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- Author or Editor: A. Reeta Pösö x
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Abstract
Objective
To study whether end products of 2 pathways of anaerobic energy metabolism, lactate and purines, that accumulate in the blood after intense exercise indicate any relation to exercise performance.
Design
Venous blood samples were taken within 1 and 15 minutes after a trotting race of 2,100 m.
Animale
16 Clinically healthy Standardbred trotters.
Procedure
Blood and plasma lactate concentrations were measured by enzymatic analyzer, and purines, uric acid and allantoin, were determined by high-performance liquid chromatography. The concentrations of metabolites were then correlated to racing time and individual performance indexes that are annually calculated from the percentage of winnings, placings, and starts rejected, average earnings per start, and the racing record.
Results
Blood lactate concentration immediately and calculated cell lactate concentration immediately and 15 minutes after the race correlated positively (P < 0.05 to P < 0.01) with the individual performance indexes. Plasma lactate concentration was not correlated to the individual performance indexes. Uric acid concentration, immediately and 15 minutes after the race, was negatively correlated (P < 0.05) to the individual performance indexes, and a positive relation (P < 0.05) was found between the highest concentration of uric acid and the racing time. Concentration of allantoin immediately or 15 minutes after the race did not have any significant correlation to the individual performance indexes.
Conclusions
Accumulation of lactate in the blood, which was greater in the superior performing horses, may prove to be an useful predictor of anaerobic capacity. The results also indicate that the loss of purine nucleotides was less in the superior performing horses, although further studies are needed to confirm this.
Abstract
Objective
To determine glycogen resynthesis rate and changes in plasma metabolite concentrations in horses before and after repeated exercise.
Animals
6 clinically normal Standardbred trotters.
Procedure
Horses trotted distances of 3,000, 3,000, and 2,000 m (trial A) and 3 days later, trotted 2, 100, 2, 100, and 1,600 m (trial B). Horses had 1 hour rest periods between bouts of exercise. Trotting speed was increased with each exercise bout, up to a near maximal. Muscle biopsy specimens and venous blood samples were obtained before each trial and 0, 4, 24, 48, and 72 hours after the third bout. Blood samples were also taken between exercise bouts. Muscle glycogen content and plasma glucose, glycerol, nonesterified fatty acid, and triglyceride concentrations were determined.
Results
Muscle glycogen content was significantly decreased immediately after exercise from 473 ± 45 to 329 ± 79 mmol/kg of dry weight in trial A, and from 472 ± 128 to 347 ± 59 mmol/kg in trial B. Further decreases were measured 4 hours after exercise. Glycogen resynthesis was negligible 24 hours after exercise. Basal muscle concentrations of glycogen were obtained 72 hours after exercise in trial A (472 ± 128 mmol/kg), but not in trial B (279 ± 52 mmol/kg). Plasma concentrations of glucose were greater than or equal to before-exercise values. Plasma concentrations of lipid metabolites, glycerol, triglycerides, and nonesterified fatty acids, were less than before-exercise values 2 to 72 hours after exercising.
Conclusions
Repeated bouts of exercise decrease glycogen repletion rate, which is not attributable to hypoglycemia, but may be influenced by limited availability of lipids for energy production. (Am J Vet Res 1997;58:162–166)
Summary
Plasma concentrations of hypoxanthine, uric acid, and allantoin, which are breakdown products of adenine nucleotides, were measured in Standardbred and Finnhorse trotters during and after an exercise test on a high-speed treadmill, after an incremental exercise test performed on a racetrack, and after a racing competition. Fiber-type composition of the middle gluteal muscle and the muscle concentrations of adenine nucleotides and inosine monophosphate were measured after the racetrack test. Changes in the concentration of hypoxanthine were not observed in any of the tests. Peak concentration of uric acid was measured between 5 and 30 minutes after exercise, and it was three- to tenfold higher than the value at rest. The variability can be explained by intensity of the exercise test and variation among horses. The concentration of allantoin after exercise was 2 to 3 times as high as that at rest, depending on the intensity of the exercise, although the absolute increase was about 10 times as high as the increase in the concentration of uric acid. Peak values of allantoin for the treadmill and the racetrack tests were obtained 4 to 6 minutes after exercise and < 30 minutes after the races. Peak concentration of allantoin correlated positively with the percentage of type-II (IIA + IIB) fibers in the middle gluteal muscle. Significant correlations were not observed between plasma concentration of uric acid or allantoin and muscle concentrations of adenosine triphosphate (atp) or inosine monophosphate. It can be concluded that in horses, breakdown of atp during and after exercise continues until allantoin is produced. The peak concentration of allantoin increases with the intensity of exercise, is reached rapidly after exercise, and the variation in the time to the peak value is small among horses. It is suggested that the main source of allantoin is the fast-twitch, type-II fibers and that the mixed muscle concentrations of adenine nucleotides are of limited value when estimating the effects of exercise on atp content of the muscle tissue.
Abstract
Objective—To detect monocarboxylate transporters (MCTs) in canine RBC membranes and to determine the distribution of lactate between plasma and RBCs.
Sample population—Blood samples obtained from 6 purpose-bred Beagles.
Procedures—Monocarboxylate transporter isoforms 1, 2, 4, 6, 7, and 8 and CD147 were evaluated in canine RBCs by use of western blot analysis. Lactate influx into RBCs was measured as incorporation of radioactive lactate.
Results—2 MCT isoforms, MCT1 and MCT7, were detected in canine RBC membranes on western blot analysis, whereas anti-MCT2, anti-MCT4, anti-MCT6, and anti-MCT8 antibodies resulted in no signal. No correlation was found between the amount of MCT1 or MCT7 and lactate transport activity, but the ancillary protein CD147 that is needed for the activity of MCT1 had a positive linear correlation with the rate of lactate influx. The apparent Michaelis constant for the lactate influx in canine RBCs was 8.8 ± 0.9mM. Results of in vitro incubation studies revealed that at lactate concentrations of 5 to 15mM, equilibrium of lactate was rapidly obtained between plasma and RBCs.
Conclusions and Clinical Relevance—These results indicated that at least half of the lactate transport in canine RBCs occurs via MCT1, whereas MCT7 may be responsible for the rest, although an additional transporter was not ruled out. For practical purposes, the rapid equilibration of lactate between plasma and RBCs indicated that blood lactate concentrations may be estimated from plasma lactate concentrations.