Skeletal muscle physiology and damage

2013 ◽  
pp. 404-408
Author(s):  
Robert Dinser ◽  
Ulf Müller-Ladner
Keyword(s):  
Molecular Structure ◽  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Muscle Tissue ◽  
Muscle Function ◽  
Clinical Analysis ◽  
Basic Function ◽  
Muscle Disease ◽  
Muscle Physiology ◽  
Physiological Ageing

This chapter summarizes muscle structure and physiology, the genesis and adaptions of muscle throughout life, and clinical assessment of muscle disease. The anatomical and molecular structure of muscle tissue is described, as well as the basic function of the neuromuscular junction, the energy metabolism of muscle tissue, and the mechanisms of fatigue. Key elements of embryological myogenesis, the adaptions of muscle to exercise and damage, and physiological ageing are depicted. A summary of the clinical analysis of muscle function including laboratory, electrophysiological, and imaging testing is provided.

Skeletal muscle physiology and damage

2018 ◽  
Author(s):  
Robert Dinser ◽  
Ulf Müller-Ladner
Keyword(s):  
Molecular Structure ◽  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Muscle Tissue ◽  
Muscle Function ◽  
Clinical Analysis ◽  
Basic Function ◽  
Muscle Disease ◽  
Muscle Physiology ◽  
Physiological Ageing

This chapter summarizes muscle structure and physiology, the genesis and adaptions of muscle throughout life, and clinical assessment of muscle disease. The anatomical and molecular structure of muscle tissue is described, as well as the basic function of the neuromuscular junction, the energy metabolism of muscle tissue, and the mechanisms of fatigue. Key elements of embryological myogenesis, the adaptions of muscle to exercise and damage, and physiological ageing are depicted. A summary of the clinical analysis of muscle function including laboratory, electrophysiological, and imaging testing is provided.

Skeletal muscle physiology and damage

2013 ◽  
Author(s):  
Robert Dinser ◽  
Ulf Müller-Ladner
Keyword(s):  
Molecular Structure ◽  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Muscle Tissue ◽  
Muscle Function ◽  
Clinical Analysis ◽  
Basic Function ◽  
Muscle Disease ◽  
Muscle Physiology ◽  
Physiological Ageing

This chapter summarizes muscle structure and physiology, the genesis and adaptions of muscle throughout life, and clinical assessment of muscle disease. The anatomical and molecular structure of muscle tissue is described, as well as the basic function of the neuromuscular junction, the energy metabolism of muscle tissue, and the mechanisms of fatigue. Key elements of embryological myogenesis, the adaptions of muscle to exercise and damage, and physiological ageing are depicted. A summary of the clinical analysis of muscle function including laboratory, electrophysiological, and imaging testing is provided.

Alterations in activin A–myostatin–follistatin system associate with disease activity in inflammatory myopathies

Rheumatology ◽  
2020 ◽  
Vol 59 (9) ◽  
pp. 2491-2501 ◽  
Author(s):  
Lucia Vernerová ◽  
Veronika Horváthová ◽  
Tereza Kropáčková ◽  
Martina Vokurková ◽  
Martin Klein ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Disease Activity ◽  
Muscle Tissue ◽  
Activin A ◽  
Muscle Disease ◽  
Manual Muscle Testing ◽  
Healthy Controls ◽  
Inflammatory Myopathies ◽  
Muscle Testing ◽  
Tgf Β1

Abstract Objectives The aim of this study was to investigate the systemic and skeletal muscle levels of atrophy-associated myokines in patients with idiopathic inflammatory myopathies (IIM) and their association with clinical characteristics of myositis. Methods A total of 94 IIM patients and 162 healthy controls were recruited. Of those, 20 IIM patients and 28 healthy controls underwent a muscle biopsy. Circulating concentrations of myostatin, follistatin, activin A and TGF-β1 were assessed by ELISA. The expression of myokines and associated genes involved in the myostatin signalling pathway in muscle tissue was determined by real-time PCR. Results We report decreased levels of circulating myostatin (median 1817 vs 2659 pg/ml; P = 0.003) and increased follistatin (1319 vs 1055 pg/ml; P = 0.028) in IIM compared with healthy controls. Activin A levels were also higher in IIM (414 vs 309 pg/ml; P = 0.0005) compared with controls. Myostatin was negatively correlated to muscle disease activity assessed by physician on visual analogue scale (MDA) (r = −0.289, P = 0.015) and positively to manual muscle testing of eight muscles (r = 0.366, P = 0.002). On the other hand, follistatin correlated positively with MDA (r = 0.235, P = 0.047). Gene expression analysis showed higher follistatin (P = 0.003) and myostatin inhibitor follistatin-like 3 protein (FSTL3) (P = 0.008) and lower expression of activin receptor type 1B (ALK4) (P = 0.034), signal transducer SMAD3 (P = 0.023) and atrophy marker atrogin-1 (P = 0.0009) in IIM muscle tissue compared with controls. Conclusion This study shows lower myostatin and higher follistatin levels in circulation and attenuated expression of myostatin pathway signalling components in skeletal muscle of patients with myositis, a newly emerging pattern of the activin A–myostatin–follistatin system in muscle wasting diseases.

scholarly journals Global and local tension measurements in biomimetic skeletal muscle tissues reveals early mechanical homeostasis

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Arne D Hofemeier ◽  
Tamara Limon ◽  
Till Moritz Muenker ◽  
Bernhard Wallmeyer ◽  
Alejandro Jurado ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Resolution ◽  
Muscle Tissue ◽  
Muscle Function ◽  
Force Measurements ◽  
Skeletal Muscle Function ◽  
Hydrogel Beads ◽  
Investigation Methods ◽  
Global Force

Tension and mechanical properties of muscle tissue are tightly related to proper skeletal muscle function, which makes experimental access to the biomechanics of muscle tissue formation a key requirement to advance our understanding of muscle function and development. Recently developed elastic in vitro culture chambers allow for raising 3D muscle tissue under controlled conditions and to measure global tissue force generation. However, these chambers are inherently incompatible with high-resolution microscopy limiting their usability to global force measurements, and preventing the exploitation of modern fluorescence based investigation methods for live and dynamic measurements. Here, we present a new chamber design pairing global force measurements, quantified from post-deflection, with local tension measurements obtained from elastic hydrogel beads embedded in muscle tissue. High-resolution 3D video microscopy of engineered muscle formation, enabled by the new chamber, shows an early mechanical tissue homeostasis that remains stable in spite of continued myotube maturation.

scholarly journals Evaluation of Skeletal Muscle Function and Effects of Early Rehabilitation during Acute Heart Failure: Rationale and Study Design

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Kinga Węgrzynowska-Teodorczyk ◽  
Agnieszka Siennicka ◽  
Krystian Josiak ◽  
Robert Zymliński ◽  
Monika Kasztura ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Acute Heart Failure ◽  
Muscle Tissue ◽  
Muscle Function ◽  
Skeletal Muscles ◽  
Group Versus ◽  
The Body ◽  
Skeletal Muscle Function ◽  
Peripheral Tissues

Background. Acute heart failure (AHF) is associated with disturbances of the peripheral perfusion leading to the dysfunction of many organs. Consequently, an episode of AHF constitutes a “multiple organ failure” which may also affect the skeletal muscles. However, the abnormalities within skeletal muscles during AHF have not been investigated so far. The aim of this project is to comprehensively evaluate skeletal muscles (at a functional and tissue level) during AHF. Methods. The study will include ≥63 consecutive AHF patients who will be randomized into 2 groups: ≥42 with cardiac rehabilitation group versus ≥21 with standard pharmacotherapy alone. The following tests will be conducted on the first and last day of hospitalization, at rest and after exercise, and 30 days following the discharge: clinical evaluation, medical interview, routine physical examination, echocardiography, and laboratory tests (including the assessment of NT-proBNP, inflammatory markers, and parameters reflecting the status of the kidneys and the liver); hemodynamic evaluation, noninvasive determination of cardiac output and systemic vascular resistance using the impedance cardiography; evaluation of biomarkers reflecting myocyte damage, immunochemical measurements of tissue-specific enzymatic isoforms; evaluation of skeletal muscle function, using surface electromyography (sEMG) (maximum tonus of the muscles will be determined along with the level of muscular fatigability); evaluation of muscle tissue perfusion, assessed on the basis of the oxygenation level, with noninvasive direct continuous recording of perfusion in peripheral tissues by local tissue oximetry, measured by near-infrared spectroscopy (NIRS). Results and Conclusions. Our findings will demonstrate that the muscle tissue is another area of the body which should be taken into consideration in the course of treatment of AHF, requiring a development of targeted therapeutic strategies, such as a properly conducted rehabilitation.

scholarly journals Skeletal muscle function and water permeability in aquaporin-4 deficient mice

2000 ◽  
Vol 278 (6) ◽  
pp. C1108-C1115 ◽  
Author(s):  
Baoxue Yang ◽  
Jean-Marc Verbavatz ◽  
Yuanlin Song ◽  
L. Vetrivel ◽  
Geoffrey Manley ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Water Permeability ◽  
Muscle Function ◽  
Force Generation ◽  
Muscle Physiology ◽  
Wild Type ◽  
Volume Changes ◽  
Skeletal Muscle Function ◽  
Performance Time ◽  
Aqp4 Protein

It has been proposed that aquaporin-4 (AQP4), a water channel expressed at the plasmalemma of skeletal muscle cells, is important in normal muscle physiology and in the pathophysiology of Duchenne's muscular dystrophy. To test this hypothesis, muscle water permeability and function were compared in wild-type and AQP4 knockout mice. Immunofluorescence and freeze-fracture electron microscopy showed AQP4 protein expression in plasmalemma of fast-twitch skeletal muscle fibers of wild-type mice. Osmotic water permeability was measured in microdissected muscle fibers from the extensor digitorum longus (EDL) and fractionated membrane vesicles from EDL homogenates. With the use of spatial-filtering microscopy to measure osmotically induced volume changes in EDL fibers, half times ( t 1/2) for osmotic equilibration (7.5–8.5 s) were not affected by AQP4 deletion. Stopped-flow light-scattering measurements of osmotically induced volume changes in plasmalemma vesicles also showed no significant differences in water permeability. Similar water permeability, yet ∼90% decreased AQP4 protein expression was found in EDL from mdx mice that lack dystrophin. Skeletal muscle function was measured by force generation in isolated EDL, treadmill performance time, and in vivo muscle swelling in response to water intoxication. No differences were found in EDL force generation after electrical stimulation [42 ± 2 (wild-type) vs. 41 ± 2 (knockout) g/s], treadmill performance time (22 vs. 26 min; 29 m/min, 13° incline), or muscle swelling (2.8 vs. 2.9% increased water content at 90 min after intraperitoneal water infusion). Together these results provide evidence against a significant role of AQP4 in skeletal muscle physiology in mice.

scholarly journals Working around the clock: circadian rhythms and skeletal muscle

2009 ◽  
Vol 107 (5) ◽  
pp. 1647-1654 ◽  
Author(s):  
Xiping Zhang ◽  
Thomas J. Dube ◽  
Karyn A. Esser
Keyword(s):  
Skeletal Muscle ◽  
Molecular Clock ◽  
Time Of Day ◽  
Muscle Disease ◽  
Muscle Physiology ◽  
Skeletal Muscle Function ◽  
Temporal Specificity ◽  
Muscle Research ◽  
Normal Expression ◽  
Normal Metabolism

The study of the circadian molecular clock in skeletal muscle is in the very early stages. Initial research has demonstrated the presence of the molecular clock in skeletal muscle and that skeletal muscle of a clock-compromised mouse, Clock mutant, exhibits significant disruption in normal expression of many genes required for adult muscle structure and metabolism. In light of the growing association between the molecular clock, metabolism, and metabolic disease, it will also be important to understand the contribution of circadian factors to normal metabolism, metabolic responses to muscle training, and contribution of the molecular clock in muscle-to-muscle disease (e.g., insulin resistance). Consistent with the potential for the skeletal muscle molecular clock modulating skeletal muscle physiology, there are findings in the literature that there is significant time-of-day effects for strength and metabolism. Additionally, there is some recent evidence that temporal specificity is important for optimizing training for muscular performance. While these studies do not prove that the molecular clock in skeletal muscle is important, they are suggestive of a circadian contribution to skeletal muscle function. The application of well-established models of skeletal muscle research in function and metabolism with available genetic models of molecular clock disruption will allow for more mechanistic understanding of potential relationships.

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