Horses were exercised at 40, 65, and 90% of their maximum O2 uptake (VO2max) until moderately fatigued (approximately 38, 15, and 9 min, respectively) to assess heat loss through different routes. Approximately 4,232, 3,195, and 2,333 kcal of heat were generated in response to exercise at these intensities. Of this, approximately 7, 16, and 20% remained as stored heat 30 min postexercise. Respiratory heat loss, estimated from the temperature difference between blood in the pulmonary and carotid arteries and the cardiac output, was estimated to be 30, 19, and 23% of the heat produced during exercise at the three intensities. The kinetics of the increases in muscle and blood temperature were similar, with the greatest change in temperature occurring in muscle (+3.8, 5.2, and 6.1 degrees C after exercise at 40, 65, and 90% of VO2max, respectively). The temperature of blood in the superficial thoracic vein was approximately 2 degrees C below that of arterial blood at rest. This difference had increased to approximately 3 degrees C during the last minute of exercise. The rate of sweating at sites on the back and neck increased with exercise intensity to a common peak of approximately 40 ml.m-2.min-1. If complete evaporation had occurred, water loss in response to exercise (estimated to be 12, 10, and 7.7 liters for the different intensities of exercise) greatly surpassed that required for dissipation of the metabolic heat load.

Objective—To determine the effects of diet-induced weight gain on glucose and insulin dynamics and plasma hormone and lipid concentrations in horses. Animals—13 adult geldings. Procedures—Horses were fed 200% of their digestible energy requirements for maintenance for 16 weeks to induce weight gain. Frequently sampled IV glucose tolerance tests were performed before and after weight gain to evaluate glucose and insulin dynamics. Adiposity (assessed via condition scoring, morphometric measurements, and subcutaneous fat depth) and plasma concentrations of insulin, glucose, nonesterified fatty acids, triglycerides, and leptin were measured on a weekly or biweekly basis. Results—Mean ± SD body weight increased by 20% from 440 ± 44 kg to 526 ± 53 kg, and body condition score (scale, 1 to 9) increased from 6 ± 1to8 ± 1. Plasma glucose, triglyceride, and nonesterified fatty acid concentrations were similar before and after weight gain. Leptin and insulin concentrations increased with weight gain. Mean ± SD insulin sensitivity decreased by 71 ± 28%, accompanied by a 408 ± 201% increase in acute insulin response to glucose, which resulted in similar disposition index before and after weight gain. Conclusions and Clinical Relevance—Diet-induced weight gain in horses occurred concurrently with decreased insulin sensitivity that was effectively compensated for by an increase in insulin secretory response. Obesity resulted in hyperinsulinemia and hyperleptinemia, compared with baseline values, but no changes in lipid concentrations were apparent. Preventing obesity is a potential strategy to help avoid insulin resistance, hyperinsulinemia, and hyperleptinemia in horses.

Background: Insulin resistance has been associated with risk of laminitis in horses. Genes coding for proinflammatory cytokines and chemokines are expressed more in visceral adipose tissue than in subcutaneous adipose tissue of insulin-resistant (IR) humans and rodents.Hypothesis/Objectives: To investigate adipose depot-specific cytokine and chemokine gene expression in horses and its relationship to insulin sensitivity (SI).Animals: Eleven light breed mares. Methods: Animals were classified as IR (SI 5 0.58 AE 0.31 Â 10 À4 L/min/mU; n 5 5) or insulin sensitive (IS; SI 5 2.59 AE 1.21 Â 10 À4 L/min/mU; n 5 6) based on results of a frequently sampled intravenous glucose tolerance test. Omental, retroperitoneal, and mesocolonic fat was collected by ventral midline celiotomy; incisional nuchal ligament and tail head adipose tissue biopsy specimens were collected concurrently. The expression of tumor necrosis factor-a (TNF-a), interleukin (IL)-1b, IL-6, plasminogen activator inhibitor-1 (PAI-1), and monocyte chemoattractant protein-1 (MCP-1) in each depot was measured by real-time quantitative polymerase chain reaction. Data were analyzed by 2-way analysis of variance for repeated measures (P o .05).Results: No differences in TNF-a, IL-1b, IL-6, PAI-1, or MCP-1 mRNA concentrations were noted between IR and IS groups for each depot. Concentrations of mRNA coding for IL-1b (P 5 .0005) and IL-6 (P 5 .004) were significantly higher in nuchal ligament adipose tissue than in other depots.Conclusions and Clinical Importance: These data suggest that the nuchal ligament depot has unique biological behavior in the horse and is more likely to adopt an inflammatory phenotype than other depots examined. Visceral fat may not contribute to the pathogenesis of obesity-related disorders in the horse as in other species.

This study examined the effects of acute high-intensity exercise on the rate and capacity of Ca2+ uptake and Ca2+-stimulated adenosinetriphosphatase (ATPase) activity of the sarcoplasmic reticulum and the reversibility of these effects. Thoroughbred horses were run at maximal O2 uptake on a high-speed treadmill until fatigued. Muscle temperatures and biopsy samples were collected at rest, immediately after exercise, and 30 and 60 min after exercise. Blood samples were collected at rest and 5 min after exercise. Muscle and blood (lactate concentration) were three- and fivefold greater than pre-exercise values. Muscle temperature and pH immediately after post-exercise were 43 degrees C and 6.55, respectively, but approached rest values by 60 min after exercise. The initial rate and maximal capacity of Ca2+ uptake of muscle homogenates and isolated sarcoplasmic reticulum were significantly depressed immediately after exercise. This depression was paralleled by decreased activity of the Ca2+-stimulated ATPase. However, both Ca2+ uptake (rate and capacity) and Ca2+4-ATPase activity had returned to normal by 60 min after exercise. These findings demonstrate that changes in sarcoplasmic reticulum function after high-intensity exercise may be induced but not sustained by local changes in muscle pH and/or temperature.

The effect of humid heat acclimation on thermoregulatory responses to humid and dry exercise-heat stress was studied in six exercise-trained Thoroughbred horses. Horses were heat acclimated by performing moderate-intensity exercise for 21 days in heat and humidity (HH) [34.2-35.7 degrees C; 84-86% relative humidity (RH); wet bulb globe temperature (WBGT) index approximately 32 degrees C]. Horses completed exercise tests at 50% of peak O(2) uptake until a pulmonary arterial temperature (T(pa)) of 41.5 degrees C was attained in cool dry (CD) (20-21.5 degrees C; 45-50% RH; WBGT approximately 16 degrees C), hot dry (HD 0) [32-34 degrees C room temperature (RT); 45-55% RH; WBGT approximately 25 degrees C], and HH conditions (HH 0), and during the second hour of HH on days 3, 7, 14, and 21, and in HD on the 18th day (HD 18) of heat acclimation. The ratios of required evaporative capacity to maximal evaporative capacity of the environment (E(req)/E(max)) for CD, HD, and HH were approximately 1.2, 1.6, and 2.5, respectively. Preexercise T(pa) and rectal temperature were approximately 0.5 degrees C lower (P < 0. 05) on days 7, 14, and 21 compared with day 0. With exercise in HH, there was no effect of heat acclimation on the rate of rise in T(pa) (and therefore exercise duration) nor the rate of heat storage. In contrast, exercise duration was longer, rate of rise in T(pa) was significantly slower, and rate of heat storage was decreased on HD 18 compared with HD 0. It was concluded that, during uncompensable heat stress in horses, heat acclimation provided modest heat strain advantages when E(req)/E(max) was approximately 1.6, but at higher E(req)/E(max) no advantages were observed.