论文部分内容阅读
本文以ＳＤ大鼠三级递增负荷力竭性跑台运动为疲劳模型，分别测定了运动后即刻肝脏线粒体：１．呼吸链复合体Ⅰ＋Ⅲ和Ⅱ＋Ⅲ电子传递与质子泵出比值（Ｈ＋／２ｅ）；２．以苹果酸＋谷氨酸（Ｍ＋Ｇ）和琥珀酸（Ｓ）为底物的呼吸控制：态３呼吸速率（Ｒ３）、态４呼吸速率（Ｒ４）、呼吸控制率（ＲＣＲ）和磷／氧比（Ｐ／Ｏ）。结果表明：两种呼吸底物启动的线粒体态４呼吸速率分别升高６４．４６和２３．５４％（Ｐ＜０．００１和Ｐ＜０．０５）；呼吸链复合体Ⅰ＋Ⅲ和Ⅱ＋Ⅲ的总Ｈ＋／２ｅ分别降低１８．６３和１５．８９％（均Ｐ＜０．０１）。两种呼吸底物的ＲＣＲ和Ｐ／Ｏ呈显著降低（均Ｐ＜０．０５）；Ｍ＋Ｇ为呼吸底物的态３呼吸速率也呈显著增加（Ｐ＜０．０１），Ｓ为呼吸底物的态３呼吸速率略有增高（Ｐ＞０．０５）。提示，线粒体质子漏增加，呼吸链电子传递与质子泵出偶联程度下降，氧化磷酸化脱偶联导致无效氧耗增多，可能是运动性疲劳状态下线粒体氧利用率下降的重要机制。
In this paper, SD rat three-level incremental load exhaustive treadmill exercise as a fatigue model were measured immediately after exercise liver mitochondria: 1. Respiratory chain complex Ⅰ + Ⅲ and Ⅱ + Ⅲ electron transfer and proton pumping ratio (H + / 2e); 2. Respiratory control with malate + glutamate (M + G) and succinate (S) as substrates: state 3 respiration (R3), state 4 respiration (R4), respiratory control (RCR) (P / O). The results showed that the respiration rate of mitochondrial state 4 increased by 64.46% and 23.54% (P <0.001 and P <0.05), respectively. The respiratory rate of respiratory chain complex Ⅰ + Ⅲ and Ⅱ + Ⅲ of total H + / 2e decreased by 18.63 and 15.89% (all P <0.01). The RCR and P / O of the two respiratory substrates were significantly decreased (all P <0.05); the respiratory rate of M + G was also increased significantly (P <0.01), and S was the respiratory substrate The respiratory rate of state 3 increased slightly (P> 0.05). Suggesting that mitochondrial proton leak increases, the respiratory chain electron transfer and the proton pump decoupling degree of decline, oxidative phosphorylation of uncoupling lead to increased oxygen consumption may be exercise fatigue state mitochondrial oxygen utilization rate is an important mechanism.