Uridine increases endurance and improves the rehabilitation of experimental animals after physical performance

BACKCROUND: Pharmacological correction of metabolic processes, providing an increase in the efficiency and duration of the physical performance and contributing to the rapid rehabilitation, is an important component of the regulation of adaptation. Previously, we found that the pyrimidine nucleoside uridine exhibits antihypoxic properties, activates mitochondrial K+ATP channels (mitoKATP), normalizes energy metabolism, reduces lipid peroxidation, activates the antioxidant system, and also increases glycogen content. It can be assumed that the substance with such properties will increase endurance and improve recovery after physical performance. AIM is to study the effect of uridine on the endurance of experimental animals in the forced swimming test under physical performance of different intensity and on their rehabilitation. MATERIALS AND METHODS: Experiments were performed on male Wistar rats (350-380 g) and male outbred mice (25-30 g). In the 1st series the effect of uridine on the rats endurance was studied in the forced swimming test with a load of 5%, 7%, or 10% of the animal weight. In the second series, the effect of uridine on the first phase of recovery processes was evaluated in a three-load swimming test. Mice with a 10% load were subjected to a swimming test three times, after which the trail index - the ratio of time of trail 3rd to trail 1st - was determined. The frequency of occurrence of animals with low, medium and high recovery ability was estimated. Uridine 30 mg/kg or physiological saline (control) was administered 30 min before, 5-hydroxidecanoate (5-HD, mitoKATP blocker) 5 mg/kg - 45 min before, and mexidol (reference drug) 200 mg/kg 50 min before testing. RESULTS. Uridine increased critical swimming duration (CSD) by 58% and 44% at 5% and 7% exercise, respectively in comparison with controle. At 7% load the drug increased the period before the appearance of the first signs of fatigue by 100%. Effect of uridine decreased by 40% in the case of fatigue and by 24% in the case of CSD when injected after the blockade of mitoKATP channels. In the three-load swimming test, uridine increased the trail index by 1.5 times, which was comparable to the effect of mexidol, and increased the number of animals with a high ability to recover by 2.6 times. The use of the drug after mitoKATP channels blockade did not lead to a decrease of its positive effect, and also the blockade of channels with 5-HD did not affect the rehabilitation. CONCLUSIONS. Uridine increases the endurance of rats with medium load in forced swimming test and the rehabilitation of mice in three-load swimming test. It also increases the number of animals with a high ability to recover after swimming performance. The mechanism of its effects is realized both through the activation of mitoKATP channels and, probably, through the stimulation of glycogenesis.