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

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.

Exercise Capacity Is Limited In Diabetic Mice Due To The Impairment Of Skeletal Muscle Function

2007 ◽  
Vol 39 (Supplement) ◽  
pp. S360
Author(s):  
Takashi Yokota ◽  
Shintaro Kinugawa ◽  
Syoji Matsushima ◽  
Naoki Inoue ◽  
Yukihiro Ohta ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Capacity ◽  
Muscle Function ◽  
Diabetic Mice ◽  
Skeletal Muscle Function

Quantitative assessment of cardiorespiratory fitness, skeletal muscle function, and body composition in adults with primary malignant glioma

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e13002-e13002
Author(s):  
L. Jones ◽  
A. Friedman ◽  
M. West ◽  
S. Mabe ◽  
J. Fraser ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Composition ◽  
Muscle Strength ◽  
Malignant Glioma ◽  
Exercise Capacity ◽  
Muscle Function ◽  
Isokinetic Strength ◽  
Safe Procedure ◽  
Skeletal Muscle Function ◽  
Cross Sectional

e13002 Background: The neuropsychological impact of malignant glioma is well documented; the physiological and functional effects are not known. We conducted a pilot study to quantitatively assess cardiorespiratiory fitness, skeletal muscle function, and body composition of patients with primary malignant glioma. Methods: Using a cross-sectional design, patients with clinically stable postsurgical (10 ± 7 days post surgery) high-grade glioma (HGG; n=25) and low-grade glioma (LGG) were studied. Participants performed a cardiopulmonary exercise test (CPET) with expired gas analysis to assess peak exercise capacity (VO2peak) and other parameters of cardiovascular function. Other physiological outcomes included skeletal muscle cross-sectional area (CSA; magnetic resonance imaging), isokinetic muscle strength (isokinetic dynamometer), and body composition (air displacement plethysmography). QOL was assessed by the Functional Assessment of Cancer Therapy-Brain scale (FACT-BR). Results: CPET was a feasible and safe procedure for malignant glioma patients with no serious adverse events. Peak VO2 indexed to total body weight and lean body mass for both groups was 13.0 mL.min-1 and 19 mL.min-1; the equivalent to 59% and 38% below age and sex-predicted normative values, respectively. Skeletal muscle isokinetic strength was significantly lower in HGG relative to LGG patients (83 vs. 125 Nm, p=.025) and predicted peak VO2 (r = 0.44, p<0.05). In patients with HGG, only self-reported exercise behavior was correlated with QOL (r = 0.42; p=.046) while sex (male) (r = 0.44; p=.037), lean mass (r = -0.41; p=.049), and VO2peak (r = -0.40; p=.052) were associated with fatigue. Conclusions: CPET is a safe and feasible tool to evaluate physical functioning in select patients with malignant glioma. Postsurgical glioma patients have markedly reduced exercise capacity, isokinetic strength and CSA. Muscle strength is an important contributor to poor VO2peak in this population. Prospective studies are now required to determine whether such abnormalities influence prognosis as well as test the effect of appropriately selected interventions to prevent and/or mitigate dysfunction. No significant financial relationships to disclose.

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.

Maximal exercise capacity and peripheral skeletal muscle function following lung transplantation

1999 ◽  
Vol 18 (2) ◽  
pp. 113-120 ◽  
Author(s):  
Larry C Lands ◽  
Argyrios A Smountas ◽  
Giulia Mesiano ◽  
L Brosseau ◽  
Hani Shennib ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lung Transplantation ◽  
Exercise Capacity ◽  
Muscle Function ◽  
Maximal Exercise ◽  
Skeletal Muscle Function ◽  
Maximal Exercise Capacity

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.

scholarly journals Impaired exercise capacity and skeletal muscle function in a mouse model of pulmonary inflammation

2013 ◽  
Vol 114 (9) ◽  
pp. 1340-1350 ◽  
Author(s):  
Kechun Tang ◽  
George Murano ◽  
Harrieth Wagner ◽  
Leonardo Nogueira ◽  
Peter D. Wagner ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Capacity ◽  
Muscle Function ◽  
Citrate Synthase ◽  
Left Ventricular ◽  
Lv Function ◽  
Male Mice ◽  
Skeletal Muscle Function ◽  
Exercise Limitation ◽  
Maximal Pressure

Pulmonary TNFα has been linked to reduced exercise capacity in a subset of patients with moderate to severe chronic obstructive pulmonary disease (COPD). We hypothesized that prolonged, high expression of pulmonary TNFα impairs cardiac and skeletal muscle function, and both contribute to exercise limitation. Using a surfactant protein C promoter-TNFα construct, TNFα was overexpressed throughout life in mouse lungs (SP-C/TNFα+). TNFα levels in wild-type (WT) female serum and lung were two- and threefold higher than in WT male mice. In SP-C/TNFα+ mice, TNFα increased similarly in both sexes. Treadmill exercise was impaired only in male SP-C/TNFα+ mice. While increases in lung volume and airspace size induced by TNFα were comparable in both sexes, pulmonary hypertension along with lower body and muscle mass were evident only in male mice. Left ventricular (LV) function (cardiac output, stroke volume, LV maximal pressure, and LV maximal pressure dP/d t) was not altered by TNFα overexpression. Fatigue measured in isolated soleus and EDL was more rapid only in soleus of male SP-C/TNFα+ mice and accompanied by a loss of oxidative IIa fibers, citrate synthase activity, and PGC-1α mRNA and increase in atrogin-1 and MuRF1 expression also only in male mice. In situ gastrocnemius fatigue resistance, reflecting both oxygen availability and contractility, was decreased similarly in female and male SP-C/TNFα+ mice. These data indicate that male, but not female, mice overexpressing pulmonary TNFα are susceptible to exercise limitation, possibly due to muscle wasting and loss of the oxidative muscle phenotype, with protection in females possibly due to estrogen.

scholarly journals Relationship between intermuscular adipose tissue infiltration and myostatin before and after aerobic exercise training

2018 ◽  
Vol 315 (3) ◽  
pp. R461-R468 ◽  
Author(s):  
Adam R. Konopka ◽  
Christopher A. Wolff ◽  
Miranda K. Suer ◽  
Matthew P. Harber
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Exercise Capacity ◽  
Muscle Function ◽  
Aerobic Exercise Training ◽  
Skeletal Muscle Function ◽  
Intermuscular Adipose Tissue ◽  
Before And After

Intermuscular adipose tissue (IMAT) is associated with impaired skeletal muscle contractile and metabolic function. Myostatin and downstream signaling proteins such as cyclin-dependent kinase 2 (CDK2) contribute to the regulation of adipose and skeletal muscle mass in cell culture and animals models, but this relationship remains incompletely understood in humans. The purpose of this study was to determine if the infiltration of IMAT was associated with skeletal muscle myostatin and downstream proteins before and after 12 wk of aerobic exercise training (AET) in healthy older women (OW; 69 ± 2 yr), older men (OM; 74 ± 3 yr), and young men (YM; 20 ± 1 yr). We found that the infiltration of IMAT was correlated with myostatin and phosphorylated CDK2 at tyrosine 15 [P-CDK2(Tyr15)]. IMAT infiltration was greater in the older subjects and was associated with lower skeletal muscle function and exercise capacity. After 12 wk of AET, there was no change in body weight. Myostatin and P-CDK2(Tyr15) were both decreased after AET, and the reduction in myostatin was associated with decreased IMAT infiltration. The decrease in myostatin and IMAT occurred concomitantly with increased exercise capacity, skeletal muscle size, and function after AET. These findings demonstrate that the reduction in IMAT infiltration after AET in weight stable individuals was accompanied by improvements in skeletal muscle function and exercise capacity. Moreover, the association between myostatin and IMAT was present in the untrained state and in response to exercise training, strengthening the potential regulatory role of myostatin on IMAT.

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