In order to compare the metabolic responses to exercise in 2 similarly managed breeds of horses, 5 Arabian (AR) and 5 Thoroughbred (TB) horses, fed an identical diet with a similar diet and exercise training programme for the 2 preceding months, undertook 3 treadmill (3 degree incline) trials with a minimum of 7 days between tests: 1) an incremental test (MAX) for determination of aerobic capacity, V(LA4) and lactate threshold (LT; the percentage of VO2max when plasma lactate = 4 mmol/l); 2) a single high-speed exercise test (SPR) at 115% VO2max for estimation of maximal accumulated oxygen deficit (MAOD) and 3) a 90 min test at 35% VO2max (LO). VO2max (P<0.001) and running speed (P<0.05) at VO2max were higher in TB (mean +/- s.e. 154 +/- 3 ml/kg/min at 12.9 +/- 0.5 m/s) than in AR (129 +/- 2.5 ml/kg/min at 11.8 +/- 0.2 m/s). Total run time during MAX was greater (P<0.05) in TB (10.5 +/- 0.5 min) than in AR (93 +/- 0.3 min). However, V(LA4) and LT were not different between groups. Run time during SPR (TB 149 +/- 16; AR 109 +/- 11 s) and MAOD (TB 88 +/- 4; AR 70 +/- 6 ml O2/kg) were higher (P<0.05) in the TB group. During LO, FFA were higher (P<0.05) and the respiratory exchange ratio (RER) lower (P<0.05) in AR than in TB between 60 and 90 min, of exercise, indicating a greater use of fat for energy. These metabolic differences may reflect breed variation in muscle fibre types. However, further studies are needed to determine the mechanisms underlying the apparent breed differences in energy metabolism during exercise.
SummaryThis study was designed to determine the effects of fat adaptation on carbohydrate and fat oxidation in conditioned horses during low-intensity exercise. Five mature Arabians were studied. The study was conducted as a crossover design with 2 dietary periods, each of 10 week's duration: a) a control (CON) diet, and b) a fat-supplemented (FAT) diet. The total amount of digestible energy (DE) supplied by the fat in the CON and FAT diets was 7% and 29%, respectively. During each period, the horses completed exercise tests at the beginning of the period (Week 0) and after 5 and 10 weeks on the diet. Tests consisted of 90 min of exercise at a speed calculated to elicit 35% VO 2max on a treadmill inclined to 3°. Oxygen consumption (VO 2 ), carbon dioxide production (VCO 2 ), and respiratory exchange ratio (RER) were measured at 15-min intervals. For determination of glucose kinetics, a stable isotope ([6-6-d 2 ] glucose) technique was used. Compared to the CON diet, FAT diet consumption for 5-10 weeks was associated with an altered metabolic response to low-intensity exercise, as evidenced by a more than 30% reduction in the production and utilisation of glucose; a decrease in RER; a decrease in the estimated rate of whole-body carbohydrate utilisation; and an increase in the whole-body rate of lipid oxidation during exercise.
The effects of propylthiouracil (PTU)-induced thyroid deficiency on the postnatal development of synaptic markers for cholinergic, GABA, dopaminergic and glutamate neurons in the rat corpus striatum were investigated. Similar effects were also assessed on β-alanine uptake by fine prisms and on DNA concentrations in striatal samples from 3- and 6-week-old rats. Thyroid deficiency (Tx) in rats markedly impaired the development of choline acetyltransferase activity and [(3)H]spiroperidol and [(3)H]-glutamate binding capacities. In contrast, small but significant increases were evident in γ-aminobutyric acid uptake and glutamate decarboxylase activity. β-Alanine uptake, a possible glial marker, was increased by up to 50% in samples from the Tx rats compared to controls. Consistent with deficits in striatal weight and greater DNA concentrations in the striatum of the Tx rats those neuronal markers which showed impairments on a mg tissue basis manifest even greater impairments expressed per whole striatum. Present findings suggest differential effects on neuronal markers, with the greatest impairments in the presynaptic markers for cholinergic interneurons in striatum during neonatal thyroid deficiency. The differential sensitivity on neuronal markers of the relatively late onset of thyroid deficiency seems likely to reflect the timing of the morphological differentiation of cholinergic and the other neurons in striatum.
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