OBJECTIVE:To determine lactate breakpoint of horses and test for effects of training and dietary supplementation with corn oil on that breakpoint.ANIMALS:7 healthy Arabian horses.PROCEDURES:Horses received a control diet (n = 4) or a diet supplemented with 10% corn oil (4). A training program, which comprised two 5-week conditioning periods with 1 week of rest, was initiated. Submaximal incremental exercise tests (IET) were conducted before the first and after both conditioning periods. Blood samples for determination of blood lactate and plasma glucose concentrations were collected 1 minute before IET and during the 15 seconds immediately preceding each speed change. Data collected were fit to one- and two-slope broken-line models and an exponential model.RESULTS:Good fits were obtained by application of the broken-line models (adjusted R2 > 0.92) to blood lactate concentration versus speed curves. Lactate breakpoints increased 41% after training. After training, slope 2 and peak blood lactate concentrations were greater in the corn oil group, compared with controls. Mean blood lactate concentration at the breakpoint was not affected by training or diet. Plasma glucose concentration versus speed curves also fit the broken-line models, and glucose breakpoints preceded lactate breakpoints by approximately 1 m/s in the second and third IET.CONCLUSIONS AND CLINICAL RELEVANCE:Lactate breakpoints can be determined for horses, using blood lactate concentration versus speed curves generated during submaximal IET and may be useful for assessing fitness and monitoring training programs in equine athletes.

Rectal temperature (Tre) is often used to adjust measurements of blood gases, but these adjusted measurements may not approximate temperatures during intense exercise at main sites of gas exchange: muscle and lung. To evaluate differences in blood gases between sites, temperatures (T) were measured with thermocouples in the rectum (re), in mixed venous blood (v), in gluteal muscle (mu), and on the skin (sk) in seven Arabian horses as they underwent an incremental exercise test on a treadmill. Blood samples were drawn from the carotid artery and pulmonary artery (mixed venous) 30 s before each increase in speed and during recovery. Blood gases and pH were measured at 37 degreesC, and all variables were adjusted to Tre, Tv, and Tmu. Adjusted variables during exercise and recovery were significantly different from each other at the three sites. Linear and polynomial equations described the time course of venous temperature and from Tre and Tsk during exercise and from Tsk during recovery. Interpretation of changes in muscle metabolism and gas exchanges based on blood-gas measurements is improved if they are adjusted appropriately to Tmu or Tv, which may be predicted from Tsk in addition to Tre during strenuous exercise and from Tsk during recovery.

Feeding and training may affect acid-base responses to strenuous exercise. Acidosis usually correlates with higher blood lactate concentrations during intense exercise, but alkalosis has been found in several studies of horses, and higher lactate responses during sprints have been found in fat adapted horses. To elucidate these unexpected findings, we applied a comprehensive physicochemical approach to evaluate acid-base responses during exercise in fat adapted horses. In incremental tests and repeated sprints, changes in blood [H+] were dependent upon corresponding changes in pCO(2) but not strong ion difference (SID, the algebraic sum of ions of sodium, potassium, chloride and lactate). The influence of changes in [Lac(-)] were largely offset by changes in [Na+], [K+] and [Cl-], so that SID was unchanged and did not contribute to the exercise induced acidemia, so it may be inaccurate to term this a lacticacidosis. During repeated sprints, central venous [H+] increased (acidosis) but arterial [H+] decreased (alkalosis). These changes were consistent with concurrent changes in venous and arterial pCO(2) but not SID. Fat adaptation decreased mixed venous pCO(2) during repeated sprints, which is consistent with the lower respiratory quotient associated with fat oxidation. Less pulmonary work to eliminate CO2 could benefit horses under hot and humid conditions, especially those with mildly reduced pulmonary function. The blood lactate response was decreased during aerobic tests but increased during anaerobic tests on fat adapted horses. Fat adaptation appears to facilitate the metabolic regulation of glycolysis, by sparing glucose and glycogen at work of low intensity, but by promoting glycolysis when power is needed for high intensity exercise. The blood lactate response to repeated sprints was increased more by the combination of fat adaptation and oral supplementation of sodium bicarbonate than by the sum of the responses to fat alone or bicarbonate alone. This synergism suggests that need for further studies of the interaction of fat adaptation with dietary cation-anion balance, especially under hot conditions. These results integrate harmoniously with previous findings of lower feed intake and fecal output, lower loads of heat and CO2, lower water losses in the feces and by evaporation, and less spontaneous activity and reactivity in fat adapted horses. Thus fat adaptation confers several advantages on horses and presumably other equids used for hard work, especially in the heat. (C) 1998 Elsevier Science B.V. All rights reserved.

Seven Arabian horses performed a standard incremental exercise test on a high-speed treadmill at 6% slope then were randomly assigned to two diets, a control diet of ground hay and concentrates and a similar diet with 10% added fat (by weight). Horses were sprint-trained 4 d/wk, and two additional exercise tests were performed at 5-wk intervals. Heart rates and rectal temperatures were monitored and venous blood samples were collected at rest and at each speed increment. Whole blood was analyzed for glucose, lactate, and hemoglobin concentrations, and plasma was analyzed for pH, pCO2, albumin, total protein, and sodium, potassium, and chloride concentrations. Bicarbonate concentration ([HCO3-]) and strong ion difference ([SID]) were calculated, and total weak acid ([Atot]) was estimated from total protein. During exercise, there were increases in plasma sodium and potassium concentrations (P < .001), whole blood lactate and glucose (P < .001), and hemoglobin concentrations (P < .01). There were decreases in plasma pH, [HCO3-], and chloride concentrations (P < .001). The decrease in plasma pH was associated with changes in [SID] and [Atot] that combined to offset a decrease in pCO2. After sprint training, heart rates at rest and during submaximal exercise were decreased (P < .01), whereas heart rates at the end of exercise were increased (P < .05). Sprint training also increased workrate and estimated oxygen consumption at a heart rate of 200 beats/min (P < .001). Training increased the duration of exercise and the speed attained at the end of exercise (P < .05). Training increased the blood hemoglobin response to exercise and decreased the pCO2 response (P < .01). There were diet x training interactions for pH, pCO2, and [SID] (P < .05). Horses consuming the high-fat diet had higher blood glucose during both standard exercise tests and higher lactate concentrations at fatigue (P < .05) during the last test. Fat adaptation involving sprint training of horses may influence glucolysis at the level of pyruvate during an incremental exercise test.

Collection of a satisfactory blood sample requires special procedures to prevent changes in glucose and lactate content after the sample has been obtained. Changes in measured plasma glucose and blood lactate concentrations attributable to anticoagulants and storage procedures, respectively, were examined in blood samples obtained from horses at rest and after exercise. To evaluate the effect of anticoagulants on measured plasma glucose concentration, blood was preserved with either sodium fluoride/potassium oxalate or lithium heparin. Measured plasma glucose concentration in blood obtained at rest and after exercise was 6 and 10% lower (P = 0.0038), respectively, when blood was preserved with fluoride/oxalate, compared with heparin. The erythrocyte volume in the blood sample was 15% smaller (P = 0.0001) in samples preserved with fluoride/oxalate, indicating a movement of water out of erythrocytes in the blood sample mixed with that anticoagulant. To evaluate the effect of storage procedure on measured blood lactate concentration, part of the blood sample was immediately deproteinized for blood lactate analysis, and the remaining blood was maintained for 30 and 60 minutes at either 0 or 22 C before deproteinization. When blood samples were maintained at 0 C prior to deproteinization, there was no difference in blood lactate concentration, regardless of the incubation time, compared with that in samples immediately deproteinized. Blood lactate concentration was greater (P < 0.01) in samples maintained at 22 C, compared with that in samples immediately deproteinized, and with that in equivalent samples maintained at 0 C.(ABSTRACT TRUNCATED AT 250 WORDS)

Multicompartmental analysis was applied to study the kinetics of D-xylose distribution after its intragastric administration to healthy mares deprived of food for 12, 36, 72, and 96 hours. Disposition of D-xylose was described by a 5-compartment model. Maximal plasma D-xylose concentration was similar for 12 and 36 hours of food deprivation and was greater (P = 0.0001) than the values for 72 and 96 hours. Peak concentration of D-xylose appeared progressively later as food deprivation proceeded (P = 0.0001). Fractional rate of transfer (k1,6) was less after 96 hours of food deprivation, compared with 12 hours (P = 0.0001), and percentage of D-xylose absorbed was reduced (P = 0.0441) after food deprivation. Fractional rate of transfer (k6,5), representing gastric emptying, tended to progressively decrease with food deprivation. Results indicated that formal kinetic analysis can be applied to D-xylose absorption kinetics in horses. Reduction in the extent of D-xylose absorption after food deprivation may be partly caused by decreased rate of D-xylose absorption across the small intestinal mucosa, but other factors, such as gastric emptying and nonabsorptive losses, may also be involved.

Multicompartmental analysis was applied to study the kinetics of D-xylose distribution after IV administration to healthy mares deprived of food for 12 and 96 hours. Urinary excretion of D-xylose was measured over a 15-hour period after administration. The plasma D-xylose concentrations in this study were in the range found after oral tolerance testing. The disposition of D-xylose was described by a two-compartment model with linear kinetic characteristics. Total volume of distribution decreased significantly (P < 0.025) from 0.270 L/kg of body weight after the 12-hour period of food deprivation to 0.235 L/kg after the 96-hour period. Fractional rate of transfer between the central and peripheral compartments did not change after 96 hours without food. Approximately a third of the D-xylose administered was recovered in the urine. Difference in urinary elimination between the 12- and 96-hour periods was not significant. Nonrenal elimination rate was determined to be twice the renal elimination rate. The results indicated that formal kinetic analysis can provide useful information about D-xylose distribution in horses. The decreased D-xylose space found after a 96-hour period of food deprivation would tend to increase the plasma D-xylose concentration, and this may help in the interpretation of the D-xylose absorption test applied to anorectic horses.

A Latin square design was used to compare the effects of laxatives and a corresponding volume of water on gastrointestinal tract function in 4 healthy horses. Horses were intragastrically infused with each of the following: dioctyl sodium sulfosuccinate (DSS; 50 mg/kg of body weight); magnesium sulfate (0.5 g/kg--low dosage); magnesium sulfate (1.0 g/kg--high dosage); and an equal volume of water (6 L) given as a control infusion. From 5 to 33 hours after the high dosage of magnesium sulfate, feces were slightly softer than usual in all horses. In 1 horse, DSS caused mild colic, hyperpnea, and diarrhea from 0.3 to 3 hours after administration. After all laxative treatments and the control infusion, fecal output, fecal water, number of defecations, and fecal water percentage were greater during the first 6 and 12 hours, compared with each subsequent 6-hour period (P less than 0.05). The high dosage of magnesium sulfate had greater effect on fecal output and fecal water than did the low dosage and control infusion (P less than 0.05). However, this effect preceded arrival of the liquid transit marker, polyethylene glycol, and magnesium at their highest concentrations in feces by 12 to 18 hours. Compared with the control infusion, none of the laxative treatments affected excretion of polyethylene glycol and plastic particulate markers, nor did they increase water consumption. It was concluded that the response to intragastric infusions may involve reflex mechanisms in the gastrointestinal tract and that these responses could be used for treatment of colon impactions.(ABSTRACT TRUNCATED AT 250 WORDS)

Four mares fed a low fiber, high soluble carbohydrate diet were used in a crossover design to evaluate the effects of dietary sodium bicarbonate (NaHCO3) supplementation during daily low-intensity submaximal working conditions. Mares were fed the diet at 1.7 times the maintenance energy requirement for mature horses at work. The horses tolerated the diet well and had no clinical abnormalities. Resting venous blood bicarbonate (HCO3), standard HCO3, and base excess (BE) concentrations significantly (P less than 0.05) increased with NaHCO3 supplementation, but no significant changes in resting venous blood pH or carbon dioxide tension (PCO2) were recorded. Venous blood HCO3, standard HCO3, BE, hemoglobin, and heart rate were significantly (P less than 0.05) increased and plasma lactate concentration was significantly (P less than 0.05) decreased in the control horses and in the horses given the NaHCO3 supplement during low-intensity submaximal exercise. There were no significant changes in venous blood pH, PCO2, or plasma protein concentration with exercise. Venous blood HCO3, standard HCO3, and BE concentrations were significantly (P less than 0.05) greater during submaximal exercise in horses given the NaHCO3 supplement. There were no significant differences in plasma lactate or total protein concentrations, blood pH, PCO2, or hemoglobin concentration between the 2 groups during exercise.

The authors review the main substances used as ergogenic supports in sporting animals. Even in the abence of objective and qualitative data on sporting dogs, certain appear to present a definite interest, particularly L-carnitine, ascorbic acid, dimethylglycine, arginine and inosine. The borders between nutrional supplement and doping are not however always clear.

A D-xylose absorption test was conducted on 4 healthy mares deprived of food for 12, 36, 72, and 96 hours before the test, with a 13- to 15-day adjustment period between each test. Maximal plasma concentrations after 72 and 96 hours of food deprivation were approximately 36% lower than those obtained after the 12- and 36-hour periods (P = 0.0001). Absorption curves were flatter and the decrease in plasma concentration was slower after the 72- and 96-hour periods of food deprivation. The rate of D-xylose absorption (P = 0.0108) and the initial rate of urinary excretion (P = 0.0117) were slower at 72 and 96 hours. Gastric emptying appeared to be progressively delayed with food deprivation, as evident by the delay in peak D-xylose excretion in urine (P = 0.0268). Areas under the plasma concentration-time curves and quantitites of D-xylose excreted in urine were similar for all periods of food deprivation, evidence that the same amounts of D-xylose were absorbed, despite changes in the plasma curve. A 15-hour collection period was sufficient to recover all D-xylose excreted in the urine, and during all periods 9.8 +/- 0.6% (mean +/- SEM) of the oral dose was eliminated in the urine.

Thin sheets of mucosa from small intestine of neonatal calves were mounted in incubation chambers for in vitro studies. These mucosal sheets generated a potential difference (PD) of 2.05 +/- 0.02 mV (mean +/- SEM), short-circuit current (SCC) of 23.32 +/- 3.81 microA x cm2, and tissue resistance of 86.22 +/- 4.41 ohms x cm2 (n = 6). Ouabain in the serosal bathing solution caused a sharp decrease in the SCC (P less than 0.01) and PD (P less than 0.005), a decrease in tissue K content (P less than 0.05), and an increase in tissue Na content (P less than 0.05). The mucosa responded to D-glucose by an increase in PD (P less than 0.001) and SCC (P less than 0.001). In vitro methods used in the calf were validated in similar experiments on rabbit ileum.