Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Healthy untrained men performed 10 series of 12 knee eccentric extension repetitions (EE) at 160 degrees /s. The maximal voluntary isometric contraction force of the quadriceps muscle, the maximal rate of electrically induced torque development (RTD) and relaxation (RTR), isokinetic concentric torque at 30 degrees /s, the electrostimulation-induced torque at 20 and 100Hz frequencies were established before and after EE at shorter and longer muscle lengths. Besides, voluntary activation (VA) index and central activation ratio (CAR) were tested. There was more peripheral fatigue than central after EE. We established more central fatigue as well as low frequency fatigue at a shorter muscle length compared to the longer muscle length. Relative RTD as well as relative RTR, improved after EE and did not depend on the muscle length. Finally, central fatigue is inversely significantly related with the eccentric torque reduction during eccentric exercise and with the changes in muscle torque induced by low frequency stimulation.
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PMID:Peripheral and central fatigue after muscle-damaging exercise is muscle length dependent and inversely related. 2034 33

The stress-responsive epigenetic repressor histone deacetylase 4 (HDAC4) regulates cardiac gene expression. Here we show that the levels of an N-terminal proteolytically derived fragment of HDAC4, termed HDAC4-NT, are lower in failing mouse hearts than in healthy control hearts. Virus-mediated transfer of the portion of the Hdac4 gene encoding HDAC4-NT into the mouse myocardium protected the heart from remodeling and failure; this was associated with decreased expression of Nr4a1, which encodes a nuclear orphan receptor, and decreased NR4A1-dependent activation of the hexosamine biosynthetic pathway (HBP). Conversely, exercise enhanced HDAC4-NT levels, and mice with a cardiomyocyte-specific deletion of Hdac4 show reduced exercise capacity, which was characterized by cardiac fatigue and increased expression of Nr4a1. Mechanistically, we found that NR4A1 negatively regulated contractile function in a manner that depended on the HBP and the calcium sensor STIM1. Our work describes a new regulatory axis in which epigenetic regulation of a metabolic pathway affects calcium handling. Activation of this axis during intermittent physiological stress promotes cardiac function, whereas its impairment in sustained pathological cardiac stress leads to heart failure.
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PMID:A proteolytic fragment of histone deacetylase 4 protects the heart from failure by regulating the hexosamine biosynthetic pathway. 2922 74