Metabolic causes of exercise intolerance can be subtle and difficult to document in horses. Because of increased metabolic rate in exercising muscle, most metabolic causes of exercise intolerance are clinically manifested by muscle abnormalities such as ER. Newer causes of ER are being documented by current research and are summarized in the article on muscular causes of equine exercise intolerance. Endocrine causes of exercise intolerance have been poorly documented, but recent work has shown the detrimental effects of hypothyroidism on exercise tolerance in horses. Many metabolic manifestations of exercise intolerance are cumulative in heat exhaustion; prevention by veterinary monitoring is the best treatment, followed by cold water bathing and oral or intravenous fluid and electrolyte replacement. Several ergogenic aids have been proposed and marketed for use in horses, but each has its own problems and few have been shown clearly to have positive effects on performance.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/s0749-0739(17)30271-7 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Paradoxical improvement in exercise tolerance and peak VO2 consumption after treatment with ivabradine and beta-blockers in a patient with mild dilated cardiomyopathy and inappropriate sinus tachycardia-a case report.
Eur Heart J Case Rep
January 2025
Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padova, Via Giustiniani 2, 35128 Padova, Italy.
Background: Left bundle branch block (LBBB) is a rare conduction disorder in athletes associated with ventricular dyssynchrony, which can lead to left ventricular systolic dysfunction and exercise intolerance. Inappropriate sinus tachycardia (IST) is characterized by an excessive heart rate (HR) that is not related to physiological needs, often resulting in reduced exercise capacity. Managing these conditions in athletes can be challenging, as standard treatments like beta-blockers and ivabradine, while effective in controlling HR, are described to be associated with a reduction in maximal exercise performance.
View Article and Find Full Text PDFTwo-hit mouse model of heart failure with preserved ejection fraction combining diet-induced obesity and renin-mediated hypertension.
Sci 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 PDFPantothenate kinase 4 controls skeletal muscle substrate metabolism.
Nat Commun
January 2025
Department of Molecular Physiology of Exercise and Nutrition, German Institute of Human Nutrition (DIfE), Potsdam-Rehbruecke, Nuthetal, Germany.
Metabolic flexibility in skeletal muscle is essential for maintaining healthy glucose and lipid metabolism, and its dysfunction is closely linked to metabolic diseases. Exercise enhances metabolic flexibility, making it an important tool for discovering mechanisms that promote metabolic health. Here we show that pantothenate kinase 4 (PanK4) is a new conserved exercise target with high abundance in muscle.
View Article and Find Full Text PDFCardiac Presynaptic Sympathetic Nervous Function Evaluated by Cardiac PET in Patients with Chronotropic Incompetence Without Heart Failure.
J Nucl Med
January 2025
Department of Cardiology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Chronotropic incompetence (CTI), the inability of the heart to increase its rate with increased activity, leads to exercise intolerance and predicts overall mortality. We previously reported that cardiac β-adrenergic receptor downregulation occurs in patients with CTI without heart failure (HF), indicating postsynaptic sympathetic nervous dysfunction. However, cardiac presynaptic sympathetic nervous system function in CTI is not fully understood.
View Article and Find Full Text PDFA founder variant in the RYR1 gene is associated with hyperCKemia, myalgia and muscle cramps.
Eur J Neurol
January 2025
Genetics Department, Institut de Recerca Sant Pau (IR SANT PAU), Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
Background And Purpose: Pathogenic variants in the RYR1 gene have been associated with a variety of conditions, ranging from congenital myopathy to adult manifestations. Our aim was to characterize the p.Leu2286Val variant in 17 Basque patients, to accurately determine its correlation with clinical features and to explore the possible founder effect of the variant.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!