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耐力训练期间骨骼肌HSP72水平:外周动脉供血不足的影响

Skeletal muscle HSP72 level during endurance training: influence of peripheral arterial insufficiency.

作者信息

Ecochard L, Lhenry F, Sempore B, Favier R

机构信息

Unité Mixte de Recherche 5578 Centre National de la Recherche Scientifique, Université Claude Bernard, Lyon, France.

出版信息

Pflugers Arch. 2000 Oct;440(6):918-24. doi: 10.1007/s004240000362.

Abstract

Heat shock protein 72 (HSP72), the inducible isoform of the HSP70 family, is synthesized in exercised rat muscles and in the ischaemic heart. To determine the isolated and combined effects of chronic ischaemia and repeated exercise on skeletal muscle HSP72 expression, male Wistar rats were subjected to unilateral occlusion of the iliac artery. Beginning 1 week after ischaemia, half the rats were exercised on a motor-driven treadmill once a day, 5 days/week, the other half were restricted to cage activity. Rats were sacrificed after 2, 4, or 8 weeks of endurance training, together with the age-matched sedentary rats. Tissue samples were obtained from the plantaris and the red portion of the quadriceps of both hind-limbs. Endurance-trained rats displayed significantly increased HSP72 levels in skeletal muscles. Occlusion of iliac artery did not affect the HSP72 level in muscle from sedentary rats but enhanced that in the trained rats. Mitochondrial oxidative capacity, as assessed from cytochrome oxidase and citrate synthase activities, decreased during growth in sedentary animals, but was significantly improved by endurance training. Nevertheless, increased oxidative capacity induced by endurance training was partially prevented by arterial occlusion. It is concluded that both HSP72 levels and mitochondrial oxidative capacity are affected by ischaemia and training but these changes are not necessarily related. Whereas superimposition of chronic exercise on peripheral arterial insufficiency increased HSP72 levels, our results demonstrate that endurance training even for extended period of time is not effective for improving oxidative capacity of ischaemic muscle.

摘要

热休克蛋白72(HSP72)是热休克蛋白70家族的诱导型异构体,在运动的大鼠肌肉和缺血心脏中合成。为了确定慢性缺血和重复运动对骨骼肌HSP72表达的单独和联合影响,对雄性Wistar大鼠进行了单侧髂动脉闭塞。在缺血1周后开始,一半的大鼠每天在电动跑步机上运动一次,每周5天,另一半则限制在笼内活动。在进行2、4或8周的耐力训练后,将大鼠与年龄匹配的久坐不动的大鼠一起处死。从双后肢的比目鱼肌和股四头肌的红色部分获取组织样本。耐力训练的大鼠骨骼肌中的HSP72水平显著升高。髂动脉闭塞对久坐不动大鼠肌肉中的HSP72水平没有影响,但增强了训练大鼠的HSP72水平。从细胞色素氧化酶和柠檬酸合酶活性评估的线粒体氧化能力,在久坐不动的动物生长过程中下降,但通过耐力训练得到显著改善。然而,耐力训练诱导的氧化能力增加被动脉闭塞部分阻止。得出的结论是,HSP72水平和线粒体氧化能力都受到缺血和训练的影响,但这些变化不一定相关。虽然将慢性运动叠加在外周动脉供血不足上会增加HSP72水平,但我们的结果表明,即使长时间进行耐力训练也不能有效提高缺血肌肉的氧化能力。

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