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Grassi 2017 J Appl Physiol (1985) - Revision history
2024-03-28T11:13:51Z
Revision history for this page on the wiki
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Krumschnabel Gerhard at 11:57, 11 June 2018
2018-06-11T11:57:22Z
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Krumschnabel Gerhard
https://wiki.oroboros.at/index.php?title=Grassi_2017_J_Appl_Physiol_(1985)&diff=145393&oldid=prev
Kandolf Georg at 12:24, 13 November 2017
2017-11-13T12:24:55Z
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Kandolf Georg
https://wiki.oroboros.at/index.php?title=Grassi_2017_J_Appl_Physiol_(1985)&diff=141699&oldid=prev
Kandolf Georg: Created page with "{{Publication |title=Grassi B, Majerczak J, Bardi E, Buso A, Comelli M, Chlopicki S, Guzik M, Mavelli I, Nieckarz Z, Salvadego D, Tyrankiewicz U, Skórka T, Bottinelli R, Zola..."
2017-08-23T14:20:07Z
<p>Created page with "{{Publication |title=Grassi B, Majerczak J, Bardi E, Buso A, Comelli M, Chlopicki S, Guzik M, Mavelli I, Nieckarz Z, Salvadego D, Tyrankiewicz U, Skórka T, Bottinelli R, Zola..."</p>
<p><b>New page</b></p><div>{{Publication<br />
|title=Grassi B, Majerczak J, Bardi E, Buso A, Comelli M, Chlopicki S, Guzik M, Mavelli I, Nieckarz Z, Salvadego D, Tyrankiewicz U, Skórka T, Bottinelli R, Zoladz JA, Pellegrino MA (2017) Exercise training in Tgα<sub>q</sub>*44 mice during the progression of chronic heart failure: cardiac vs. peripheral (soleus muscle) impairments to oxidative metabolism. J Appl Physiol (1985) 123:326-36.<br />
|info=[https://www.ncbi.nlm.nih.gov/pubmed/28522765 PMID: 28522765]<br />
|authors=Grassi B, Majerczak J, Bardi E, Buso A, Comelli M, Chlopicki S, Guzik M, Mavelli I, Nieckarz Z, Salvadego D, Tyrankiewicz U, Skórka T, Bottinelli R, Zoladz JA, Pellegrino MA<br />
|year=2017<br />
|journal=J Appl Physiol (1985)<br />
|abstract=Cardiac function, skeletal (soleus) muscle oxidative metabolism, and the effects of exercise training were evaluated in a transgenic murine model (Tgα<sub>q</sub>*44) of chronic heart failure during the critical period between the occurrence of an impairment of cardiac function and the stage at which overt cardiac failure ensues (i.e., from 10 to 12 mo of age). Forty-eight Tgα<sub>q</sub>*44 mice and 43 wild-type FVB controls were randomly assigned to control groups and to groups undergoing 2 mo of intense exercise training (spontaneous running on an instrumented wheel). In mice evaluated at the beginning and at the end of training we determined: exercise performance (mean distance covered daily on the wheel); cardiac function ''in vivo'' (by magnetic resonance imaging); soleus mitochondrial respiration ''ex vivo'' (by high-resolution respirometry); muscle phenotype [myosin heavy chain (MHC) isoform content; citrate synthase (CS) activity]; and variables related to the energy status of muscle fibers [ratio of phosphorylated 5'-AMP-activated protein kinase (AMPK) to unphosphorylated AMPK] and mitochondrial biogenesis and function [peroxisome proliferative-activated receptor-γ coactivator-α (PGC-1α)]. In the untrained Tgα<sub>q</sub>*44 mice functional impairments of exercise performance, cardiac function, and soleus muscle mitochondrial respiration were observed. The impairment of mitochondrial respiration was related to the function of complex I of the respiratory chain, and it was not associated with differences in CS activity, MHC isoforms, p-AMPK/AMPK, and PGC-1α levels. Exercise training improved exercise performance and cardiac function, but it did not affect mitochondrial respiration, even in the presence of an increased percentage of type 1 MHC isoforms. Factors "upstream" of mitochondria were likely mainly responsible for the improved exercise performance.<br />
<br />
Functional impairments in exercise performance, cardiac function, and soleus muscle mitochondrial respiration were observed in transgenic chronic heart failure mice, evaluated in the critical period between the occurrence of an impairment of cardiac function and the terminal stage of the disease. Exercise training improved exercise performance and cardiac function, but it did not affect the impaired mitochondrial respiration. Factors "upstream" of mitochondria, including an enhanced cardiovascular O<sub>2</sub> delivery, were mainly responsible for the functional improvement.<br />
<br />
Copyright © 2017 the American Physiological Society.<br />
|keywords=Transgenic murine model, Chronic heart failure, Skeletal muscle oxidative 59 metabolism, Exercise training<br />
|editor=[[Kandolf G]]<br />
|mipnetlab=IT Udine Grassi B, IT Udine Mavelli I<br />
}}<br />
{{Labeling<br />
|area=Respiration, mt-Biogenesis;mt-density, Exercise physiology;nutrition;life style<br />
|diseases=Cardiovascular<br />
|organism=Mouse<br />
|tissues=Skeletal muscle<br />
|couplingstates=LEAK, OXPHOS, ETS<br />
|pathways=N, NS<br />
|instruments=Oxygraph-2k<br />
|additional=Labels, 2017-08<br />
}}</div>
Kandolf Georg