Oxidative Stress and Skeletal Muscle Dysfunction with Aging

2011 ◽  
Vol 4 (2) ◽  
pp. 101-109 ◽  
Author(s):  
Wataru Aoi ◽  
Kunihiro Sakuma
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Dysfunction ◽  
Skeletal Muscle Dysfunction

scholarly journals Ascorbate infusion increases skeletal muscle fatigue resistance in patients with chronic obstructive pulmonary disease

2013 ◽  
Vol 305 (10) ◽  
pp. R1163-R1170 ◽  
Author(s):  
Matthew J. Rossman ◽  
Ryan S. Garten ◽  
H. Jonathan Groot ◽  
Van Reese ◽  
Jia Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Skeletal Muscle ◽  
Antioxidant Capacity ◽  
Chronic Obstructive ◽  
Muscle Dysfunction ◽  
Obstructive Pulmonary Disease ◽  
Skeletal Muscle Fatigue ◽  
Systemic Oxidative Stress ◽  
Skeletal Muscle Dysfunction

Chronic obstructive pulmonary disease (COPD) is associated with systemic oxidative stress and skeletal muscle dysfunction. The purpose of this study was to examine the impact of intravenous ascorbate administration (AO) on biological markers of antioxidant capacity and oxidative stress, and subsequently skeletal muscle function during dynamic, small muscle mass exercise in patients with COPD. Ten patients with spirometric evidence of COPD performed single-leg knee extensor (KE) trials matched for intensity and time (isotime) following intravenous ascorbate (2 g) or saline infusion (PL). Quadriceps fatigue was quantified by changes in force elicited by maximal voluntary contraction (MVC) and magnetic femoral nerve stimulation (Qtw,pot). AO administration significantly increased antioxidant capacity, as measured by the ferric-reducing ability of plasma (PL: 1 ± 0.1 vs. AO: 5 ± 0.2 mM), and significantly reduced malondialdehyde levels (PL: 1.16 ± 0.1 vs. AO: 0.97 ± 0.1 mmol). Additionally, resting blood pressure was significantly reduced (PL: 104 ± 4 vs. AO: 93 ± 6 mmHg) and resting femoral vascular conductance was significantly elevated after AO (PL: 2.4 ± 0.2 vs. AO: 3.6 ± 0.4 ml·min−1·mmHg−1). During isotime exercise, the AO significantly attenuated both the ventilatory and metabolic responses, and patients accumulated significantly less peripheral quadriceps fatigue, as illustrated by less of a fall in MVC (PL: −11 ± 2% vs. AO: −5 ± 1%) and Qtw,pot (PL: −37 ± 1% vs. AO: −30 ± 2%). These data demonstrate a beneficial role of AO administration on skeletal muscle fatigue in patients with COPD and further implicate systemic oxidative stress as a causative factor in the skeletal muscle dysfunction observed in this population.

scholarly journals Fibroblast growth factor 23 does not directly influence skeletal muscle cell proliferation and differentiation or ex vivo muscle contractility

2018 ◽  
Vol 315 (4) ◽  
pp. E594-E604 ◽  
Author(s):  
Keith G. Avin ◽  
Julian A. Vallejo ◽  
Neal X. Chen ◽  
Kun Wang ◽  
Chad D. Touchberry ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Ex Vivo ◽  
Fibroblast Growth Factor 23 ◽  
Hypophosphatemic Rickets ◽  
Muscle Dysfunction ◽  
Fibroblast Growth ◽  
Muscle Contractility ◽  
Skeletal Muscle Dysfunction

Skeletal muscle dysfunction accompanies the clinical disorders of chronic kidney disease (CKD) and hereditary hypophosphatemic rickets. In both disorders, fibroblast growth factor 23 (FGF23), a bone-derived hormone regulating phosphate and vitamin D metabolism, becomes chronically elevated. FGF23 has been shown to play a direct role in cardiac muscle dysfunction; however, it is unknown whether FGF23 signaling can also directly induce skeletal muscle dysfunction. We found expression of potential FGF23 receptors ( Fgfr1–4) and α-Klotho in muscles of two animal models (CD-1 and Cy/+ rat, a naturally occurring rat model of chronic kidney disease-mineral bone disorder) as well as C2C12 myoblasts and myotubes. C2C12 proliferation, myogenic gene expression, oxidative stress marker 8-OHdG, intracellular Ca2+ ([Ca2+]i), and ex vivo contractility of extensor digitorum longus (EDL) or soleus muscles were assessed after treatment with various amounts of FGF23. FGF23 (2–100 ng/ml) did not alter C2C12 proliferation, expression of myogenic genes, or oxidative stress after 24- to 72-h treatment. Acute or prolonged FGF23 treatment up to 6 days did not alter C2C12 [Ca2+]i handling, nor did acute treatment with FGF23 (9–100 ng/ml) affect EDL and soleus muscle contractility. In conclusion, although skeletal muscles express the receptors involved in FGF23-mediated signaling, in vitro FGF23 treatments failed to directly alter skeletal muscle development or function under the conditions tested. We hypothesize that other endogenous substances may be required to act in concert with FGF23 or apart from FGF23 to promote muscle dysfunction in hereditary hypophosphatemic rickets and CKD.

scholarly journals Prevention of Doxorubicin-Induced Autophagy Attenuates Oxidative Stress and Skeletal Muscle Dysfunction

Antioxidants ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 263 ◽  
Author(s):  
Vivian Doerr ◽  
Ryan N. Montalvo ◽  
Oh Sung Kwon ◽  
Erin E. Talbert ◽  
Brian A. Hain ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Dominant Negative ◽  
Skeletal Muscle Atrophy ◽  
Muscle Dysfunction ◽  
Related Factor ◽  
Skeletal Muscle Dysfunction ◽  
Dominant Negative Mutation

Clinical use of the chemotherapeutic doxorubicin (DOX) promotes skeletal muscle atrophy and weakness, adversely affecting patient mobility and strength. Although the mechanisms responsible for DOX-induced skeletal muscle dysfunction remain unclear, studies implicate the significant production of reactive oxygen species (ROS) in this pathology. Supraphysiological ROS levels can enhance protein degradation via autophagy, and it is established that DOX upregulates autophagic signaling in skeletal muscle. To determine the precise contribution of accelerated autophagy to DOX-induced skeletal muscle dysfunction, we inhibited autophagy in the soleus via transduction of a dominant negative mutation of the autophagy related 5 (ATG5) protein. Targeted inhibition of autophagy prevented soleus muscle atrophy and contractile dysfunction acutely following DOX administration, which was associated with a reduction in mitochondrial ROS and maintenance of mitochondrial respiratory capacity. These beneficial modifications were potentially the result of enhanced transcription of antioxidant response element-related genes and increased antioxidant capacity. Specifically, our results showed significant upregulation of peroxisome proliferator-activated receptor gamma co-activator 1-alpha, nuclear respiratory factor-1, nuclear factor erythroid-2-related factor-2, nicotinamide-adenine dinucleotide phosphate quinone dehydrogenase-1, and catalase in the soleus with DOX treatment when autophagy was inhibited. These findings establish a significant role of autophagy in the development of oxidative stress and skeletal muscle weakness following DOX administration.

scholarly journals Oxidative stress and skeletal muscle dysfunction are present in healthy smokers

2016 ◽  
Vol 49 (11) ◽  
Author(s):  
C.D.C. Neves ◽  
A.C.R. Lacerda ◽  
V.K.S. Lage ◽  
L.P. Lima ◽  
R. Tossige-Gomes ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Dysfunction ◽  
Skeletal Muscle Dysfunction

scholarly journals Oxidative Stress and Exercise‐Induced Flow‐Mediated Dilation in COPD: Insight into Skeletal Muscle Dysfunction

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Ryan Alan Harris ◽  
Steven K. Nishiyama ◽  
D. Walter Wray ◽  
Kimberly A. Berkstressor ◽  
Russell S. Richardson
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Dysfunction ◽  
Flow Mediated Dilation ◽  
Skeletal Muscle Dysfunction ◽  
Induced Flow ◽  
Exercise Induced ◽  
Insight Into

scholarly journals Autophagy promotes cancer chemotherapy‐induced oxidative stress and skeletal muscle dysfunction

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Ashley J. Smuder ◽  
Oh Sung Kwon ◽  
Brian A. Hain ◽  
Fraser E. Houston ◽  
Erin E. Talbert
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Cancer Chemotherapy ◽  
Muscle Dysfunction ◽  
Skeletal Muscle Dysfunction
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