scholarly journals Acute Elevated Glucose Promotes Abnormal Action Potential-Induced Ca2+Transients in Cultured Skeletal Muscle Fibers

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Erick O. Hernández-Ochoa ◽  
Quinton Banks ◽  
Martin F. Schneider
Keyword(s):  
Skeletal Muscle ◽  
High Speed ◽  
Muscle Fibers ◽  
Muscle Dysfunction ◽  
Intermediate Step ◽  
Temporal Properties ◽  
Intracellular Ca ◽  
Elevated Glucose ◽  
Underlying Mechanisms ◽  
The Impact

A common comorbidity of diabetes is skeletal muscle dysfunction, which leads to compromised physical function. Previous studies of diabetes in skeletal muscle have shown alterations in excitation-contraction coupling (ECC)—the sequential link between action potentials (AP), intracellular Ca2+release, and the contractile machinery. Yet, little is known about the impact of acute elevated glucose on the temporal properties of AP-induced Ca2+transients and ionic underlying mechanisms that lead to muscle dysfunction. Here, we used high-speed confocal Ca2+imaging to investigate the temporal properties of AP-induced Ca2+transients, an intermediate step of ECC, using an acute in cellulo model of uncontrolled hyperglycemia (25 mM, 48 h.). Control and elevated glucose-exposed muscle fibers cultured for five days displayed four distinct patterns of AP-induced Ca2+transients (phasic, biphasic, phasic-delayed, and phasic-slow decay); most control muscle fibers show phasic AP-induced Ca2+transients, while most fibers exposed to elevated D-glucose displayed biphasic Ca2+transients upon single field stimulation. We hypothesize that these changes in the temporal profile of the AP-induced Ca2+transients are due to changes in the intrinsic excitable properties of the muscle fibers. We propose that these changes accompany early stages of diabetic myopathy.

scholarly journals Re-Setting the Circadian Clock Using Exercise against Sarcopenia

2020 ◽  
Vol 21 (9) ◽  
pp. 3106 ◽  
Author(s):  
Youngju Choi ◽  
Jinkyung Cho ◽  
Mi-Hyun No ◽  
Jun-Won Heo ◽  
Eun-Jeong Cho ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Circadian Rhythms ◽  
Circadian Clock ◽  
Intervention Strategy ◽  
Muscle Metabolism ◽  
Circadian Disruption ◽  
Adverse Health Outcomes ◽  
Exercise Timing ◽  
Underlying Mechanisms ◽  
The Impact

Sarcopenia is defined as the involuntary loss of skeletal muscle mass and function with aging and is associated with several adverse health outcomes. Recently, the disruption of regular circadian rhythms, due to shift work or nocturnal lifestyle, is emerging as a novel deleterious factor for the development of sarcopenia. The underlying mechanisms responsible for circadian disruption-induced sarcopenia include molecular circadian clock and mitochondrial function associated with the regulation of circadian rhythms. Exercise is a potent modulator of skeletal muscle metabolism and is considered to be a crucial preventative and therapeutic intervention strategy for sarcopenia. Moreover, emerging evidence shows that exercise, acting as a zeitgeber (time cue) of the skeletal muscle clock, can be an efficacious tool for re-setting the clock in sarcopenia. In this review, we provide the evidence of the impact of circadian disruption on skeletal muscle loss resulting in sarcopenia. Furthermore, we highlight the importance of exercise timing (i.e., scheduled physical activity) as a novel therapeutic strategy to target circadian disruption in skeletal muscle.

scholarly journals Sarcopenia in chronic kidney disease – A brief review

2021 ◽  
Vol 35 (2) ◽  
Author(s):  
Beatriz Donato ◽  
◽  
Catarina Teixeira ◽  
Sónia Velho ◽  
Edgar Almeida ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Muscle Mass ◽  
Physical Performance ◽  
Functional Independence ◽  
Muscle Dysfunction ◽  
Skeletal Muscle Dysfunction ◽  
Age Related ◽  
The Impact

Sarcopenia is a progressive age -related loss of muscle mass associated with a decline in muscle function and physical performance. Patients with chronic kidney disease experience substantial loss of muscle mass, weakness, and poor physical performance. Indeed, with the progression of chronic kidney disease, skeletal muscle dysfunction contributes to mobility limitation, loss of functional independence, and vulnerability to disease complications. There is a lack of robust data on the negative effect of the impact of kidney disease on skeletal muscle dysfunction, as well as on screening and treatment strategies that can be used in clinical practice to prevent functional decline and disability. Therefore, sarcopenia may be an underestimated condition with major implications for people with chronic kidney disease, even before the start of dialysis, which makes research into this topic necessary. The purpose of this review is to expand on some fundamental topics of sarcopenia, with an emphasis on the setting of chronic kidney disease patients.

Differential Effects of Bupivacaine and Ropivacaine Enantiomers on Intracellular Ca2+Regulation in Murine Skeletal Muscle Fibers

2005 ◽  
Vol 102 (4) ◽  
pp. 793-798 ◽  
Author(s):  
Wolfgang Zink ◽  
Goetz Missler ◽  
Barbara Sinner ◽  
Eike Martin ◽  
Rainer H. A. Fink ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Local Anesthetic ◽  
Muscle Fibers ◽  
Optical Isomers ◽  
Skinned Muscle ◽  
Skeletal Muscle Fibers ◽  
Racemic Mixtures ◽  
Intracellular Ca ◽  
Murine Skeletal Muscle

Background Increased intracellular Ca concentrations are considered to be a major pathomechanism in local anesthetic myotoxicity. Racemic bupivacaine and S-ropivacaine cause Ca release from the sarcoplasmic reticulum of skeletal muscle fibers and simultaneously inhibit Ca reuptake. Examining the optical isomers of both agents, the authors investigated stereoselective effects on muscular Ca regulation to get a closer insight in subcellular mechanisms of local anesthetic myotoxicity. Methods R- and S-enantiomers as well as racemic mixtures of both agents were tested in concentrations of 1, 5, 10, and 15 mm. Saponin-skinned muscle fibers from the extensor digitorum longus muscle of BALB/c mice were examined according to a standardized procedure. For the assessment of effects on Ca uptake and release from the sarcoplasmic reticulum, agents were added to the loading solution and the release solution, respectively, and force and Ca transients were monitored. Results The effects of S-enantiomers on both Ca release and reuptake were significantly more pronounced than those of racemic mixtures and R-enantiomers, respectively. In addition, the effects of racemates were markedly stronger than those of R-enantiomers. With regard to Ca release, the effects of bupivacaine isomers were more pronounced than the isomers of ropivacaine. Conclusions These data show that stereoselectivity is involved in alterations of intracellular Ca regulation by bupivacaine and ropivacaine. S-enantiomers seem to be more potent than R-enantiomers, with intermediate effects of racemic mixtures. In addition, lipophilicity also seems to determine the extent of Ca release by local anesthetics.

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.

Myofibrillar distribution of succinate dehydrogenase activity and lipid stores differs in skeletal muscle tissue of paraplegic subjects

2012 ◽  
Vol 302 (3) ◽  
pp. E365-E373 ◽  
Author(s):  
Richard A. M. Jonkers ◽  
Marlou L. Dirks ◽  
Christine I. H. C. Nabuurs ◽  
Henk M. De Feyter ◽  
Stephan F. E. Praet ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Succinate Dehydrogenase ◽  
Muscle Tissue ◽  
Muscle Fiber ◽  
Muscle Fibers ◽  
Oxidative Capacity ◽  
Skeletal Muscle Tissue ◽  
Whole Body ◽  
The Impact

Lack of physical activity has been related to an increased risk of developing insulin resistance. This study aimed to assess the impact of chronic muscle deconditioning on whole body insulin sensitivity, muscle oxidative capacity, and intramyocellular lipid (IMCL) content in subjects with paraplegia. Nine subjects with paraplegia and nine able-bodied, lean controls were recruited. An oral glucose tolerance test was performed to assess whole body insulin sensitivity. IMCL content was determined both in vivo and in vitro using1H-magnetic resonance spectroscopy and fluorescence microscopy, respectively. Muscle biopsy samples were stained for succinate dehydrogenase (SDH) activity to measure muscle fiber oxidative capacity. Subcellular distributions of IMCL and SDH activity were determined by defining subsarcolemmal and intermyofibrillar areas on histological samples. SDH activity was 57 ± 14% lower in muscle fibers derived from subjects with paraplegia when compared with controls ( P < 0.05), but IMCL content and whole body insulin sensitivity did not differ between groups. In muscle fibers taken from controls, both SDH activity and IMCL content were higher in the subsarcolemmal region than in the intermyofibrillar area. This typical subcellular SDH and IMCL distribution pattern was lost in muscle fibers collected from subjects with paraplegia and had changed toward a more uniform distribution. In conclusion, the lower metabolic demand in deconditioned muscle of subjects with paraplegia results in a significant decline in muscle fiber oxidative capacity and is accompanied by changes in the subcellular distribution patterns of SDH activity and IMCL. However, loss of muscle activity due to paraplegia is not associated with substantial lipid accumulation in skeletal muscle tissue.

scholarly journals Role of autophagy in sepsis-induced skeletal muscle dysfunction, whole-body metabolism, and survival

2021 ◽  
Author(s):  
Jean-Philippe Leduc-Gaudet ◽  
Kayla Miguez ◽  
Marina Cefis ◽  
Alaa Moamer ◽  
Tomer Jordi Chaffer ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Dysfunction ◽  
Skeletal Muscles ◽  
Muscle Wasting ◽  
26S Proteasome ◽  
Whole Body ◽  
Protective Mechanism ◽  
Muscle Dysfunction ◽  
Sham Operation ◽  
The Impact

Septic patients frequently develop skeletal muscle wasting and weakness, resulting in severe clinical consequences and adverse outcomes. Autophagy is a stress-induced degradative process essential to cell survival. Recent studies have demonstrated that sepsis triggers sustained induction of autophagy in skeletal muscles, although the impact of this enhanced autophagy on sepsis-induced muscle dysfunction remains unclear. Atg7 is an autophagy gene that plays a major role in autophagosome formation. Using an inducible and muscle-specific Atg7 knockout mouse model (Atg7iSkM-KO), we investigated the functional importance of skeletal muscle autophagy in sepsis. Sepsis was induced using cecal ligation and perforation (CLP) with a sham operation serving as a control. Atg7iSkM-KO mice exhibited a more severe phenotype in response to sepsis, marked by severe muscle wasting and contractile dysfunction, hypoglycemia, higher ketone levels and a decreased in survival as compared to mice with intact Atg7. Several genes that encode 26S proteasome subunits were upregulated, suggesting that activation of the ubiquitin-proteasome system is responsible for the severe muscle atrophy that was seen in these mice. Sepsis and Atg7 deletion resulted in the accumulation of mitochondrial dysfunction, although sepsis did not further worsen mitochondrial dysfunction in Atg7iSkM-KO mice. Overall, our study demonstrates that autophagy inactivation in skeletal muscles triggers significant worsening of sepsis-induced contractile and metabolic dysfunctions and negatively impacts survival. Induction of autophagy in skeletal muscles in response to sepsis thus represents a protective mechanism.

scholarly journals Sarcopenia: Etiology, Nutritional Approaches, and miRNAs

2021 ◽  
Vol 22 (18) ◽  
pp. 9724
Author(s):  
Roberto Cannataro ◽  
Leandro Carbone ◽  
Jorge L. Petro ◽  
Erika Cione ◽  
Salvador Vargas ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Intake ◽  
Nutritional Interventions ◽  
Age Related ◽  
Early Biomarker ◽  
Underlying Mechanisms ◽  
And Function ◽  
The Impact

Sarcopenia, an age-related decline in skeletal muscle mass and function, dramatically affects the quality of life. Although there is a consensus that sarcopenia is a multifactorial syndrome, the etiology and underlying mechanisms are not yet delineated. Moreover, research about nutritional interventions to prevent the development of sarcopenia is mainly focused on the amount and quality of protein intake. The impact of several nutrition strategies that consider timing of food intake, anti-inflammatory nutrients, metabolic control, and the role of mitochondrial function on the progression of sarcopenia is not fully understood. This narrative review summarizes the metabolic background of this phenomenon and proposes an integral nutritional approach (including dietary supplements such as creatine monohydrate) to target potential molecular pathways that may affect reduce or ameliorate the adverse effects of sarcopenia. Lastly, miRNAs, in particular those produced by skeletal muscle (MyomiR), might represent a valid tool to evaluate sarcopenia progression as a potential rapid and early biomarker for diagnosis and characterization.

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