"All things are poison, and nothing is without poison; the dosage alone makes it so a thing is not a poison" (Paracelsus, ~ 1538 AD). This well-known quote seems to aptly summarize the current understanding of the interaction between exercise and atrial fibrillation (AF). A host of data strongly suggests that regular exercise has a protective effect against developing AF. A small but well-conducted group of trials also demonstrates beneficial effects of exercise in the treatment of AF. Recently, however, potentially detrimental effects of large volumes of high-intensity exercise on the probability of developing AF have moved into the sports-cardiological focus. This effect is well documented for elite athletes; data regarding the general population is less clear. This review presents the current data regarding the protective, therapeutic and potentially risk-enhancing effects of exercise regarding AF. The authors demonstrate that the benefits are clear and strongly outweigh the potential disadvantages.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10776210 | PMC |
http://dx.doi.org/10.1055/a-2152-7628 | DOI Listing |
Front Cardiovasc Med
December 2024
Cardiology Department, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Atrial fibrillation (AF), the most prevalent cardiac arrhythmia, is closely linked to metabolic dysfunctions, including obesity, diabetes, and dyslipidemia. These lead to pathological changes in myocardial metabolism and mitochondrial energy metabolism, thereby aggravating AF's incidence and severity. This review introduces the role of metabolic dysfunctions in exacerbating AF, assesses the therapeutic potential of physical exercise and investigates it as a non-pharmacological intervention to alleviate these metabolic disturbances.
View Article and Find Full Text PDFSci Rep
January 2025
Cardiovascular Institute, Children's Hospital of Philadelphia, Philadelphia, PA, USA.
Heart failure with preserved ejection fraction (HFpEF) is increasingly common but its pathogenesis is poorly understood. The ability to assess genetic and pharmacologic interventions is hampered by the lack of robust preclinical mouse models of HFpEF. We developed a novel "two-hit" model, which combines obesity and insulin resistance with chronic pressure overload to recapitulate clinical features of HFpEF.
View Article and Find Full Text PDFFront Physiol
December 2024
NextGen Precision Health, University of Missouri, Columbia, MO, United States.
The Lim Kinase (LIMK) family of serine/threonine kinases is comprised of LIMK1 and LIMK2, which are central regulators of cytoskeletal dynamics via their well-characterized roles in promoting actin polymerization and destabilizing the cellular microtubular network. The LIMKs have been demonstrated to modulate several fundamental physiological processes, including cell cycle progression, cell motility and migration, and cell differentiation. These processes play important roles in maintaining cardiovascular health.
View Article and Find Full Text PDFFront Cardiovasc Med
December 2024
School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Objective: The left atrial stiffness index (LASI) holds significance in the atrioventricular coupling function and heart failure progression. To assess left atrial function and evaluate the relationship between LASI and exercise capacity in hypertension-related heart failure with preserved ejection fraction (HT-HFpEF).
Methods: The study involved 62 healthy subjects and 163 patients with HT (112 patients in simple HT group and 51 patients in HT-HFpEF group).
Front Cardiovasc Med
December 2024
Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Pok Fu Lam, Hong Kong SAR, China.
Background: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare inherited arrhythmia disorder characterized by ventricular arrhythmia triggered by adrenergic stimulation.
Case Presentation: A 9-year-old boy presented with convulsions following physical exertion. Bidirectional ventricular tachycardia (VT) during a treadmill test led to the diagnosis of catecholaminergic polymorphic ventricular tachycardia (CPVT).
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