Changes in skeletal muscle biochemistry and histology relative to fiber type in rats with heart failure
Changes in skeletal muscle biochemistry and histology relative to fiber type in rats with heart failure
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DOI：
10.1152/jappl.1997.83.4.1291
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发表时间：
1997-10-01
影响因子：
3.3
通讯作者：
Musch, TI
中科院分区：
文献类型：
--
作者：
Delp, MD;Duan, CP;Musch, TI
心肌梗死后左心功能不全(LVD)的主要后果之一是运动能力的下降。有几个因素被认为是造成这种下降的原因，包括骨骼肌代谢和有氧能力的改变。本研究的目的是确定LVD引起的骨骼肌酶活性、纤维组成和纤维大小的改变是否1)在肌肉中普遍存在，或仅限于主要由特定纤维类型组成的肌肉；2)与LVD的严重程度有关。雌性Wistar大鼠分为3组：假手术对照组(n=13)和LVD中度组(n=10)和重度组(n=7)。结扎左冠状动脉主干造成LVD，并导致左心室舒张末压升高(P<；0.05)(假手术组，5+/-1 mm Hg；中度LVD，11+/-1 mm Hg；重度LVD，25+/-1 mm Hg)。适度的LVD降低了由类型领带纤维组成的肌肉中磷酸果糖激酶(PFK)和柠檬酸合成酶的活性，但不改变所研究的任何肌肉的纤维组成或大小。然而，严重的LVD降低了肌肉中参与末端和β-氧化的酶的活性，这些酶主要由I型纤维、IIA型纤维和IIB型纤维组成。此外，严重的LVD导致IIB型肌肉中PFK活性降低，IID/X型纤维的百分比减少10%，而Tie型纤维的比例相应增加。重度LVD大鼠比目鱼肌和足底肌I型纤维、IIA型纤维和/或IIB型纤维萎缩。这些数据表明，心肌梗死后严重LVD的大鼠表现为1)不依赖于肌肉纤维组成的线粒体酶活性降低，2)IIB型肌肉中PFK活性降低，3)IID/X型向IIB型纤维转化，以及4)I型、IIA和IIB型纤维萎缩。
One of the primary consequences of left ventricular dysfunction (LVD) after myocardial infarction is a decrement in exercise capacity. Several factors have been hypothesized to account for this decrement, including alterations in skeletal muscle metabolism and aerobic capacity. The purpose of this study was to determine whether LVD-induced alterations in skeletal muscle enzyme activities, fiber composition, and fiber size are I) generalized in muscles or specific to muscles composed primarily of a given fiber type and 2) related to the severity of the LVD. Female Wistar rats were divided into three groups: sham-operated controls (n = 13) and rats with moderate (n = 10) and severe (n = 7) LVD. LVD was surgically induced by ligating the left main coronary artery and resulted in elevations (P < 0.05) in left ventricular end-diastolic pressure (sham, 5 +/- 1 mmHg; moderate LVD, 11 +/- I mmHg; severe LVD, 25 +/- 1 mmHg). Moderate LVD decreased the activities of phosphofructokinase (PFK) and citrate synthase in one muscle composed of type TIE fibers but did not modify fiber Composition or size of any muscle studied. However, severe LVD diminished the activity of enzymes involved in terminal and beta-oxidation in muscles composed primarily of type I fibers, type IIA fibers, and type IIB fibers. In addition, severe LVD induced a reduction in the activity of PFK in type IIB muscle, a 10% reduction in the percentage of type IID/X fibers, and a corresponding increase in the portion of type TIE fibers. Atrophy of type I fibers, type IIA fibers, and/or type IIB fibers occurred in soleus and plantaris muscles of rats with severe LVD. These data indicate that rats with severe LVD after myocardial infarction exhibit 1) decrements in mitochondrial enzyme activities independent of muscle fiber composition, 2) a reduction in PFK activity in type IIB muscle, 3) transformation of type IID/X to type IIB fibers, and 4) atrophy of type I, IIA, and IIB fibers.