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运动可导致暂时的线粒体和收缩功能障碍,与呼吸链复合物活性受损有关。

Exercise can induce temporary mitochondrial and contractile dysfunction linked to impaired respiratory chain complex activity.

机构信息

Department of Cardiac Surgery, Heart Center Leipzig, University of Leipzig, Germany.

出版信息

Metabolism. 2012 Jan;61(1):117-26. doi: 10.1016/j.metabol.2011.05.023. Epub 2011 Aug 3.

DOI:10.1016/j.metabol.2011.05.023
PMID:21816448
Abstract

Exercise is considered to elicit a physiological response of the heart. Previous studies investigated the influence of repetitive exercise only at the end of the training period. We assessed the impact of 2 exercise protocols, differing in their treadmill inclination, on cardiac and mitochondrial function at different times during the training period. Within 10 weeks, animals trained with 16% incline developed hypertrophy (left ventricular posterior wall thickness: 1.6 ± 0.1 vs 2.4 ± 0.1 mm; P < .05) with normal function (ejection fraction: 75.2% ± 2.5% vs 75.6% ± 2.1%). However, at 6 weeks, there was temporary impairment of contractile function (ejection fraction: 74.5% ± 1.67% vs 65.8% ± 2.3%; P < .05) associated with decreased mitochondrial respiratory capacity (state 3 respiration: 326 ± 71 vs 161 ± 22 natoms/[min mg protein]; P < .05) and a gene expression shift from the adult (α) to the fetal (β) myosin heavy chain isoform. Although peroxisome proliferator-activated receptor gamma coactivator-1α expression was normal, nuclear respiratory factors (NRFs)-1 and -2 were significantly reduced (NRF-1: 1.00 ± 0.16 vs 0.55 ± 0.09; NRF-2: 1.00 ± 0.11 vs 0.63 ± 0.07; P < .05) after 6 weeks. These findings were associated with a reduction of electron transport chain complexes I and IV activity (complex I: 1016 ± 67 vs 758 ± 71 nmol/[min mg protein]; complex IV: 18768 ± 1394 vs 14692 ± 960 nmol/[min mg protein]; P < .05). Messenger RNA expression of selected nuclear encoded subunits of the electron transport chain was unchanged at all investigated time points. In contrast, animals trained with 10% incline showed less hypertrophy and normal function in echocardiography, normal maximal respiratory capacity, and unchanged complex activities at all 3 time points. Repetitive exercise may cause contractile and mitochondrial dysfunction characterized by impaired respiratory chain complex activities. This activity reduction is temporary and intensity related.

摘要

运动被认为会引起心脏的生理反应。先前的研究仅在训练期末评估了重复运动对心脏的影响。我们评估了两种不同倾斜度的跑步机训练方案对训练期不同时间的心脏和线粒体功能的影响。在 10 周内,以 16%坡度训练的动物出现了肥厚(左心室后壁厚度:1.6 ± 0.1 与 2.4 ± 0.1 毫米;P <.05),但功能正常(射血分数:75.2% ± 2.5%与 75.6% ± 2.1%)。然而,在 6 周时,收缩功能暂时受损(射血分数:74.5% ± 1.67%与 65.8% ± 2.3%;P <.05),与线粒体呼吸能力下降(状态 3 呼吸:326 ± 71 与 161 ± 22 纳原子/[分钟毫克蛋白];P <.05)和从成人(α)到胎儿(β)肌球蛋白重链同工型的基因表达转变相关。虽然过氧化物酶体增殖物激活受体 γ 共激活因子 1α 的表达正常,但核呼吸因子(NRFs)-1 和 -2 明显减少(NRF-1:1.00 ± 0.16 与 0.55 ± 0.09;NRF-2:1.00 ± 0.11 与 0.63 ± 0.07;P <.05)。这些发现与电子传递链复合物 I 和 IV 活性降低有关(复合物 I:1016 ± 67 与 758 ± 71 纳摩尔/[分钟毫克蛋白];复合物 IV:18768 ± 1394 与 14692 ± 960 纳摩尔/[分钟毫克蛋白];P <.05)。在所有研究的时间点,电子传递链的选定核编码亚基的信使 RNA 表达均未改变。相比之下,以 10%坡度训练的动物的心脏超声心动图肥厚程度较小,功能正常,最大呼吸能力正常,在所有 3 个时间点,复合物活性均未改变。重复运动可能导致收缩和线粒体功能障碍,表现为呼吸链复合物活性受损。这种活性降低是暂时的,与强度有关。

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