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

2020 ◽  
Author(s):  
Arne D. Hofemeier ◽  
Tamara Limon ◽  
Till M. Muenker ◽  
Bernhard Wallmeyer ◽  
Alejandro Jurado ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Resolution ◽  
Muscle Tissue ◽  
Muscle Function ◽  
Muscle Development ◽  
Force Measurements ◽  
Skeletal Muscle Function ◽  
Investigation Methods ◽  
Global Force

AbstractThe mechanical properties and tension of muscle tissue are tightly related to proper skeletal muscle function, which makes experimental access to the biomechanics of muscle tissue development 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 measurements of 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 the muscle tissue. High resolution 3D video microscopy of engineered muscle development, enabled by the new chamber, shows an early mechanical tissue homeostasis that remains stable in spite of continued myotube maturation.

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 Role of TRPC1 channel in skeletal muscle function

2010 ◽  
Vol 298 (1) ◽  
pp. C149-C162 ◽  
Author(s):  
Nadège Zanou ◽  
Georges Shapovalov ◽  
Magali Louis ◽  
Nicolas Tajeddine ◽  
Chiara Gallo ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Transient Receptor Potential ◽  
Force Production ◽  
Receptor Potential ◽  
Cross Sectional Area ◽  
Sectional Area ◽  
Skeletal Muscle Function ◽  
Cross Sectional

Skeletal muscle contraction is reputed not to depend on extracellular Ca2+. Indeed, stricto sensu , excitation-contraction coupling does not necessitate entry of Ca2+. However, we previously observed that, during sustained activity (repeated contractions), entry of Ca2+is needed to maintain force production. In the present study, we evaluated the possible involvement of the canonical transient receptor potential (TRPC)1 ion channel in this entry of Ca2+and investigated its possible role in muscle function. Patch-clamp experiments reveal the presence of a small-conductance channel (13 pS) that is completely lost in adult fibers from TRPC1−/−mice. The influx of Ca2+through TRPC1 channels represents a minor part of the entry of Ca2+into muscle fibers at rest, and the activity of the channel is not store dependent. The lack of TRPC1 does not affect intracellular Ca2+concentration ([Ca2+]i) transients reached during a single isometric contraction. However, the involvement of TRPC1-related Ca2+entry is clearly emphasized in muscle fatigue. Indeed, muscles from TRPC1−/−mice stimulated repeatedly progressively display lower [Ca2+]itransients than those observed in TRPC1+/+fibers, and they also present an accentuated progressive loss of force. Interestingly, muscles from TRPC1−/−mice display a smaller fiber cross-sectional area, generate less force per cross-sectional area, and contain less myofibrillar proteins than their controls. They do not present other signs of myopathy. In agreement with in vitro experiments, TRPC1−/−mice present an important decrease of endurance of physical activity. We conclude that TRPC1 ion channels modulate the entry of Ca2+during repeated contractions and help muscles to maintain their force during sustained repeated contractions.

scholarly journals The Influence of Supplemental Dietary Linoleic Acid on Skeletal Muscle Contractile Function in a Rodent Model of Barth Syndrome

2021 ◽  
Vol 12 ◽  
Author(s):  
Mario Elkes ◽  
Martin Andonovski ◽  
Daislyn Vidal ◽  
Madison Farago ◽  
Ryan Modafferi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Linoleic Acid ◽  
Muscle Function ◽  
Barth Syndrome ◽  
Dietary Linoleic Acid ◽  
Skeletal Muscle Function ◽  
Contractile Phenotype ◽  
Muscle Contractile

Barth syndrome is a rare and incurable X-linked (male-specific) genetic disease that affects the protein tafazzin (Taz). Taz is an important enzyme responsible for synthesizing biologically relevant cardiolipin (for heart and skeletal muscle, cardiolipin rich in linoleic acid), a critical phospholipid of mitochondrial form and function. Mutations to Taz cause dysfunctional mitochondria, resulting in exercise intolerance due to skeletal muscle weakness. To date, there has been limited research on improving skeletal muscle function, with interventions focused on endurance and resistance exercise. Previous cell culture research has shown therapeutic potential for the addition of exogenous linoleic acid in improving Taz-deficient mitochondrial function but has not been examined in vivo. The purpose of this study was to examine the influence of supplemental dietary linoleic acid on skeletal muscle function in a rodent model of Barth syndrome, the inducible Taz knockdown (TazKD) mouse. One of the main findings was that TazKD soleus demonstrated an impaired contractile phenotype (slower force development and rates of relaxation) in vitro compared to their WT littermates. Interestingly, this impaired contractile phenotype seen in vitro did not translate to altered muscle function in vivo at the whole-body level. Also, supplemental linoleic acid attenuated, to some degree, in vitro impaired contractile phenotype in TazKD soleus, and these findings appear to be partially mediated by improvements in cardiolipin content and resulting mitochondrial supercomplex formation. Future research will further examine alternative mechanisms of dietary supplemental LA on improving skeletal muscle contractile dysfunction in TazKD mice.

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 Effect of pulmonary TNF-α overexpression on mouse isolated skeletal muscle function

2011 ◽  
Vol 301 (4) ◽  
pp. R1025-R1031 ◽  
Author(s):  
Li Zuo ◽  
Leonardo Nogueira ◽  
Michael C. Hogan
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Weight Ratio ◽  
The Body ◽  
Chronic Obstructive ◽  
Skeletal Muscle Function ◽  
Muscle Weight ◽  
Peak Rate ◽  
Tnf Α

TNF-α is a proinflammatory cytokine that is involved in numerous pathological processes including chronic obstructive pulmonary disease (COPD). In the present study, we used a transgenic mouse model that overexpresses TNF-α in the lung (Tg+) to test the hypothesis that chronic exposure to TNF-α (as seen in COPD) reduces skeletal muscle force production and fatigue resistance, particularly under low Po2 conditions. At 7–12 mo, body and muscle weight of both extensor digitorum longus (EDL) and soleus were significantly smaller in Tg+ compared with littermate wild-type (WT) mice; however, the body-to-muscle weight ratio was not different between groups. EDL and soleus muscles were subjected to in vitro fatiguing contractile periods under high (∼550 Torr) and low Po2 (∼40 Torr). Although all muscles were less fatigue-resistant during low Po2 compared with high Po2, only the soleus fatigued more rapidly in Tg+ mice (∼12%) compared with WT at high Po2. The maximal tension of EDL was equally reduced in Tg+ mice (28–34% decrease from WT under both Po2 conditions); but for soleus this parameter was smaller only under low Po2 in Tg+ mice (∼31% decrease from WT). The peak rate of relaxation and the peak rate of contraction were both significantly reduced in Tg+ EDL muscles compared with WT EDL under low Po2 conditions, but not in soleus. These results demonstrate that TNF-α upregulation in the lung impairs peripheral skeletal muscle function but affects fast- and slow-twitch muscles differentially at high and low Po2.

scholarly journals Ang-(1-7) Protects Skeletal Muscle Function in Aged Mice

2021 ◽  
Author(s):  
Xiaoli Huang ◽  
Jiao Song ◽  
Yangyang Jiang ◽  
Xue Yang ◽  
Li Cao ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Glucose Transporter ◽  
C2c12 Cells ◽  
Protective Effects ◽  
Skeletal Muscle Function ◽  
Aged Mice ◽  
Age Related ◽  
The Impact

Abstract Background: The angiotensin-converting enzyme 2 (ACE2)/angiotensin 1-7 (Ang-(1-7)) axis has been shown to perform a protective task in the decline of the function of skeletal muscle correlated with the process of aging. In the present investigation, the protective effects of ACE2 in mitigating the age-associated decline of skeletal function and identified the potential underlying molecular mechanism mediating the process have been extensively evaluated.Methods: We measured the expression levels of Ang-(1-7) in C57BL/6J mice of different ages and correlated these levels with measures of skeletal muscle function. Also, we determine the expression of myocyte enhancer factor 2A (MEF2A) were detected in ACE2 knockout (ACE2KO) and correlated with muscle function. We then treated ACE2KO aged mice for 4 weeks with Ang-(1-7) and characterized the levels of MEF2A and skeletal muscle function before and after treatment. We assessed the impact of Ang-(1-7) on the growth and differentiation of C2C12 cells in vitro and assessed changes in the glucose transporter type 4 (Glut4) expression.Results: Aged mice showed reduced skeletal muscle function and levels of Ang-(1-7) expression in comparison to young and middle-aged mice. In ACE2KO mice, skeletal muscle function and MEF2A protein expression were significantly lower than in age-matched WT mice. After 1 month of the treatment of Ang-(1-7), the function of skeletal muscle related to the aged ACE2KO mice improved, however, the expression of MEF2A protein was similar to that in the untreated group. In C2C12 cells, Ang-(1-7) was shown to increased cell growth and differentiation characteristics along with the upregulated expression of Glut4.Conclusions: The axis of ACE2/ Ang-(1-7) has a protective task in skeletal muscle and the administration of exogenous Ang-(1-7) can delay the age-related decline in the functions of skeletal muscle.

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