补充丙酮酸盐可预防高强度间歇运动诱导代谢性酸中毒并提高大鼠骨骼肌MCT1/MCT4的表达

Pyruvate Supplementation Can Prevent HIIE-induced Metabolic Acidosis and Increase the Expression of MCT1/MCT4 in Skeletal Muscles of Rats

运动诱导的代谢性酸中毒作为运动性疲劳的发生原因之一而备受关注。补充丙酮酸盐对运动诱导代谢性酸中毒的作用效果少有报道,且其作用机制尚未完全阐明。单羧酸转运蛋白(monocarboxylate transporter,MCTs)对机体酸碱平衡的维持有重要意义,但丙酮酸盐能否通过提高MCTs表达缓解酸中毒尚不清楚。因此,本研究通过预先给大鼠补充丙酮酸盐(616 mg/kg/d)。1周后进行急性高强度间歇运动(high intensity intermittent exercise,HIIE)。具体方案为110%VO_(2max)运动1 min结合1 min休息为1组,共13组,观察大鼠在HIIE后血液、骨骼肌酸碱平衡状态及骨骼肌MCTs表达的变化。结果表明,急性HIIE后大鼠血液pH、碳酸氢根离子(bicarbonate ion,HCO_(3)^(-))、碱剩余(base excess,BE)显著降低(P<0.05),血乳酸水平显著升高(P<0.05);并且快肌和慢肌内pH显著降低(P<0.05),肌内乳酸水平显著升高(P<0.05)。预先补充丙酮酸盐,大鼠血液pH、HCO_(3)^(-)、以及BE均显著提升(P<0.05),快肌和慢肌内pH也显著提升(P<0.05),并且快肌内乳酸水平显著降低(P<0.05)。采用免疫印迹法测定大鼠快、慢肌中MCT1、MCT4相对表达后发现,补充丙酮酸盐,能够显著增高大鼠快肌和慢肌中MCT4表达水平(P<0.05)以及慢肌中MCT1的表达(P<0.05)。以上研究结果表明,补充丙酮酸盐,能够有效预防HIIE诱导的代谢性酸中毒,其可以通过增高大鼠快肌和慢肌中MCT4及慢肌中MCT1的表达,从而改善大鼠骨骼肌和血液的酸代谢。本研究为今后丙酮酸盐缓解运动诱导的酸中毒的机制研究提供了理论基础,并为运动性疲劳的延缓提供了新的营养策略。

As one of the causes of exercise-induced fatigue, exercise-induced metabolic acidosis has attracted much attention. The effect of pyruvate supplementation on exercise-induced metabolic acidosis is rarely reported, and its mechanism has not been fully elucidated. Monocarboxylate transporters(MCTs) play an important role in the maintenance of the acid-base balance, but it is not clear whether pyruvate can alleviate acidosis by increasing the expression of MCTs. In this study, pyruvate(616 mg/kg/day) was supplemented to rats for one week, and then acute HIIE was performed. The HIIE protocol comprised 13 repeats of a 60 s sprint session at 110% VO_(2)max speed with a 60 s interval between sessions. The changes of the acid-base balance and lactate transporter in blood and skeletal muscles of rats after HIIE were observed. The results showed that after acute HIIE, the blood pH, bicarbonate ion(HCO_(3)^(-)) and base excess(BE) decreased significantly(P < 0.05), and the blood lactate level increased significantly(P < 0.05). The pH in fast and slow muscles decreased(P < 0.05), and the level of intramuscular lactate increased significantly(P < 0.05). After pyruvate supplementation, the blood pH, HCO_(3)^(-), and BE were significantly increased(P < 0.05), the pH in fast and slow muscles were also significantly increased(P < 0.05), and the lactate level in fast muscles was significantly reduced(P < 0.05). Western blotting was used to determine the relative expression of MCT1 and MCT4 in rat fast and slow muscles. Pyruvate supplementation could significantly increase the expression level of MCT4 in fast and slow muscles(P < 0.05) and MCT1 in slow muscles(P < 0.05). The results above show that pyruvate supplementation can effectively correct the metabolic acidosis induced by HIIE. Pyruvate supplementation can enhance the expression of MCT4 in fast and slow muscles and MCT1 in slow muscles, so as to improve the acid metabolism of the skeletal muscle and blood. This study provides a theoretical basis for the mechanism of pyruvate in alleviating exercise-induced acidosis in the future, and provides a new nutritional strategy for delaying exercise-induced fatigue.