scholarly journals Age-induced oxidative stress: how does it influence skeletal muscle quantity and quality?

2016 ◽  
Vol 121 (5) ◽  
pp. 1047-1052 ◽  
Author(s):  
Cory W. Baumann ◽  
Dongmin Kwak ◽  
Haiming M. Liu ◽  
LaDora V. Thompson
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Function ◽  
Strength Loss ◽  
Muscle Quality ◽  
Muscle Size ◽  
Nitrogen Species ◽  
Skeletal Muscle Function ◽  
Protein Balance ◽  
Ec Coupling

With advancing age, skeletal muscle function declines as a result of strength loss. These strength deficits are largely due to reductions in muscle size (i.e., quantity) and its intrinsic force-producing capacity (i.e., quality). Age-induced reductions in skeletal muscle quantity and quality can be the consequence of several factors, including accumulation of reactive oxygen and nitrogen species (ROS/RNS), also known as oxidative stress. Therefore, the purpose of this mini-review is to highlight the published literature that has demonstrated links between aging, oxidative stress, and skeletal muscle quantity or quality. In particular, we focused on how oxidative stress has the potential to reduce muscle quantity by shifting protein balance in a deficit, and muscle quality by impairing activation at the neuromuscular junction, excitation-contraction (EC) coupling at the ryanodine receptor (RyR), and cross-bridge cycling within the myofibrillar apparatus. Of these, muscle weakness due to EC coupling failure mediated by RyR dysfunction via oxidation and/or nitrosylation appears to be the strongest candidate based on the publications reviewed. However, it is clear that age-associated oxidative stress has the ability to alter strength through several mechanisms and at various locations of the muscle fiber.

scholarly journals Potential Utility of Electrical Impedance Myography in Evaluating Age-Related Skeletal Muscle Function Deficits

2021 ◽  
Vol 12 ◽  
Author(s):  
Brian C. Clark ◽  
Seward Rutkove ◽  
Elmer C. Lupton ◽  
Carlos J. Padilla ◽  
W. David Arnold
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Function ◽  
Electrical Impedance ◽  
Muscle Quality ◽  
Muscle Size ◽  
Current Evidence ◽  
Potential Utility ◽  
Skeletal Muscle Function ◽  
Muscle Health

Skeletal muscle function deficits associated with advancing age are due to several physiological and morphological changes including loss of muscle size and quality (conceptualized as a reduction in the intrinsic force-generating capacity of a muscle when adjusted for muscle size). Several factors can contribute to loss of muscle quality, including denervation, excitation-contraction uncoupling, increased fibrosis, and myosteatosis (excessive levels of inter- and intramuscular adipose tissue and intramyocellular lipids). These factors also adversely affect metabolic function. There is a major unmet need for tools to rapidly and easily assess muscle mass and quality in clinical settings with minimal patient and provider burden. Herein, we discuss the potential for electrical impedance myography (EIM) as a tool to evaluate muscle mass and quality in older adults. EIM applies weak, non-detectible (e.g., 400 μA), mutifrequency (e.g., 1 kHz–1 MHz) electrical currents to a muscle (or muscle group) through two excitation electrodes, and resulting voltages are measured via two sense electrodes. Measurements are fast (~5 s/muscle), simple to perform, and unaffected by factors such as hydration that may affect other simple measures of muscle status. After nearly 2 decades of study, EIM has been shown to reflect muscle health status, including the presence of atrophy, fibrosis, and fatty infiltration, in a variety of conditions (e.g., developmental growth and maturation, conditioning/deconditioning, and obesity) and neuromuscular diseases states [e.g., amyotrophic lateral sclerosis (ALS) and muscular dystrophies]. In this article, we describe prior work and current evidence of EIM’s potential utility as a measure of muscle health in aging and geriatric medicine.

scholarly journals Fourteen days of smoking cessation improves muscle fatigue resistance and reverses markers of systemic inflammation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mohammad Z. Darabseh ◽  
Thomas M. Maden-Wilkinson ◽  
George Welbourne ◽  
Rob C. I. Wüst ◽  
Nessar Ahmed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Smoking Cessation ◽  
Muscle Fatigue ◽  
Fatigue Resistance ◽  
Systemic Inflammation ◽  
Muscle Function ◽  
Low Grade ◽  
Skeletal Muscle Function ◽  
Tnf Α

AbstractCigarette smoking has a negative effect on respiratory and skeletal muscle function and is a risk factor for various chronic diseases. To assess the effects of 14 days of smoking cessation on respiratory and skeletal muscle function, markers of inflammation and oxidative stress in humans. Spirometry, skeletal muscle function, circulating carboxyhaemoglobin levels, advanced glycation end products (AGEs), markers of oxidative stress and serum cytokines were measured in 38 non-smokers, and in 48 cigarette smokers at baseline and after 14 days of smoking cessation. Peak expiratory flow (p = 0.004) and forced expiratory volume in 1 s/forced vital capacity (p = 0.037) were lower in smokers compared to non-smokers but did not change significantly after smoking cessation. Smoking cessation increased skeletal muscle fatigue resistance (p < 0.001). Haemoglobin content, haematocrit, carboxyhaemoglobin, total AGEs, malondialdehyde, TNF-α, IL-2, IL-4, IL-6 and IL-10 (p < 0.05) levels were higher, and total antioxidant status (TAS), IL-12p70 and eosinophil numbers were lower (p < 0.05) in smokers. IL-4, IL-6, IL-10 and IL-12p70 had returned towards levels seen in non-smokers after 14 days smoking cessation (p < 0.05), and IL-2 and TNF-α showed a similar pattern but had not yet fully returned to levels seen in non-smokers. Haemoglobin, haematocrit, eosinophil count, AGEs, MDA and TAS did not significantly change with smoking cessation. Two weeks of smoking cessation was accompanied with an improved muscle fatigue resistance and a reduction in low-grade systemic inflammation in smokers.

Oxidative Stress in Skeletal Muscle Function and Dysfunction

2014 ◽  
pp. 373-390
Author(s):  
Carlos da Justa Pinheiro ◽  
Marco Salomão Fortes ◽  
Rui Curi
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Function ◽  
Skeletal Muscle Function

scholarly journals Effectiveness of impedance parameters for muscle quality evaluation in healthy men

2020 ◽  
Vol 70 (1) ◽  
Author(s):  
Hiroki Sato ◽  
Takao Nakamura ◽  
Toshimasa Kusuhara ◽  
Kobara Kenichi ◽  
Katsushi Kuniyasu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Muscle Thickness ◽  
Bioelectrical Impedance ◽  
Impedance Analysis ◽  
Muscle Quality ◽  
Stepwise Multiple Regression ◽  
Skeletal Muscle Function ◽  
Healthy Men ◽  
Impedance Parameters

Abstract We investigated the relationship between impedance parameters and skeletal muscle function in the lower extremities, as well as the effectiveness of impedance parameters in evaluating muscle quality. Lower extremity impedance of 19 healthy men (aged 23–31 years) measured using the direct segmental multi-frequency bioelectrical impedance analysis were arc-optimized using the Cole–Cole model, following which phase angle (PA), $${R}_{i}/{R}_{e}$$ R i / R e , and β were estimated. Skeletal muscle function was assessed by muscle thickness, muscle intensity, and isometric knee extension force (IKEF). IKEF was positively correlated with PA (r = 0.58, p < 0.01) and β (r = 0.34, p < 0.05) was negatively correlated with $${R}_{i}/{R}_{e}$$ R i / R e (r = − 0.43, p < 0.01). Stepwise multiple regression analysis results revealed that PA, β, and $${R}_{i}/{R}_{e}$$ R i / R e were correlated with IKEF independently of muscle thickness. This study suggests that arc-optimized impedance parameters are effective for evaluating muscle quality and prediction of muscle strength.

Targeting Mitochondrial Oxidative Stress to Improve Aged Skeletal Muscle Function

2014 ◽  
Vol 76 ◽  
pp. S29
Author(s):  
Matthew David Campbell ◽  
Ying Ann Chiao ◽  
Matthew J Gaffrey ◽  
Danijel Djukovic ◽  
Haiwei Gu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Function ◽  
Skeletal Muscle Function ◽  
Mitochondrial Oxidative Stress

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.

scholarly journals Age-related changes in isolated mouse skeletal muscle function are dependent on sex, muscle, and contractility mode

2020 ◽  
Vol 319 (3) ◽  
pp. R296-R314
Author(s):  
Cameron Hill ◽  
Rob S. James ◽  
Val. M. Cox ◽  
Frank Seebacher ◽  
Jason Tallis
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Fatigue Resistance ◽  
Muscle Function ◽  
Isometric Force ◽  
Muscle Quality ◽  
Skeletal Muscle Function ◽  
Cross Sectional ◽  
Mouse Skeletal Muscle ◽  
Age Related

The present study aimed to simultaneously examine the age-related, muscle-specific, sex-specific, and contractile mode-specific changes in isolated mouse skeletal muscle function and morphology across multiple ages. Measurements of mammalian muscle morphology, isometric force and stress (force/cross-sectional area), absolute and normalized (power/muscle mass) work-loop power across a range of contractile velocities, fatigue resistance, and myosin heavy chain (MHC) isoform concentration were measured in 232 isolated mouse (CD-1) soleus, extensor digitorum longus (EDL), and diaphragm from male and female animals aged 3, 10, 30, 52, and 78 wk. Aging resulted in increased body mass and increased soleus and EDL muscle mass, with atrophy only present for female EDL by 78 wk despite no change in MHC isoform concentration. Absolute force and power output increased up to 52 wk and to a higher level for males. A 23–36% loss of isometric stress exceeded the 14–27% loss of power normalized to muscle mass between 10 wk and 52 wk, although the loss of normalized power between 52 and 78 wk continued without further changes in stress ( P > 0.23). Males had lower power normalized to muscle mass than females by 78 wk, with the greatest decline observed for male soleus. Aging did not cause a shift toward slower contractile characteristics, with reduced fatigue resistance observed in male EDL and female diaphragm. Our findings show that the loss of muscle quality precedes the loss of absolute performance as CD-1 mice age, with the greatest effect seen in male soleus, and in most instances without muscle atrophy or an alteration in MHC isoforms.

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