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The aim of this study was to investigate the effects of multiple cold-water immersions (CWIs) on muscle function, markers of muscle damage, systemic inflammation and ECM degradation following exercise-induced muscle damage (EIMD). Thirty physically active males were randomly assigned to either a control (n = 15) or cold-water immersion (CWI) group (n = 15). The CWI group performed one immersion (10 °C for 20 min) at post-exercise and every 24 h for the following 72 h, while the control group remained in a seated position during these corresponding periods. Muscle strength, vertical jump height, muscle thickness, delayed-onset muscle soreness (DOMS), systemic creatine kinase (CK), C-reactive protein (CRP), inflammatory cytokines and matrix metalloproteinase-2 (MMP-2) activity were assessed at Pre, Post, 24, 48, 72, 96 and 168 h following EIMD. No significant time × group interaction was obtained for muscle strength, vertical jump height recovery and MMP-2 activity (p > 0.05). At 24 h, muscle thickness from the CWI group returned to baseline and was lower than the control (p = 0.04). DOMS returned to baseline at 168 h for the CWI group (p = 0.109) but not for the control (p = 0.008). At 168 h, CK showed a time-group difference with a greater peak for the control group (p = 0.016). In conclusion, multiple CWIs attenuated muscle damage, but not altered systemic inflammation and muscle function recovery.
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http://dx.doi.org/10.1038/s41598-018-28942-5 | DOI Listing |
Rev Cardiovasc Med
August 2025
Henan Key Laboratory of Medical Tissue Regeneration, Xinxiang Medical University, 453003 Xinxiang, Henan, China.
Myocarditis is a life-threatening inflammatory disorder that affects the cardiac muscle tissue. Current treatments merely regulate heart function but fail to tackle the root cause of inflammation. In myocarditis, the initial wave of inflammation is characterized by the presence of neutrophils.
View Article and Find Full Text PDFCell Physiol Biochem
September 2025
Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institute of Biochemistry, 10117 Berlin, Germany.
Background/aims: The ubiquitin-like protein ISG15 and its covalent conjugation to substrates (ISGylation) represent a critical interferon (IFN)-induced antiviral mechanism. USP18 is an ISG15-specific isopeptidase and a key negative regulator of type I IFN signaling. While inactivation of USP18's catalytic activity enhances ISGylation and promotes viral resistance, its role in modulating inflammation and cardiac function during CVB3-induced myocarditis remains unclear.
View Article and Find Full Text PDFMed Eng Phys
October 2025
Departament of Electronics and Biomedical Engineering, School of Electrical and Computer Engineering (DEEB/FEEC), University of Campinas (UNICAMP), Campinas, SP, Brazil; National Laboratory for Study of Cell Calcium (LabNECC), Center for Biomedical Engineering (CEB), UNICAMP, Campinas, SP, Brazil.
High-intensity, external electric fields (HIEF) have been used in research and therapy for abnormal generation/propagation of the cardiac electrical activity (e.g., defibrillation), and for promoting access of membrane-impermeant molecules into the cytosol through electropores.
View Article and Find Full Text PDFBiomed Pharmacother
September 2025
Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Electronic address:
Immune-mediated necrotizing myopathy (IMNM) is an emerging and severe form of myositis. Most patients experience persistent muscle weakness or recurrent attacks within their lifetime. The previous view suggests that autoimmune and complement activation play a key role in muscle damage, and aggressive immunotherapy may benefit patients.
View Article and Find Full Text PDFRedox Biol
August 2025
Department of Medicine, School of Medicine, Universidad Autónoma de Madrid, Madrid, Spain; Instituto Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain; Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES), Instituto de Salud Carlos III, Madrid, Spain. Electronic
Tobacco smoke is the main risk factor for the development of chronic obstructive pulmonary disease (COPD). Despite current therapies alleviate symptoms there are limitations in the efficacy of treatments to curb its cardiovascular morbidities, particularly vascular dysfunction and the development of pulmonary hypertension. Our previous studies demonstrate that cigarette smoke directly contributes to pulmonary arterial dysfunction.
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