Changes in circulating equine erythrocytes induced by brief, high-speed exercise

Five horses were exercised at 10m/sec at a 3 degree incline for 2 mins. Packed cell volume, erythrocyte count, haemoglobin concentration, mean corpuscular volume, plasma protein, total white cell count and lymphocytes increased significantly in blood samples taken after exercise, compared with those taken before exercise; but mean corpuscular haemoglobin and mean corpuscular haemoglobin concentration decreased. Erythrocytes were more resistant to osmotic stress after exercise, but their shape and degree of deformity were unaffected by exercise.     

The effect of exercise and conditioning on equine red blood cell characteristics

The effect of exercise and conditioning on 2,3-diphosphoglycerate levels was studied in nine mature horses. During a 12 minute exercise bout producing heart rates of 165 bpm, 2,3-DPG was significantly increased (p<.05). In addition, exercising levels of 2,3-DPG were increased (p<.05) approximately 8% after a six-week submaximal conditioning program. These increases could not be entirely attributed to changes in erythrocyte number. Mean corpuscular volume was also increased during exercise (p<.05) but was not altered by conditioning.     

Biochemical and metabolic changes due to exercise in sprint-racing sled dogs: implications for postexercise carbohydrate supplements and hydration management

Evaluations of biochemical changes associated with spring-style sled dog racing indicate that differences in cortisol, lactate, and serum glucose levels suggest exercise of moderate duration (but high intensity) has metabolic demands that dif-fer from those for typical endurance sled dog racing. Additionally, hematocrit, albumin, sodium, chloride, and blood urea nitrogen levels decreased in one team of dogs, whereas there were mild increases in sodium, chloride, and blood urea nitrogen in the other team. These opposing biochemical findings suggest physiologic changes associated with differences in hydration status, likely attributed to different dietary and hydration strategies used by the respective kennels.     

ECEIM consensus statement on equine metabolic syndrome

Equine metabolic syndrome (EMS) is a widely recognized collection of risk factors for endocrinopathic laminitis. The most important of these risk factors is insulin dysregulation (ID). Clinicians and horse owners must recognize the presence of these risk factors so that they can be targeted and controlled to reduce the risk of laminitis attacks. Diagnosis of EMS is based partly on the horse's history and clinical examination findings, and partly on laboratory testing. Several choices of test exist which examine different facets of ID and other related metabolic disturbances. EMS is controlled mainly by dietary strategies and exercise programs that aim to improve insulin regulation and decrease obesity where present. In some cases, pharmacologic aids might be useful. Management of an EMS case is a long‐term strategy requiring diligence and discipline by the horse's carer and support and guidance from their veterinarians.     

The equine metabolic syndrome peripheral Cushing's syndrome.

Certain management practices tend to promote the development of obesity (metabolic syndrome) in mature horses as they enter their teenage years. These management practices include the provision of starch-rich (high glycemic index) and fat-supplemented rations to healthy horses that are relatively inactive. Some horse breeds and ponies appear to be genetically predisposed to metabolic syndrome. The accretion of intra-abdominal adiposity by equids is associated with the development of insulin insensitivity (hyperinsulinemia), glucose intolerance, dyslipidemia, hypertension, and insidious-onset laminitis. Omental adipocytes are metabolically active, secreting free fatty acids and hormonally active mediators including cortisol, leptin, and resistin that might contribute to persistence and worsening of insulin refractoriness and the obese phenotype. We have hypothesized that obesity-associated laminitis arises as a consequence of vascular changes and a hypercoagulable state, similar to the development of atherosclerosis in human type 2 diabetes. Several molecular mechanisms that might serve to explain the development of insulin insensitivity as a result of excessive adiposity have been incriminated. Little investigation into the relationship between obesity, insulin insensitivity, and laminitis in horses has been reported to date. Insulin sensitivity and glucose tolerance can be improved by dietary restriction and exercise aimed at reversing omental obesity. Management practices that promote the development of obesity are likely initiated during the first 10 years of the horse's life. Veterinarians and horse owners must recognize that mature-onset obesity in adult horses is associated with a risk for development of laminitis. Obesity and insulin insensitivity might be prevented if horse owners can be educated to feed rations with a relatively lower glycemic index to inactive horses. Investigative research pertaining to the development of antiobesity drugs for human patients is continuing. Greater than 30 new pharmaceuticals are in various stages of research. However, it will likely take many years before any of these drugs are shown to be useful and safe in horses. Lifestyle changes in the form of diet and exercise patterns are still the crux of therapy for both human and equine patients.