scholarly journals Skeletal Muscle Function Deficit: A New Terminology to Embrace the Evolving Concepts of Sarcopenia and Age-Related Muscle Dysfunction

2014 ◽  
Vol 69 (5) ◽  
pp. 591-594 ◽  
Author(s):  
R. Correa-de-Araujo ◽  
E. Hadley
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Muscle Dysfunction ◽  
Skeletal Muscle Function ◽  
Age Related

scholarly journals Gait disturbances and muscle dysfunction in fibroblast growth factor 2 knockout mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
C. Homer-Bouthiette ◽  
L. Xiao ◽  
Marja M. Hurley
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Muscle Strength ◽  
Fibroblast Growth Factor ◽  
Muscle Function ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Skeletal Muscle Function ◽  
Age Related ◽  
Gait Disturbances

AbstractFibroblast growth factor 2 (FGF2) is important in musculoskeletal homeostasis, therefore the impact of reduction or Fgf2 knockout on skeletal muscle function and phenotype was determined. Gait analysis as well as muscle strength testing in young and old WT and Fgf2KO demonstrated age-related gait disturbances and reduction in muscle strength that were exacerbated in the KO condition. Fgf2 mRNA and protein were significantly decreased in skeletal muscle of old WT compared with young WT. Muscle fiber cross-sectional area was significantly reduced with increased fibrosis and inflammatory infiltrates in old WT and Fgf2KO vs. young WT. Inflammatory cells were further significantly increased in old Fgf2KO compared with old WT. Lipid-related genes and intramuscular fat was increased in old WT and old Fgf2KO with a further increase in fibro-adipocytes in old Fgf2KO compared with old WT. Impaired FGF signaling including Increased β-Klotho, Fgf21 mRNA, FGF21 protein, phosphorylated FGF receptors 1 and 3, was observed in old WT and old Fgf2KO. MAPK/ ERK1/2 was significantly increased in young and old Fgf2KO. We conclude that Fgf2KO, age-related decreased FGF2 in WT mice, and increased FGF21 in the setting of impaired Fgf2 expression likely contribute to impaired skeletal muscle function and sarcopenia in mice.

The Effects of Aging and Training on Skeletal Muscle

1998 ◽  
Vol 26 (4) ◽  
pp. 598-602 ◽  
Author(s):  
Donald T. Kirkendall ◽  
William E. Garrett
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Function ◽  
Cellular Level ◽  
Type I ◽  
Loss Of Function ◽  
Skeletal Muscle Function ◽  
Cross Sectional ◽  
Age Related ◽  
General Slowing

Aging results in a gradual loss of muscle function, and there are predictable age-related alterations in skeletal muscle function. The typical adult will lose muscle mass with age; the loss varies according to sex and the level of muscle activity. At the cellular level, muscles loose both cross-sectional area and fiber numbers, with type II muscle fibers being the most affected by aging. Some denervation of fibers may occur. The combination of these factors leads to an increased percentage of type I fibers in older adults. Metabolically, the glycolytic enzymes seem to be little affected by aging, but the aerobic enzymes appear to decline with age. Aged skeletal muscle produces less force and there is a general “slowing” of the mechanical characteristics of muscle. However, neither reduced muscle demand nor the subsequent loss of function is inevitable with aging. These losses can be minimized or even reversed with training. Endurance training can improve the aerobic capacity of muscle, and resistance training can improve central nervous system recruitment of muscle and increase muscle mass. Therefore, physical activity throughout life is encouraged to prevent much of the age-related impact on skeletal muscle.

scholarly journals Measuring skeletal muscle strength and endurance, from bench to bedside

2008 ◽  
Vol 31 (5) ◽  
pp. 307 ◽  
Author(s):  
Didier Saey ◽  
Thierry Troosters
Keyword(s):  
Skeletal Muscle ◽  
Muscle Strength ◽  
Exercise Training ◽  
Muscle Weakness ◽  
Muscle Function ◽  
Muscle Endurance ◽  
Muscle Dysfunction ◽  
Skeletal Muscle Function ◽  
Peripheral Muscle ◽  
Skeletal Muscle Strength

Peripheral muscle dysfunction is a recognized and important systemic consequence of many chronic diseases. Peripheral muscle weakness is associated with excess utilization of health care recourses, morbidity and /or mortality in patients with COPD, congestive heart failure, liver and frail elderly. In the latter group, muscle weakness was associated with significant increase in falling and falling related injury. Exercise training does enhance skeletal muscle function and exercise performance. In addition, patients who start a training program with impaired skeletal muscle function may be more likely to respond adequately to an exercise training program. It is beyond the scope of the present review to discuss in detail the factors that may contribute to muscle dysfunction in chronic conditions. Clearly, muscle weakness is multi-factorial. Factors associated with skeletal muscle force are general factors (such as age, body weight, sex), disease related factors (such as inactivity) and disease specific factors (for example in COPD drug treatment, i.e. corticosteroid treatment, inflammation, oxidative stress and hypoxia have been shown to contribute to muscle dysfunction). This review will focus on the different ways to assess skeletal muscle function in patients with chronic disease. More specifically, techniques to assess skeletal muscle strength, skeletal muscle endurance and skeletal muscle fatigue will be discussed. For the American College of Sport Medicine (ACSM) not only muscle strength but also muscle endurance are health- related fitness components. Loss in one of these muscle characteristics results in impaired muscle. Muscle function tests are very specific to the muscle group tested, the type of contraction, the velocity of muscle motion, the type of equipment and the joint range of motion. Results of any test are specific to the procedures used. Individuals should participate in familiarization sessions with the equipment, and adhere to a specific protocol in order to obtain a true and reliable score. A change in one’s muscular fitness over time can be based on the absolute value of the external force (Newton (N)), but when comparisons are made between individuals, the values should be expressed as relative values (percentage of a predicted normal value). In both cases, caution must be taken in the interpretation of the result because the norms may not include a representative sample of the individual being measured, a standardized protocol may be absent, or the exact test being used may differ.

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 Nesprin 1α2 is essential for mouse postnatal viability and nuclear positioning in skeletal muscle

2017 ◽  
Vol 216 (7) ◽  
pp. 1915-1924 ◽  
Author(s):  
Matthew J. Stroud ◽  
Wei Feng ◽  
Jianlin Zhang ◽  
Jennifer Veevers ◽  
Xi Fang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Knockout Mice ◽  
Muscle Function ◽  
Actin Binding ◽  
Muscle Dysfunction ◽  
Linc Complex ◽  
Nuclear Positioning ◽  
Skeletal Muscle Function ◽  
Binding Domains ◽  
A Cell

The position of the nucleus in a cell is controlled by interactions between the linker of nucleoskeleton and cytoskeleton (LINC) complex and the cytoskeleton. Defects in nuclear positioning and abnormal aggregation of nuclei occur in many muscle diseases and correlate with muscle dysfunction. Nesprin 1, which includes multiple isoforms, is an integral component of the LINC complex, critical for nuclear positioning and anchorage in skeletal muscle, and is thought to provide an essential link between nuclei and actin. However, previous studies have yet to identify which isoform is responsible. To elucidate this, we generated a series of nesprin 1 mutant mice. We showed that the actin-binding domains of nesprin 1 were dispensable, whereas nesprin 1α2, which lacks actin-binding domains, was crucial for postnatal viability, nuclear positioning, and skeletal muscle function. Furthermore, we revealed that kinesin 1 was displaced in fibers of nesprin 1α2–knockout mice, suggesting that this interaction may play an important role in positioning of myonuclei and functional skeletal muscle.

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 Improper Remodeling of Organelles Deputed to Ca2+ Handling and Aerobic ATP Production Underlies Muscle Dysfunction in Ageing

2021 ◽  
Vol 22 (12) ◽  
pp. 6195
Author(s):  
Feliciano Protasi ◽  
Laura Pietrangelo ◽  
Simona Boncompagni
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Calcium Release ◽  
Muscle Dysfunction ◽  
Efficient Production ◽  
Membrane Systems ◽  
Skeletal Muscle Function ◽  
Atp Production ◽  
Functional Changes ◽  
Ec Coupling

Proper skeletal muscle function is controlled by intracellular Ca2+ concentration and by efficient production of energy (ATP), which, in turn, depend on: (a) the release and re-uptake of Ca2+ from sarcoplasmic-reticulum (SR) during excitation–contraction (EC) coupling, which controls the contraction and relaxation of sarcomeres; (b) the uptake of Ca2+ into the mitochondrial matrix, which stimulates aerobic ATP production; and finally (c) the entry of Ca2+ from the extracellular space via store-operated Ca2+ entry (SOCE), a mechanism that is important to limit/delay muscle fatigue. Abnormalities in Ca2+ handling underlie many physio-pathological conditions, including dysfunction in ageing. The specific focus of this review is to discuss the importance of the proper architecture of organelles and membrane systems involved in the mechanisms introduced above for the correct skeletal muscle function. We reviewed the existing literature about EC coupling, mitochondrial Ca2+ uptake, SOCE and about the structural membranes and organelles deputed to those functions and Finally, we summarized the data collected in different, but complementary, projects studying changes caused by denervation and ageing to the structure and positioning of those organelles: a. denervation of muscle fibers—an event that contributes, to some degree, to muscle loss in ageing (known as sarcopenia)—causes misplacement and damage: (i) of membrane structures involved in EC coupling (calcium release units, CRUs) and (ii) of the mitochondrial network; b. sedentary ageing causes partial disarray/damage of CRUs and of calcium entry units (CEUs, structures involved in SOCE) and loss/misplacement of mitochondria; c. functional electrical stimulation (FES) and regular exercise promote the rescue/maintenance of the proper architecture of CRUs, CEUs, and of mitochondria in both denervation and ageing. All these structural changes were accompanied by related functional changes, i.e., loss/decay in function caused by denervation and ageing, and improved function following FES or exercise. These data suggest that the integrity and proper disposition of intracellular organelles deputed to Ca2+ handling and aerobic generation of ATP is challenged by inactivity (or reduced activity); modifications in the architecture of these intracellular membrane systems may contribute to muscle dysfunction in ageing and sarcopenia.

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