| Summary: | ObjectiveTo explore the correlation between adaptation to exercise-induced fatigue and lactate transport and metabolism in the cerebral cortex under high-altitude hypoxia.MethodsA total of 63 SD rats were randomly divided into control, normal exercise, rush-entry-into-altitude, 3-day-altitude acclimatization, 1-week-altitude acclimatization, 2-week-altitude acclimatization, and monocarboxylate-transporter-inhibitor (altitude inhibitor injection) groups. Except for the control group, rats were subjected to exhaustive-load treadmill exercises under either normal pressure and normoxic conditions or low pressure and hypoxic conditions. The average time-to-exhaustion was used to determine variation trends in exercise-induced fatigue. The expression of monocarboxylate transporters (MCT)2 and MCT4 in the cerebral motor cortex was detected using western blotting and immunohistochemistry. The pathological evaluation of neuronal death in the cortex was carried out using Nissl staining, and the lactate content was also determined in rat brains.ResultsThe average time-to-exhaustion in the rush-entry-into-altitude and the altitude inhibitor injection groups were (61.00±6.55) min and (71.25±9.59) min, respectively, which was significantly lower than that in the normal exercise (124.75±9.36) min and the 2-week-altitude acclimatization groups (100.25±9.74) min (P<0.05). Western blotting showed that, compared with the control group, the expression of MCT2 in the motor cortex in the 2-week-altitude acclimatization and the altitude inhibitor injection groups increased significantly by 120.6% and 164.4% (P<0.05), respectively; the expression of MCT4 in the two groups increased significantly by 174.6% and 168.8% (P<0.05). The results of western blotting were confirmed by the results of immunohistochemistry. In the high-altitude environment, the average lactate content in rat brains was significantly higher than that in the normal exercise group (0.175±0.021) mmol/g, P<0.05]. Neuropathological evaluation showed that the average neuronal density [neurons per high power field (HPF)] in the motor cortex in the rush-entry-into-altitude and the altitude inhibitor injection groups were (46.75±8.65) cells/HPF and (63.50±7.65) cells/HPF, respectively, which were significantly lower than that in the control group [(135.88±8.59) cells/HPF](P<0.05). Differences between the 2-week-altitude acclimatization [(121.75±16.00) cells/HPF] and the control groups were not statistically significant (P > 0.05).ConclusionThe adaptability of the body to exercise fatigue after altitude acclimatization is correlated with changes in the expression of MCT2 and MCT4 in the brain, which can be used as targets for medical intervention for exercise-induced fatigue.
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