scholarly journals Voluntary physical activity counteracts Chronic Heart Failure progression affecting both cardiac function and skeletal muscle in the transgenic Tgαq*44 mouse model

2019 ◽  
Vol 7 (13) ◽  
Author(s):  
Eleonora Bardi ◽  
Joanna Majerczak ◽  
Jerzy A. Zoladz ◽  
Urszula Tyrankiewicz ◽  
Tomasz Skorka ◽  
...  
2015 ◽  
Vol 38 (5) ◽  
pp. 409-415 ◽  
Author(s):  
Sumihito Haseba ◽  
Harutoshi Sakakima ◽  
Takuro Kubozono ◽  
Syuhei Nakao ◽  
Satoshi Ikeda

2007 ◽  
Vol 26 (2) ◽  
pp. S209
Author(s):  
S. Maybaum ◽  
I. George ◽  
C. Petrilli ◽  
E. Shane ◽  
G. Kamalakkannan ◽  
...  

2011 ◽  
Vol 110 (4) ◽  
pp. 892-900 ◽  
Author(s):  
Michael J. Toth ◽  
Kimberly Ward ◽  
Jos van der Velden ◽  
Mark S. Miller ◽  
Peter VanBuren ◽  
...  

Patients with chronic heart failure (HF) frequently lose muscle mass and function during the course of the disease. A reduction in anabolic stimuli to the muscle has been put forth as a potential mechanism underlying these alterations. The present study examined the hypothesis that skeletal muscle tissue from HF patients would show reduced IGF-1 expression and phosphorylation of signaling molecules downstream of receptor activation. To isolate the unique effect of HF on these variables, we limited the confounding effects of muscle disuse and/or acute disease exacerbation by recruiting controls ( n = 11) with similar physical activity levels as HF patients ( n = 11) and by testing patients at least 6 mo following any bouts of disease exacerbation/hospitalization. IGF-1 expression in skeletal muscle was similar between patients and controls. Despite this, HF patients were characterized by reduced levels of phospho-Akt/Akt (S473; −43%; P < 0.05), whereas no differences were found in total Akt protein content or phospho- or total protein content of mammalian target of rapamycin (mTOR; S2448), glycogen synthase kinase-3β (GSK-3β; S9), eukaryotic translation initiation factor 4E binding protein-1 (eIF4E-BP; T37/46), p70 ribosomal S6 kinase (p70 S6K; T389), or eIF2Bε (S540). Reduced phospho-Akt/Akt levels and phospho-mTOR/mTOR were related to decreased skeletal muscle myosin protein content ( r = 0.602; P < 0.02) and knee extensor isometric torque ( r = 0.550; P < 0.05), respectively. Because patients and controls were similar for age, muscle mass, and physical activity, we ascribe the observed alterations in Akt phosphorylation and its relationship to myosin protein content to the unique effects of the HF syndrome.


2018 ◽  
Vol 1 (2) ◽  
Author(s):  
Lingjie Li ◽  
Jing Zhang ◽  
Xuefei Chen

Objective To investigate the effects of vascular endothelial growth factor B in aerobic exercise mediated chronic heart failure rats cardiac function improvement and skeletal muscle remodeling. Methods We employed transverse abdominal aortic constriction (TAC) inducing CHF in Sprague Dawley rats. Controls were sham-operated animals. At 4 weeks after surgery, rats were randomized to 4 weeks of aerobic exercise (CHF+E) or to untrained groups (CHF). After 8 weeks, all rats went echocardiography test. After which, rats were sacrificed and samples were collected. Muscular cytokine VEGFB and its receptor NRP1 expression were analyzed. Expression of apoptosis and muscle atrophy markers were assessed in cardiac muscle、gastrocnemius. Results TAC rats developed CHF (preserved LV ejection fraction, hypertrophy of myocardial cells, decreased FS, increased LVAW d and LVID s). Exercise ameliorate CHF rat cardiac function. TAC rat skeletal muscle developed irregular muscle fiber distribution.The two atrophy-related ubiquitin ligases atrogin-1 and MuRF1, as well as genes involved in apoptosis and autophagy were upregulated in muscles in CHF rats. Exercise inhibited muscle atrophy and skeletal muscle apoptosis.VEGFB and its receptor NRPI decreased significantly in CHF muscle. Exercise promoted VEGFB and NRP1 expression in cardiac tissue, gastrocnemius. Conclusions Exercise ameliorates CHF rat cardiac function. VEGFB inhibits cardiac muscle and gastrocnemius apoptosis in CHF rats.


Author(s):  
Kazuhiro P. Izawa ◽  
Satoshi Watanabe ◽  
Koichiro Oka ◽  
Koji Hiraki ◽  
Yuji Morio ◽  
...  

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