Burn-induced hypermetabolism and skeletal muscle dysfunction

2021 ◽  
Author(s):  
Carly M Knuth ◽  
Christopher Auger ◽  
Marc G. Jeschke
Keyword(s):  
Skeletal Muscle ◽  
Wound Healing ◽  
Burn Injury ◽  
Improve Patient Care ◽  
Morbidity And Mortality ◽  
Muscle Dysfunction ◽  
Comprehensive Overview ◽  
Skeletal Muscle Function ◽  
Skeletal Muscle Dysfunction ◽  
Muscle Catabolism

Critical illnesses, including sepsis, cancer cachexia and burn injury, invoke a milieu of systemic metabolic and inflammatory derangements that ultimately results in increased energy expenditure leading to fat and lean mass catabolism. Burn injuries present a unique clinical challenge given the magnitude and duration of the hypermetabolic response in comparison to other forms of critical illness, which drastically increase the risk of morbidity and mortality. Skeletal muscle metabolism is particularly altered as a consequence of burn-induced hypermetabolism as it primarily provides a main source of fuel in support of wound healing. Interestingly, muscle catabolism is sustained long after the wound has healed, indicating that additional mechanisms beyond wound healing are involved. In this review, we discuss the distinctive pathophysiological response to burn injury with a focus on skeletal muscle function and metabolism. We first examine the diverse consequences on skeletal muscle dysfunction between thermal, electrical and chemical burns. We then provide a comprehensive overview of the known mechanisms underlying skeletal muscle dysfunction that may be attributed to hypermetabolism. Lastly, we review the most promising current treatment options to mitigate muscle catabolism, and by extension improve morbidity and mortality, and end with future directions which have the potential to significantly improve patient care.

Changes in calmodulin concentration and cyclic 3′,5′-nucleotide phosphodiesterase activity in skeletal muscle of hyper- and hypothyroid rats

1995 ◽  
Vol 146 (2) ◽  
pp. 287-292 ◽  
Author(s):  
T Mano ◽  
K Iwase ◽  
I Yoshimochi ◽  
Y Sawai ◽  
N Oda ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Hydrolytic Activity ◽  
Periodic Paralysis ◽  
Metabolic Enzyme ◽  
Muscle Dysfunction ◽  
Skeletal Muscle Function ◽  
Skeletal Muscle Dysfunction ◽  
Camp System ◽  
Β Receptor

Abstract Hyper- and hypothyroid states occasionally induce skeletal muscle dysfunction i.e. periodic paralysis and thyroid myopathy. The etiology of these diseases remains unclear, but several findings suggest that the catecholamine-β-receptor-cAMP system or other messenger systems are disturbed in these diseases. In this context, we evaluated changes in the cyclic 3′,5′-nucleotide metabolic enzyme, cyclic 3′,5′-nucleotide phosphodiesterase (PDE) and calmodulin concentrations in skeletal muscles of hyper- and hypothyroid rats. Activities of cyclic AMP-PDE were low in skeletal muscle both from hyper- and hypothyroid rats, and calmodulin concentration was high in hyperthyroid and low in hypothyroid rats, as compared with normal rats. DE-52 column chromatographic analysis showed that the cGMP hydrolytic activity in peak I and the cAMP hydrolytic activity in peak II were decreased in hypothyroid rats, whereas cAMP hydrolytic activity in peak III was unchanged. The cAMP hydrolytic activity in peak III was decreased in hyperthyroid rats, but the activities in peaks I and II were unchanged. These findings indicate that cAMP and calmodulin may have some role in skeletal muscle function in the hyperthyroid state, and that cAMP and calmodulin-dependent metabolism may be suppressed in the hypothyroid state. Journal of Endocrinology (1995) 146, 287–292

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.

scholarly journals Pseudomonas aeruginosa Quorum Sensing Molecule Alters Skeletal Muscle Protein Homeostasis by Perturbing the Antioxidant Defense System

mBio ◽  
2019 ◽  
Vol 10 (5) ◽  
Author(s):  
Arunava Bandyopadhaya ◽  
A. Aria Tzika ◽  
Laurence G. Rahme
Keyword(s):  
Skeletal Muscle ◽  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Muscle Function ◽  
Muscle Dysfunction ◽  
Chronic Infections ◽  
Skeletal Muscle Function ◽  
Content Type ◽  
Skeletal Muscle Dysfunction ◽  
Ros Homeostasis

ABSTRACT Skeletal muscle function is compromised in many illnesses, including chronic infections. The Pseudomonas aeruginosa quorum sensing (QS) signal, 2-amino acetophenone (2-AA), is produced during acute and chronic infections and excreted in human tissues, including the lungs of cystic fibrosis patients. We have shown that 2-AA facilitates pathogen persistence, likely via its ability to promote the formation of bacterial persister cells, and that it acts as an interkingdom immunomodulatory signal that epigenetically reprograms innate immune functions. Moreover, 2-AA compromises muscle contractility and impacts the expression of genes involved in reactive oxygen species (ROS) homeostasis in skeletal muscle and in mitochondrial functions. Here, we elucidate the molecular mechanisms of 2-AA’s impairment of skeletal muscle function and ROS homeostasis. Murine in vivo and differentiated C2C12 myotube cell studies showed that 2-AA promotes ROS generation in skeletal muscle via the modulation of xanthine oxidase (XO) activity, NAD(P)H oxidase2 (NOX2) protein level, and the activity of antioxidant enzymes. ROS accumulation triggers the activity of AMP-activated protein kinase (AMPK), likely upstream of the observed locations of induction of ubiquitin ligases Muscle RING Finger 1 (MuRF1) and Muscle Atrophy F-box (MAFbx), and induces autophagy-related proteins. The protein-level perturbation in skeletal muscle of silent mating type information regulation 2 homolog 1 (SIRT1), peroxisome proliferator-activated receptor gamma coactivator 1 (PGC-1), and uncoupling protein 3 (UCP3) is rescued by the antioxidant N-acetyl-l-cysteine (NAC). Together, these results unveil a novel form of action of a QS bacterial molecule and provide molecular insights into the 2-AA-mediated skeletal muscle dysfunction caused by P. aeruginosa. IMPORTANCE Pseudomonas aeruginosa, a bacterium that is resistant to treatment, causes serious acute, persistent, and relapsing infections in humans. There is increasing evidence that bacterial excreted small molecules play a critical role during infection. We have shown that a quorum sensing (QS)-regulated excreted small molecule, 2-AA, which is abundantly produced by P. aeruginosa, promotes persistent infections, dampens host inflammation, and triggers mitochondrial dysfunction in skeletal muscle. QS is a cell-to-cell communication system utilized by bacteria to promote collective behaviors. The significance of our study in identifying a mechanism that leads to skeletal muscle dysfunction, via the action of a QS molecule, is that it may open new avenues in the control of muscle loss as a result of infection and sepsis. Given that QS is a common characteristic of prokaryotes, it is possible that 2-AA-like molecules promoting similar effects may exist in other pathogens.

scholarly journals Skeletal muscle dysfunction in chronic renal failure: effects of exercise

2006 ◽  
Vol 290 (4) ◽  
pp. F753-F761 ◽  
Author(s):  
Gregory R. Adams ◽  
Nosratola D. Vaziri
Keyword(s):  
Skeletal Muscle ◽  
Renal Failure ◽  
Exercise Capacity ◽  
Muscle Function ◽  
Chronic Illnesses ◽  
Treatment Modalities ◽  
Muscle Dysfunction ◽  
Obstructive Pulmonary Disease ◽  
Skeletal Muscle Dysfunction

A number of chronic illnesses such as renal failure (CRF), obstructive pulmonary disease, and congestive heart failure result in a significant decrease in exercise tolerance. There is an increasing awareness that prescribed exercise, designed to restore some level of physical performance and quality of life, can be beneficial in these conditions. In CRF patients, muscle function can be affected by a number of direct and indirect mechanisms caused by renal disease as well as various treatment modalities. The aims of this review are twofold: first, to briefly discuss the mechanisms by which CRF negatively impacts skeletal muscle and, therefore, exercise capacity, and, second, to discuss the available data on the effects of programmed exercise on muscle function, exercise capacity, and various other parameters in CRF.

scholarly journals Targeted overexpression of mitochondrial catalase protects against cancer chemotherapy-induced skeletal muscle dysfunction

2016 ◽  
Vol 311 (2) ◽  
pp. E293-E301 ◽  
Author(s):  
Laura A. A. Gilliam ◽  
Daniel S. Lark ◽  
Lauren R. Reese ◽  
Maria J. Torres ◽  
Terence E. Ryan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cancer Chemotherapy ◽  
Protein Oxidation ◽  
Muscle Function ◽  
Contractile Function ◽  
Muscle Dysfunction ◽  
Skeletal Muscle Dysfunction ◽  
Whole Muscle ◽  
Loss Of Strength ◽  
Mitochondrial Respiratory

The loss of strength in combination with constant fatigue is a burden on cancer patients undergoing chemotherapy. Doxorubicin, a standard chemotherapy drug used in the clinic, causes skeletal muscle dysfunction and increases mitochondrial H2O2. We hypothesized that the combined effect of cancer and chemotherapy in an immunocompetent breast cancer mouse model (E0771) would compromise skeletal muscle mitochondrial respiratory function, leading to an increase in H2O2-emitting potential and impaired muscle function. Here, we demonstrate that cancer chemotherapy decreases mitochondrial respiratory capacity supported with complex I (pyruvate/glutamate/malate) and complex II (succinate) substrates. Mitochondrial H2O2-emitting potential was altered in skeletal muscle, and global protein oxidation was elevated with cancer chemotherapy. Muscle contractile function was impaired following exposure to cancer chemotherapy. Genetically engineering the overexpression of catalase in mitochondria of muscle attenuated mitochondrial H2O2 emission and protein oxidation, preserving mitochondrial and whole muscle function despite cancer chemotherapy. These findings suggest mitochondrial oxidants as a mediator of cancer chemotherapy-induced skeletal muscle dysfunction.

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