zoophysiology, Vol 1). Springer, 1986.
Find full text
15
Hu, Xiaogang, Francesco Negro, and Jun Yao, eds. Understanding Altered Muscle Activation After Central or Peripheral Neuromuscular Injuries. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-398-1.
Full text
16
H, Vandenburgh Herman, and United States. National Aeronautics and Space Administration., eds. Mechanical stimulation of skeletal muscle generates lipid-related second messengers by phospholipase activation. [Washington, DC?: National Aeronautics and Space Administration, 1991.
Find full text
17
Buckley, Bernadette Drew. Comparison of muscle activation pattens in boys and girls during a simple landing task. 2003.
Find full text
18
Zwarts, Machiel J. Nerve, muscle, and neuromuscular junction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0001.
Full textAbstract:
Essential to all living creatures is the ability to convey information. In addition motor responses are required, for example running. This all is possible due to the ability of specialized cells to conduct information along the cell membrane by means of action potentials (AP) made possible by the charged cell membrane, which has selective permeability for different ions. Voltage and ligand sensitive ion channels are responsible for sudden changes in selective permeability of the membrane resulting in local depolarization of the membrane. The neuromuscular junction is a highly specialized region of the distal motor axon that is responsible for the transferring of activation from nerve to muscle. All these systems and subsystems can fail and a thorough understanding is necessary in order to understand the changes a clinical neurophysiologist can encounter while recording from the human nervous system in cases of disorders of brain, nerve and muscle.
19
Effects of concentric and eccentric isokinetic heavy-resistance training on quadriceps muscle strength, cross-sectional area and neural activation in women. 1994.
Find full text
20
Dutto, Darren John. Leg spring model related to muscle activation, force, and kinematic patterns during endurance running to voluntary exhaustion. 1999.
Find full text
21
Luppi, Pierre-Hervé, Olivier Clément, Christelle Peyron, and Patrice Fort. Neurobiology of REM sleep. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0003.
Full textAbstract:
REM (paradoxical) sleep is a state characterized by rapid eye movements, EEG activation, and muscle atonia. REM sleep behavior disorder (RBD) is a parasomnia characterized by loss of muscle atonia during REM sleep. Cataplexy, a key symptom of narcolepsy, is a striking sudden episode of muscle weakness comparable to REM sleep atonia triggered by emotions during wakefulness. This chapter presents recent results on the neuronal network responsible for REM sleep and explores hypotheses explaining RBD and cataplexy. RBD could be due to a specific degeneration of glutamatergic neurons responsible for muscle atonia, localized in the pontine sublaterodorsal tegmental nucleus (SLD) or the glycinergic/GABAergic premotoneurons localized in the ventral medullary reticular nuclei. Cataplexy in narcoleptics could be due to activation during waking of SLD neurons. In normal conditions, activation of SLD neurons would be blocked by simultaneous excitation by hypocretins of REM sleep-off GABAergic neurons localized in the ventrolateral periaqueductal gray.
22
Biewener, Andrew A., and Shelia N. Patek, eds. Muscles and Skeletons. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198743156.003.0002.
Full textAbstract:
Animal locomotion depends on the organization, physiology and biomechanical properties of muscles and skeletons. Musculoskeletal systems encompass the mechanical interactions of muscles and skeletal elements that ultimately transmit force for movement and support. Muscles not only perform work by contracting and shortening to generate force, they can also operate as brakes to slow the whole body or a single appendage. Muscles can also function as struts (rod-like) to maintain the position of a joint and facilitate elastic energy storage and recovery. Skeletal muscles share a basic organization and all rely on the same protein machinery for generating force and movement. Variation in muscle function, therefore, depends on the underlying mechanical and energetic components, enzymatic properties, and activation by the nervous system. Muscles require either an internal, external or hydrostatic skeletal system to transmit force for movement and support.
23
Steenland, Hendrick William. Respiratory activation of the genioglossus muscle involves both non-NMDA and NMDA glutamate receptors at the hypoglossal motor nucleus in-vivo. 2005.
Find full text
24
Cellek, Selim. Mechanism of penile erection. Edited by David John Ralph. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0101.
Full textAbstract:
Sexual stimuli (tactile, visual, olfactory, and imaginative) are processed and integrated in the central nervous system which then activates certain autonomic and somatic pathways within the peripheral nervous system. This coordinated activation of the central and peripheral nervous systems leads to penile erection which is actually a result of relaxation of vascular and cavernosal smooth muscle in the penis. In the flaccid (detumescent) penis, the smooth muscle tone is heightened. Penile erection (tumescence) requires a decrease in the smooth muscle tone. The tone of the penile smooth muscle therefore is the main determinant of erectile function. In this chapter, the current information on the control of erectile function by this central-peripheral-smooth muscle axis will be reviewed.
25
Jones, Barbara E. Neuroanatomical, neurochemical, and neurophysiological bases of waking and sleeping. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0004.
Full textAbstract:
Neurons distributed through the reticular core of the brainstem, hypothalamus, and basal forebrain and giving rise to ascending projections to the cortex or descending projections to the spinal cord promote the changes in cortical activity and behavior that underlie the sleep–wake cycle and three states of waking, NREM (slow wave) sleep, and REM (paradoxical) sleep. Forming the basic units of these systems, glutamate and GABA cell groups are heterogeneous in discharge profiles and projections, such that different subgroups can promote cortical activation (wake/REM(PS)-active) versus cortical deactivation (NREM(SWS)-active) by ascending influences or behavioral arousal with muscle tone (wake-active) versus behavioral quiescence with muscle atonia (NREM/REM(PS)-active) by descending influences. These different groups are in turn regulated by neuromodulatory systems, including cortical activation (wake/REM(PS)-active acetylcholine neurons), behavioral arousal (wake-active noradrenaline, histamine, serotonin, and orexin neurons), and behavioral quiescence (NREM/REM(PS)-active MCH neurons). By different projections, chemical neurotransmitters and discharge profiles, distinct cell groups thus act and interact to promote cyclic oscillations in cortical activity and behavior forming the sleep-wake cycle and states.
26
Clarke, Andrew. Temperature and reaction rate. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199551668.003.0007.
Full textAbstract:
All other things being equal, physiological reaction rate increases roughly exponentially with temperature. Organisms that have adapted over evolutionary time to live at different temperatures can have enzyme variants that exhibit similar kinetics at the temperatures to which they have adapted to operate. Within species whose distribution covers a range of temperatures, there may be differential expression of enzyme variants with different kinetics across the distribution. Enzymes adapted to different optimum temperatures differ in their amino acid sequence and thermal stability. The Gibbs energy of activation tends to be slightly lower in enzyme variants adapted to lower temperatures, but the big change is a decrease in the enthalpy of activation, with a corresponding change in the entropy of activation, both associated with a more open, flexible structure. Despite evolutionary adjustments to individual enzymes involved in intermediary metabolism (ATP regeneration), many whole-organism processes operate faster in tropical ectotherms compared with temperate or polar ectotherms. Examples include locomotion (muscle power output), ATP regeneration (mitochondrial function), nervous conduction and growth.
27
Ratel, Sébastien, and Craig A. Williams. Neuromuscular fatigue. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0009.
Full textAbstract:
Scientific evidence supports the proposition that prepubertal children fatigue less than adults when performing whole-body dynamic activities like maximal cycling, running bouts, and maximal voluntary isometric/isokinetic muscle contractions. Although the mechanisms underpinning differences in fatigue between children and adults are not all fully understood, there is a consensus that children experience less peripheral fatigue (i.e. muscular fatigue) than their older counterparts. Central factors may also account for the lower fatigability in children. Some studies report a higher reduction of muscle voluntary activation during fatiguing exercise in prepubertal children compared to adults. This could reflect a strategy of the central nervous system aimed at limiting the recruitment of motor units, in order to prevent any extensive peripheral fatigue. Further studies are required to clarify this proposition.
28
Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.
Full textAbstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
29
Rider, Lisa G., and Frederick W. Miller. Outcome assessment in the idiopathic inflammatory myopathies. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0016.
Full textAbstract:
Due to their rarity, heterogeneity, and multispecialty nature, the myositis syndromes have limited data-driven consensus on appropriate outcome measures. Recently, two international, multispecialty consortia developed new tools and consensus on core set measures of myositis disease activity and damage, as well as response criteria that are now recommended for use as clinical trial endpoints but will also be useful in clinical practice. Magnetic resonance imaging, muscle ultrasound, selected laboratory tests, and immunological biomarkers—including cytokines, chemokines, lymphocyte flow cytometry, and endothelial activation markers—can all be helpful adjuncts to serum muscle enzyme levels in assessing disease activity and damage, but these have not yet been fully validated. Definitions of clinically inactive disease, complete clinical response, and remission have also been proposed but require further validation. These advances should enhance the development of therapies by standardizing our ability to demonstrate their efficacy in treating the idiopathic inflammatory myopathies.
30
Baracos, Vickie E., Sharon M. Watanabe, and Kenneth C. H. Fearon. Aetiology, classification, assessment, and treatment of the anorexia-cachexia syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0205.
Full textAbstract:
Anorexia-cachexia is a heterogeneous and multifactorial syndrome most likely driven by systemic inflammation and neuroendocrine activation. Key diagnostic features include reduced appetite, weight loss, and muscle wasting. Key clinical problems include management of anorexia without resort to artificial nutritional support, and muscle wasting that cannot be completely arrested/reversed even with such intervention. Assessment should cover domains such as body stores of energy and protein, food intake, performance status, and factors resulting in excess catabolism. Intervention should be early rather than late, informed by the assessment process and focused on a multimodal approach (nutrition, exercise, and pharmacological agents). This chapter aims to discuss these issues and provide (a) the reader with some background principles to classification, (b) a simple approach to patient assessment and a robust algorithm for basic multimodal treatment, and (c) an overview of the evidence base for different pharmacological interventions.
31
Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.
Full textAbstract:
Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.
32
Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.
Full textAbstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
33
Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.
Full textAbstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
34
Thakore, Nimish J., and Erik P. Pioro. Clinical Presentations, Diagnostic Criteria, and Lab Testing. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0023.
Full textAbstract:
Amyotrophic lateral sclerosis (ALS) is the protypical motor neuron disease, which is characterized by the simultaneous presence of upper motor neuron (UMN) and lower motor neuron (LMN) signs in the same extremity or in the cranial-bulbar region. UMN signs at spinal levels include spasticity, slowness of motor activation, hyperactive deep tendon reflexes and extensor plantar responses, whereas UMN signs at the cranial level include spastic dysarthia (slow, labored, nasal); slowness of tongue movements, and hyperactive jaw, gag, and facial reflexes. LMN signs at the spinal level include muscle atrophy, fasciculations, and weakness and LMN signs at the cranial level include tongue atrophy and weakness, facial weakness, tongue and facial fasciculations, palatal weakness, weak cough, and dysphonia. ALA is fatal in 2 to 4 years, and the only medication known to prolong tracheostomy-free survival
35
Speer, Thimoteus, and Danilo Fliser. Abnormal endothelial vasomotor and secretory function. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0113.
Full textAbstract:
The endothelium plays a crucial role in the maintenance of vascular integrity and function. Nitric oxide produced by endothelial cells is a key player, inducing relaxation of vascular smooth muscle cells, inhibition of vascular inflammation, and prevention of coagulatory activation. Chronic kidney disease (CKD) is characterized by deterioration of different protective endothelial properties, collectively described as endothelial dysfunction. Several factors such as methylarginines, modified lipoproteins, and other substances that accumulate may be involved in the pathogenesis of endothelial dysfunction of CKD. Endothelial dysfunction is suggested to be the first critical step in the initiation of atherosclerosis. Clinical assessment of endothelial function may become important in recognition of patients with increased cardiovascular risk. Beside several invasive and non-invasive methods to assess endothelial function in vivo, measurement of circulating (bio)markers may be useful for the evaluation of endothelial dysfunction.
36
Sánchez-Quintana, Damián, and José Angel Cabrera. Normal atrial and ventricular myocardial structures. Edited by Yen Ho. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0014.
Full textAbstract:
The heart functions by means of a three-dimensional arrangement of myofibres supported by an extracellular matrix which plays an important role in maintaining the size and shape of the heart. In both atria, the structure of the walls and the atrial septum confers a three-dimensional arrangement of muscle bundles and myoarchitecture that allows preferential electrical intra- and interatrial conduction which is important for a better understanding of atrial activation and arrhythmias. The myoarchitecture within the ventricular walls has a three-dimensional arrangement of myofibres, within a supporting matrix of fibrous tissue, which changes orientation from being oblique in the subepicardium to circumferential in the middle and to longitudinal in the subendocardium, allowing the chambers to change in shape and size through the cardiac cycle. Within each ventricle, the circumferential portion is the thickest transmurally, with the longitudinal portion the thinnest. The three-dimensional arrangement of the ventricular mesh serves to realign the myocytes during ventricular contraction, accounting for the extent of systolic mural thickening. Abnormal myoarchitecture in combination with alterations in the connective tissue matrix provide the structural basis for abnormalities in myocardial function.
37
Aoki, Cynthia R. A. Activating the cAMP-PKA pathway modulates genioglossus muscle and responses to excitatory inputs. 2005.
Find full text
38
Broussal-Derval, Aurélien, and Stéphane Ganneau. The Modern Art and Science of Mobility. Human Kinetics, 2020. http://dx.doi.org/10.5040/9781718214606.
Full textAbstract:
The Modern Art and Science of Mobility is a striking visual guide to releasing muscle tension and activating muscles for functional motion. It goes beyond traditional training methods that focus on performance and aesthetics and asks these simple questions: Are you truly reaping the full benefits of training if it does not include mobility exercises? Why are the vast majority of people, even the most athletic individuals, unable to perform basic motor tasks without pain or difficulty? Why are physically active people still dealing with lack of mobility and chronic injury? Whether you are a casual exerciser or an elite athlete, you will learn how to preserve and maintain your body with over 300 exercises designed to improve mobility, facilitate recovery, reduce pain, and activate muscles. Utilize the self-tests to assess your current level of mobility, and then choose from over 50 prescriptive training routines that can be used as is or customized to target specific functional chains. You’ll find exercise recommendations based on body region, activity, and primary goal, and you’ll learn to incorporate a variety of techniques and popular equipment, including resistance bands, foam rollers, massage balls, and stability balls. The Modern Art and Science of Mobility provides a stunning visual presentation with over 1,200 photos and 100 original illustrations by Stéphane Ganneau. His illustrations highlight the muscles with precision, and his avant-garde style and the harmony of colors give this book a unique graphic signature. Mobility is the foundation for training your best and feeling your best. The Modern Art and Science of Mobility will help you do just that by helping you to alleviate pain, improve posture, and release muscle tension for a more comfortable and enjoyable quality of life.
39
Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0022.
Full textAbstract:
Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
40
Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_002.
Full textAbstract:
Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
41
Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_003.
Full textAbstract:
Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
42
The effects of lifting posture and muscular fatigue on erector spinae activation in normals and weight lifters. 1991.
Find full text
43
The effects of lifting posture and muscular fatigue on erector spinae activation in normals and weight lifters. 1991.
Find full text
44
The effects of lifting posture and muscular fatigue on erector spinae activation in normals and weight lifters. 1990.
Find full text
45
Whitworth, Caroline, and Stewart Fleming. Malignant hypertension. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0216.
Full textAbstract:
Malignant hypertension (MH) is recognized clinically by elevated blood pressure together with retinal haemorrhages or exudates with or without papilloedema (grades III or IV hypertensive retinopathy); and may constitute a hypertensive emergency or crisis when complicated by evidence of end-organ damage including microangiopathic haemolysis, encephalopathy, left ventricular failure, and renal failure. Though reversible, it remains a significant cause of end-stage renal failure, and of cardiovascular and cerebrovascular morbidity and mortality in developing countries.MH can complicate pre-existing hypertension arising from diverse aetiologies, but most commonly develops from essential hypertension. The absolute level of blood pressure appears not to be critical to the development of MH, but the rate of rise of blood pressure may well be relevant in the pathogenesis. The pathogenesis of this transformation remains unclear.The pathological hallmark of MH is the presence of fibrinoid necrosis (medial vascular smooth muscle cell necrosis and fibrin deposition within the intima) involving the resistance arterioles in many organs. Fibrinoid necrosis is not specific to MH and this appearance is seen in other conditions causing a thrombotic microangiopathy such as haemolytic uraemic syndrome, scleroderma renal crisis, antiphospholipid syndrome, and acute vascular rejection post transplant. MH can both cause a thrombotic microangiopathy (TMA) but can also complicate underlying conditions associated with TMA.The pathophysiological factors that interact to generate and sustain this condition remain poorly understood. Risk factors include Afro-Caribbean race, smoking history, younger age of onset of hypertension, previous pregnancy, and untreated hypertension associated with non-compliance or cessation of antihypertensive therapy.Evidence from clinical studies and animal models point to a central role for the intrarenal renin–angiotensin system (RAS) in MH; there is good evidence for renal vasoconstriction and activation of the renal paracrine RAS potentiating MH once established; however, there may also be a role in the predisposition of MH suggested by presence of increased risk conferred by an ACE gene polymorphism in humans and polymorphisms for both ACE and AT1 receptor in an animal model of spontaneous MH. Other vasoactive mediators such as the endothelin and the inflammatory response may be important contributing to and increasing endothelial damage. There have been no randomized controlled trials to define the best treatment approach, but progressive lowering of pressures over days is considered safest unless made more urgent by critical clinical state. It seems logical to introduce ACE inhibition cautiously and early, but in view of the risk of rapid pressure lowering some recommend delay.
46
RYAN, Natasha. Sirt Diet: A Beginner's Guide to Sirt Food, Lose Weight While Eating, Like You're Not on a Diet. Burns Fat and Increases Muscle Mass by Activating Lean Genes. Independently Published, 2020.
Find full text