■不能否认外源性丙酮酸在治疗病理性代谢性酸中毒中的临床益处。然而,是否可以预防运动生理代谢性酸中毒,延缓运动性疲劳的发生,和提高运动的有益效果及其内在机制尚不清楚。
■我们将24只雄性SD大鼠随机分为3组:一组为无运动的对照组(CC,n=8),和其他两组补充616毫克/千克/天丙酮酸(EP,n=8)或等体积蒸馏水(EC,n=8)。这些小组在补充7天后完成了急性高强度间歇运动(HIIE)。运动后立即测量酸代谢变量,包括血液pH值(pHe),碱过量(BE),HCO3-,血乳酸和骨骼肌pH(pHi)。通过测量氧化型辅酶I/还原型辅酶I(烟酰胺腺嘌呤二核苷酸[NAD+]/还原型NAD+[NADH])比率和乳酸/丙酮酸(L/P)比率来确定氧化还原状态。此外,乳酸脱氢酶A(LDHA)的活性,己糖激酶(香港),通过ELISA测定磷酸果糖激酶(PFK)和丙酮酸激酶(PK)。
■丙酮酸盐的补充显著逆转了pHe的下降,BE,HIIE后的HCO3-和pHi值(p<0.001),而LDHA的活性显着增加(p=0.048),香港(p=0.006),和PFK(p=0.047)。与CC相比,NAD+/NADH(p=0.008)比值和LDHA活性(p=0.002),香港(p<0.001),PFK(p<0.001),EP组的PK(p=0.006)显著改善。
■这项研究提供了令人信服的证据,表明口服丙酮酸可减弱HIIE诱导的细胞内和细胞外酸化,可能是由于LDHA的活性增加,这促进了LDH反应中H+的吸收。还显示了改善氧化还原状态和糖酵解速率的有益效果。我们的结果表明,丙酮酸盐可以用作口服营养补充剂,以缓解HIIE引起的代谢性酸中毒。
UNASSIGNED: There is no denying the clinical benefits of exogenous pyruvate in the treatment of pathological metabolic acidosis. However, whether it can prevent exercise physiological metabolic acidosis, delay the occurrence of exercise fatigue, and improve the beneficial effects of exercise and its internal mechanism remain unclear.
UNASSIGNED: We randomly divided 24 male SD rats into 3 groups: one group was a control without exercise (CC, n = 8), and the other two groups were supplemented with 616 mg/kg/day pyruvate (EP, n = 8) or distilled water of equal volume (EC, n = 8). These groups completed acute high-intensity interval exercise (HIIE) after 7 days of supplementation. The acid metabolism variables were measured immediately after exercise including blood pH (pHe), base excess (BE), HCO3 -, blood lactic acid and skeletal muscle pH (pHi). The redox state was determined by measuring the oxidized coenzyme I/reduced coenzyme I (nicotinamide adenine dinucleotide [NAD+]/reduced NAD+ [NADH]) ratio and lactate/pyruvate (L/P) ratio. In addition, the activities of lactate dehydrogenase A (LDHA), hexokinase (HK), phosphofructokinase (PFK) and pyruvate kinase (PK) were determined by ELISA.
UNASSIGNED: Pyruvate supplementation significantly reversed the decrease of pHe, BE, HCO3 - and pHi values after HIIE (p < 0.001), while significantly increased the activities of LDHA (p = 0.048), HK (p = 0.006), and PFK (p = 0.047). Compared with the CC, the NAD+/NADH (p = 0.008) ratio and the activities of LDHA (p = 0.002), HK (p < 0.001), PFK (p < 0.001), and PK (p = 0.006) were significantly improved in EP group.
UNASSIGNED: This study provides compelling evidence that oral pyruvate attenuates HIIE-induced intracellular and extracellular acidification, possibly due to increased activity of LDHA, which promotes the absorption of H+ in the LDH reaction. The beneficial effects of improving the redox state and glycolysis rate were also shown. Our results suggest that pyruvate can be used as an oral nutritional supplement to buffer HIIE induced metabolic acidosis.