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 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 Lung overexpression of TNF α impairs locomotor skeletal muscle function and exercise capacity

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Kechun Tang ◽  
George Murano ◽  
Peter D. Wagner ◽  
Ellen C. Breen
Keyword(s):  
Skeletal Muscle ◽  
Exercise Capacity ◽  
Muscle Function ◽  
Skeletal Muscle Function ◽  
Tnf Α

Abstract 3789: Induction of Murf-1 is Required for Tnf-alpha Induced Loss of Skeletal Muscle Function

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Volker Adams ◽  
Norman Magner ◽  
Axel Linke ◽  
Alexander Gasch ◽  
Stephanie Hirner ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Troponin T ◽  
Organ Bath ◽  
Down Regulation ◽  
Skeletal Muscle Function ◽  
Necrosis Factor Alpha ◽  
E3 Ligases ◽  
Force Development ◽  
Tnf Α

Background: Inflammatory cytokines like tumor necrosis factor alpha (TNF-α) are known to impair skeletal muscle (SM) function. Furthermore, TNF-α induces the expression of atrogin-like muscle specific ubiquitin E3-ligases, presumed to mediate muscle atrophy. The relative contributions of respective ubiquitin ligases, like MuRF1 for the TNF-α induced reduction in muscle function are not known. Methods: TNF-α or saline was injected either into C57Bl6 or MuRF1 −/− mice. After 16 –24h the expression of MuRF1 in the SM was quantified by qRT-PCR and western blot. Muscle function was measured in an organ bath. To obtain a broader overview on potential alterations, 2D-gel electrophoresis was performed. Results: WT animals injected with TNF-α had higher MuRF1 mRNA (saline: 56.6±12.1 vs. TNF-α: 133.6±30.3 arb. Units; p<0.05) and protein expression (saline: 0.38±0.11 vs. TNF-α: 1.07±0.25 arb. Units; p<0.05) as compared to saline injected littermates. However, TNF- α was unable to induce MurRF1 expression in MuRF1 −/− mice. Furthermore, TNF- α reduced force development at 150Hz by 25% in C57Bl6 animals (saline: 2412±120 vs. TNF-α: 1799±114 g/cm2; p<0.05), but not in MuRF1 −/− mice (saline: 2424±198 vs. TNF-α: 2431±180 g/cm2; p=NS). The proteome analysis revealed a significant down-regulation of fast skeletal muscle troponin T (TNNT3) in WT animals treated with TNF- α as compared to MuRF1 −/− mice receiving TNF-α . In addition, TNF-α injection into C57Bl6 animals resulted in a down-regulation of eEF1γ ( WT: 0.60±0.02 vs. WT+TNF-α: 0.39±0.05 arb. Units; p<0.05). This reduction was not seen in MuRF1 −/− mice receiving TNF- α (KO: 0.59±0.03 vs. KO+TNF-α: 0.68±0.01 arb. Units; p<0.05) Conclusion: The results of this study demonstrate for the first time, that the TNF- α induced reduction in SM force development depends on the induction of the atrophy related E3-ubiquitin ligase MuRF1. A link for the reduction in muscle force may be the TNF-α-MuRF1-mediated down-regulation of TNNT3 and the elongation factor eEF1γ.

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 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.

scholarly journals Effect of pulmonary TNF-α overexpression on mouse isolated skeletal muscle function

2011 ◽  
Vol 301 (4) ◽  
pp. R1025-R1031 ◽  
Author(s):  
Li Zuo ◽  
Leonardo Nogueira ◽  
Michael C. Hogan
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Weight Ratio ◽  
The Body ◽  
Chronic Obstructive ◽  
Skeletal Muscle Function ◽  
Muscle Weight ◽  
Peak Rate ◽  
Tnf Α

TNF-α is a proinflammatory cytokine that is involved in numerous pathological processes including chronic obstructive pulmonary disease (COPD). In the present study, we used a transgenic mouse model that overexpresses TNF-α in the lung (Tg+) to test the hypothesis that chronic exposure to TNF-α (as seen in COPD) reduces skeletal muscle force production and fatigue resistance, particularly under low Po2 conditions. At 7–12 mo, body and muscle weight of both extensor digitorum longus (EDL) and soleus were significantly smaller in Tg+ compared with littermate wild-type (WT) mice; however, the body-to-muscle weight ratio was not different between groups. EDL and soleus muscles were subjected to in vitro fatiguing contractile periods under high (∼550 Torr) and low Po2 (∼40 Torr). Although all muscles were less fatigue-resistant during low Po2 compared with high Po2, only the soleus fatigued more rapidly in Tg+ mice (∼12%) compared with WT at high Po2. The maximal tension of EDL was equally reduced in Tg+ mice (28–34% decrease from WT under both Po2 conditions); but for soleus this parameter was smaller only under low Po2 in Tg+ mice (∼31% decrease from WT). The peak rate of relaxation and the peak rate of contraction were both significantly reduced in Tg+ EDL muscles compared with WT EDL under low Po2 conditions, but not in soleus. These results demonstrate that TNF-α upregulation in the lung impairs peripheral skeletal muscle function but affects fast- and slow-twitch muscles differentially at high and low Po2.

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