Deletion of the Microtubule‐associated protein tau (Mapt−/−) results in diastolic heart failure and altered skeletal muscle function in vivo

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Sahith Rajalingam ◽  
Anuradha Valiya Kambrath ◽  
Ruben Vidal ◽  
Monte S. Willis
2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 903
Author(s):  
David S. Hydock ◽  
Chia-Ying Lien ◽  
Brock T. Jensen ◽  
Traci L. Parry ◽  
Carole M. Schneider ◽  
...  

2002 ◽  
Vol 92 (1) ◽  
pp. 18-24 ◽  
Author(s):  
Espen E. Spangenburg ◽  
Simon J. Lees ◽  
Jeff S. Otis ◽  
Timothy I. Musch ◽  
Robert J. Talmadge ◽  
...  

It is thought that changes in sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) of skeletal muscle contribute to alterations in skeletal muscle function during congestive heart failure (CHF). It is well established that exercise training can improve muscle function. However, it is unclear whether similar adaptations will result from exercise training in a CHF patient. Therefore, the purpose of this study was to determine whether skeletal muscle during moderate CHF adapts to increased activity, utilizing the functional overload (FO) model. Significant increases in plantaris mass of the CHF-FO and sham-FO groups compared with the CHF and control (sham) groups were observed. Ca2+ uptake rates were significantly elevated in the CHF group compared with all other groups. No differences were detected in Ca2+ uptake rates between the CHF-FO, sham, and sham-FO groups. Increases in Ca2+ uptake rates in moderate-CHF rats were not due to changes in SERCA isoform proportions; however, FO may have attenuated the CHF-induced increases through alterations in SERCA isoform expression. Therefore, changes in skeletal muscle Ca2+handling during moderate CHF may be due to alterations in regulatory mechanisms, which exercise may override, by possibly altering SERCA isoform expression.


1997 ◽  
Vol 18 (10) ◽  
pp. 1626-1631 ◽  
Author(s):  
C. Opasich ◽  
E. Pasini ◽  
R. Aquilani ◽  
F. Coelli ◽  
R. Solfrini ◽  
...  

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
David Hydock ◽  
Asma Omar ◽  
Eric Bredahl ◽  
Colin Quinn

2021 ◽  
Vol 12 ◽  
Author(s):  
Mario Elkes ◽  
Martin Andonovski ◽  
Daislyn Vidal ◽  
Madison Farago ◽  
Ryan Modafferi ◽  
...  

Barth syndrome is a rare and incurable X-linked (male-specific) genetic disease that affects the protein tafazzin (Taz). Taz is an important enzyme responsible for synthesizing biologically relevant cardiolipin (for heart and skeletal muscle, cardiolipin rich in linoleic acid), a critical phospholipid of mitochondrial form and function. Mutations to Taz cause dysfunctional mitochondria, resulting in exercise intolerance due to skeletal muscle weakness. To date, there has been limited research on improving skeletal muscle function, with interventions focused on endurance and resistance exercise. Previous cell culture research has shown therapeutic potential for the addition of exogenous linoleic acid in improving Taz-deficient mitochondrial function but has not been examined in vivo. The purpose of this study was to examine the influence of supplemental dietary linoleic acid on skeletal muscle function in a rodent model of Barth syndrome, the inducible Taz knockdown (TazKD) mouse. One of the main findings was that TazKD soleus demonstrated an impaired contractile phenotype (slower force development and rates of relaxation) in vitro compared to their WT littermates. Interestingly, this impaired contractile phenotype seen in vitro did not translate to altered muscle function in vivo at the whole-body level. Also, supplemental linoleic acid attenuated, to some degree, in vitro impaired contractile phenotype in TazKD soleus, and these findings appear to be partially mediated by improvements in cardiolipin content and resulting mitochondrial supercomplex formation. Future research will further examine alternative mechanisms of dietary supplemental LA on improving skeletal muscle contractile dysfunction in TazKD mice.


2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Kinga Węgrzynowska-Teodorczyk ◽  
Agnieszka Siennicka ◽  
Krystian Josiak ◽  
Robert Zymliński ◽  
Monika Kasztura ◽  
...  

Background. Acute heart failure (AHF) is associated with disturbances of the peripheral perfusion leading to the dysfunction of many organs. Consequently, an episode of AHF constitutes a “multiple organ failure” which may also affect the skeletal muscles. However, the abnormalities within skeletal muscles during AHF have not been investigated so far. The aim of this project is to comprehensively evaluate skeletal muscles (at a functional and tissue level) during AHF. Methods. The study will include ≥63 consecutive AHF patients who will be randomized into 2 groups: ≥42 with cardiac rehabilitation group versus ≥21 with standard pharmacotherapy alone. The following tests will be conducted on the first and last day of hospitalization, at rest and after exercise, and 30 days following the discharge: clinical evaluation, medical interview, routine physical examination, echocardiography, and laboratory tests (including the assessment of NT-proBNP, inflammatory markers, and parameters reflecting the status of the kidneys and the liver); hemodynamic evaluation, noninvasive determination of cardiac output and systemic vascular resistance using the impedance cardiography; evaluation of biomarkers reflecting myocyte damage, immunochemical measurements of tissue-specific enzymatic isoforms; evaluation of skeletal muscle function, using surface electromyography (sEMG) (maximum tonus of the muscles will be determined along with the level of muscular fatigability); evaluation of muscle tissue perfusion, assessed on the basis of the oxygenation level, with noninvasive direct continuous recording of perfusion in peripheral tissues by local tissue oximetry, measured by near-infrared spectroscopy (NIRS). Results and Conclusions. Our findings will demonstrate that the muscle tissue is another area of the body which should be taken into consideration in the course of treatment of AHF, requiring a development of targeted therapeutic strategies, such as a properly conducted rehabilitation.


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