Delp M D, Duan C, Mattson J P, Musch T I
Department of Health and Kinesiology, Texas A&M University, College Station, Texas 77843, USA.
J Appl Physiol (1985). 1997 Oct;83(4):1291-9. doi: 10.1152/jappl.1997.83.4.1291.
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 1) 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 +/- 1 mmHg; severe LVD, 25 +/- 1 mmHg). Moderate LVD decreased the activities of phosphofructokinase (PFK) and citrate synthase in one muscle composed of type IIB 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 IIB 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.
心肌梗死后左心室功能障碍（LVD）的主要后果之一是运动能力下降。有几种因素被认为可以解释这种下降，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，还是特定于主要由给定纤维类型组成的肌肉；2）与LVD的严重程度相关。雌性Wistar大鼠分为三组：假手术对照组（n = 13）以及中度（n = 10）和重度（n = 7）LVD大鼠。通过结扎左冠状动脉手术诱导LVD，导致左心室舒张末期压力升高（P < 0.05）（假手术组，5±1 mmHg；中度LVD组，11±1 mmHg；重度LVD组，25±1 mmHg）。中度LVD降低了一块由IIB型纤维组成的肌肉中的磷酸果糖激酶（PFK）和柠檬酸合酶的活性，但未改变所研究的任何肌肉的纤维组成或大小。然而，重度LVD降低了主要由I型纤维、IIA型纤维和IIB型纤维组成的肌肉中参与终末氧化和β氧化的酶的活性。此外，重度LVD导致IIB型肌肉中PFK活性降低，IID/X型纤维百分比降低10%，相应地IIB型纤维比例增加。重度LVD大鼠的比目鱼肌和跖肌中出现了I型纤维、IIA型纤维和/或IIB型纤维的萎缩。这些数据表明，心肌梗死后重度LVD大鼠表现出：1）线粒体酶活性下降，与肌肉纤维组成无关；2）IIB型肌肉中PFK活性降低；3）IID/X型纤维向IIB型纤维的转变；4）I型、IIA型和IIB型纤维的萎缩。
