scholarly journals The Impact of Obesity on In Vivo Human Skeletal Muscle Function

2013 ◽  
Vol 2 (3) ◽  
pp. 251-260 ◽  
Author(s):  
Nicola A. Maffiuletti ◽  
Sébastien Ratel ◽  
Alessandro Sartorio ◽  
Vincent Martin
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Human Skeletal Muscle ◽  
Skeletal Muscle Function ◽  
The Impact

Effects of In Vivo Doxorubicin Treatment on Skeletal Muscle Function

2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 903
Author(s):  
David S. Hydock ◽  
Chia-Ying Lien ◽  
Brock T. Jensen ◽  
Traci L. Parry ◽  
Carole M. Schneider ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Skeletal Muscle Function ◽  
Doxorubicin Treatment

scholarly journals In vivo Skeletal Muscle Function and Doxorubicin Treatment in the Rat

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
David Hydock ◽  
Asma Omar ◽  
Eric Bredahl ◽  
Colin Quinn
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Skeletal Muscle Function ◽  
Doxorubicin Treatment

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.

Effects of prolonged hypobaric hypoxia on human skeletal muscle function and electromyographic events

2000 ◽  
Vol 98 (3) ◽  
pp. 329 ◽  
Author(s):  
F. CAQUELARD ◽  
H. BURNET ◽  
F. TAGLIARINI ◽  
E. CAUCHY ◽  
J.P. RICHALET ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Hypobaric Hypoxia ◽  
Human Skeletal Muscle ◽  
Skeletal Muscle Function

scholarly journals Gut bacteria are critical for optimal muscle function: a potential link with glucose homeostasis

2019 ◽  
Vol 317 (1) ◽  
pp. E158-E171 ◽  
Author(s):  
Kevin Nay ◽  
Maxence Jollet ◽  
Benedicte Goustard ◽  
Narjes Baati ◽  
Barbara Vernus ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Gut Microbiota ◽  
Muscle Function ◽  
Ex Vivo ◽  
Gut Bacteria ◽  
Muscle Endurance ◽  
Endurance Capacity ◽  
Skeletal Muscle Function ◽  
Fatty Acid Chain ◽  
The Impact

Gut microbiota is involved in the development of several chronic diseases, including diabetes, obesity, and cancer, through its interactions with the host organs. It has been suggested that the cross talk between gut microbiota and skeletal muscle plays a role in different pathological conditions, such as intestinal chronic inflammation and cachexia. However, it remains unclear whether gut microbiota directly influences skeletal muscle function. In this work, we studied the impact of gut microbiota modulation on mice skeletal muscle function and investigated the underlying mechanisms. We determined the consequences of gut microbiota depletion after treatment with a mixture of a broad spectrum of antibiotics for 21 days and after 10 days of natural reseeding. We found that, in gut microbiota-depleted mice, running endurance was decreased, as well as the extensor digitorum longus muscle fatigue index in an ex vivo contractile test. Importantly, the muscle endurance capacity was efficiently normalized by natural reseeding. These endurance changes were not related to variation in muscle mass, fiber typology, or mitochondrial function. However, several pertinent glucose metabolism markers, such as ileum gene expression of short fatty acid chain and glucose transporters G protein-coupled receptor 41 and sodium-glucose cotransporter 1 and muscle glycogen level, paralleled the muscle endurance changes observed after treatment with antibiotics for 21 days and reseeding. Because glycogen is a key energetic substrate for prolonged exercise, modulating its muscle availability via gut microbiota represents one potent mechanism that can contribute to the gut microbiota-skeletal muscle axis. Taken together, our results strongly support the hypothesis that gut bacteria are required for host optimal skeletal muscle function.

scholarly journals In vivo characterization of skeletal muscle function in nebulin‐deficient mice

2020 ◽  
Vol 61 (3) ◽  
pp. 416-424
Author(s):  
Charlotte Gineste ◽  
Augustin C. Ogier ◽  
Isabelle Varlet ◽  
Zaynab Hourani ◽  
Monique Bernard ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Skeletal Muscle Function ◽  
In Vivo Characterization ◽  
Deficient Mice

141 Mild Burns Combined with Diet Induced Demyelination Does Not Affect Skeletal Muscle Function

2021 ◽  
Vol 42 (Supplement_1) ◽  
pp. S94-S94
Author(s):  
Emre Vardarli ◽  
Nisha Bhattarai ◽  
Amina El Ayadi ◽  
Y E Wang ◽  
Jayson W Jay ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Diet Group ◽  
Muscle Dysfunction ◽  
Skeletal Muscle Function ◽  
Regular Diet ◽  
Skeletal Muscle Dysfunction ◽  
Significant Difference ◽  
The Impact

Abstract Introduction Severe burns result in decreased skeletal muscle mass and function. Recent evidence suggests that massive burns disrupt the motor-neural system including motor neurons to partially explain skeletal muscle dysfunction in response to burns. However, impact of demyelination on burn induced skeletal muscle dysfunction has not been investigated. The purpose of this study was to determine the impact of exaggerated demyelination on skeletal muscle dysfunction after burn. Methods C57BL/6 (20-25g, male, n = 26) mice were separated into 6 groups (4–5 animals per group) by diet, burn injury and timepoint (burn or sham groups with two different diets measured at two different timepoints). Mice were fed with either cuprizone diet (0.2 %) to induce severe demyelination or regular diet (18 % protein) for 5 weeks prior to injury. Burns were administered by immersing the dorsal side of the animal into ~95 °C hot water for 10 seconds (~15 % body surface area, full thickness burn). In-situ gastrocnemius function was assessed by attaching the distal tendon of the muscle to a lever arm of a force transducer and stimulating the muscle via exposed sciatic nerve while the animal was under anesthesia. In-situ gastrocnemius muscle function was evaluated 3- and 7-days after burn. Results Food intake was 30 % higher in cuprizone diet group compared to the regular diet group (p=0.002). However, there was no significant difference in body weight among groups (p=0.071). No significant difference was found in gastrocnemius wet weight, peak twitch tension, time to reach peak twitch tension, peak twitch half relaxation time, force-frequency relationship, maximum tetanic force, and fatigue index among groups (burn effect, diet effect, time effect, and their interactions; NS). Conclusions Mild burns combined with demyelination by diet had no effect on skeletal muscle function on our timepoints, and 15 % TBSA burn size was not sufficient to induce skeletal muscle dysfunction. The impact of burn induced neural damage on muscle function and performance indicates further investigation.

The Versatility of the Pump-Perfused Rat Hindlimb Preparation: Examples Relating to Skeletal Muscle Function and Energy Metabolism

2005 ◽  
Vol 30 (5) ◽  
pp. 576-590 ◽  
Author(s):  
David J. Baker ◽  
Russell T. Hepple
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Muscle Function ◽  
Exercise Physiology ◽  
Muscle Metabolism ◽  
Perfusion Medium ◽  
Skeletal Muscle Function ◽  
And Control ◽  
Fast Freezing

The pump-perfused rat hindlimb model, in various forms, has been in use for several decades. There are many applications for this model, owing to the ability to control the content and rate of perfusion. In the context of exercise physiology this model has been put to particularly good use. In this report we summarize some of the central surgical differences between different versions of the pump-perfused rat hindlimb model, including the double hindlimb + trunk, double hindlimb alone, single hindlimb, and distal hindlimb-alone models. We also summarize specific elements of the perfusion medium and measurement of force used in our lab during assessment of muscle metabolic and contractile responses, and illustrate some of the differences from the in vivo condition that merit consideration. We then provide specific examples of how the single pump-perfused hindlimb and distal hindlimb-alone versions of this model have been used to study muscle function and energy metabolism. In this context we show how this model can be used to permit the experimenter to manipulate and control the rate of O2delivery and to add specific compounds that inhibit a particular aspect of muscle metabolism, such that in combination with measurements of the flux of specific substances across the muscle and/or fast-freezing of muscle after contractions, more can be understood about the metabolic state of the contracting muscles. Key words: aerobic metabolism, mitochondria, aging, adaptation

Effect of in vivo inhibition of neutrophil adherence on skeletal muscle function during ischemia in ferrets

1991 ◽  
Vol 261 (4) ◽  
pp. H1178-H1183
Author(s):  
E. O. Weselcouch ◽  
R. I. Grove ◽  
C. D. Demusz ◽  
A. J. Baird
Keyword(s):  
Skeletal Muscle ◽  
Monoclonal Antibody ◽  
Muscle Function ◽  
Peak Force ◽  
Control Group ◽  
Protective Effects ◽  
Normal Flow ◽  
Skeletal Muscle Function ◽  
Time Curve

Neutrophils are reported to play an important role in the genesis of tissue damage during reperfusion after periods of ischemia in a variety of organs and may also be involved in loss of tissue function during ischemia. To test this hypothesis, the monoclonal antibody, MoAb 60.3, which prevents the adhesion of ferret neutrophils to cultured human endothelial cells at a concentration of 30 micrograms/ml, was tested in a model of peripheral vascular disease to determine whether it would preserve skeletal muscle function during ischemia. In an anesthetized ferret the muscles of the hindlimb were stimulated electrically to contract isometrically and the force of contraction was measured. Under normal perfusion conditions the contractile force peaked within 1 or 2 min of initiation of stimulation and gradually declined to approximately 80% of peak force after 20 min. When femoral arterial pressure was reduced to 45 mmHg by partial occlusion of the abdominal aorta, peak force was reduced by 25 +/- 7%, and within 5 min the force decayed to approximately 20% of the original peak, resulting in an area under the force-time curve (AUC) of 32 +/- 5% of that seen during the normal flow period. During ischemia after treatment with MoAb 60.3 (2 mg/kg iv), peak force was 94 +/- 3% and AUC was 49 +/- 5% of that observed during the normal flow period, a significant protective effect compared with the untreated control group (P = 0.0294). When the nonneutrophil-directed monoclonal antibody, L6, was tested in this model, no protective effects were evident.(ABSTRACT TRUNCATED AT 250 WORDS)

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