Suppr超能文献

实验性心力衰竭时大鼠骨骼肌代谢:体育锻炼的影响

Rat skeletal muscle metabolism in experimental heart failure: effects of physical training.

作者信息

Brunotte F, Thompson C H, Adamopoulos S, Coats A, Unitt J, Lindsay D, Kaklamanis L, Radda G K, Rajagopalan B

机构信息

M.R.C. Biochemical & Clinical Magnetic Resonance Unit, Oxford Radcliffe Trust, Headington, UK.

出版信息

Acta Physiol Scand. 1995 Aug;154(4):439-47. doi: 10.1111/j.1748-1716.1995.tb09929.x.

Abstract

Skeletal muscle metabolic abnormalities exist in chronic heart failure. The influence of physical training on muscle metabolism after myocardial infarction was studied in a rat model. 31P magnetic resonance spectroscopy and enzyme assays were performed in Wistar rats 12 weeks after coronary artery ligation. Infarcted rats were allocated randomly to either 6 weeks of training or non-training. Spectra were collected from the calf muscles during sciatic nerve stimulation at 2 Hz. Fibre typing and enzymatic assays were performed on the muscles of the contralateral non stimulated leg. Post-mortem rats were also divided into severe and moderate heart failure according to the lung weight per body weight. At 200 g twitch tension, phosphocreatine and pH were found to be significantly lower in the non-trained severe heart failure group compared with the other groups. Phosphocreatine recovery half-time was significantly longer in the non-trained group with severe heart failure and correlated with the citrate synthase activity in the muscle. The training did not induce a change in the enzyme activities in the infarcted animals with moderate heart failure but did correct the lower citrate synthase activity in the non-trained severe heart failure animals. This normalization of muscle metabolism was achieved by training without any change in calf muscle mass, making atrophy unlikely to be the sole cause of the metabolic changes in heart failure. Training in rats with severe heart failure can reverse the abnormalities of skeletal muscle metabolism, implicating decreased physical activity in the aetiology of these changes.

摘要

慢性心力衰竭存在骨骼肌代谢异常。在大鼠模型中研究了体育锻炼对心肌梗死后肌肉代谢的影响。在冠状动脉结扎12周后的Wistar大鼠中进行了31P磁共振波谱分析和酶活性测定。将梗死大鼠随机分为训练6周组或非训练组。在坐骨神经以2Hz频率刺激期间从小腿肌肉采集波谱。对侧未受刺激腿的肌肉进行纤维分型和酶活性测定。死后大鼠也根据每体重的肺重量分为重度和中度心力衰竭组。在200g抽搐张力下,发现未训练的重度心力衰竭组的磷酸肌酸和pH值显著低于其他组。重度心力衰竭的未训练组中磷酸肌酸恢复半衰期显著延长,且与肌肉中的柠檬酸合酶活性相关。训练未引起中度心力衰竭梗死动物的酶活性变化,但确实纠正了未训练的重度心力衰竭动物中较低的柠檬酸合酶活性。肌肉代谢的这种正常化是通过训练实现的,小腿肌肉质量没有任何变化,这使得萎缩不太可能是心力衰竭代谢变化的唯一原因。重度心力衰竭大鼠的训练可以逆转骨骼肌代谢异常,这表明身体活动减少是这些变化病因的一个因素。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验