Thomas D P, Molé P A
Int J Sports Med. 1981 Aug;2(3):171-7. doi: 10.1055/s-2008-1034606.
Integrity of the myocardium following a swim to exhaustion (STE) was assessed by quantitative light and electron microscopy in young adult female rats. Myocardial fiber diameter and mitochondrial (MITO) number, size, and volume fraction (VF) were unaffected by the STE, Also, the STE did not alter ventricular water content. In contrast, myofibrillar (MYO) VF was reduced and sarcoplasmic (SARCO) VF elevated (both P less than 0.05) at exhaustion. As both cell and MITO absolute volume were apparently unchanged at exhaustion, an intracellular fluid shift from MYO to SARCO space must have occurred, without affecting MITO volume. Neither swim training nor low-protein diet modified these exhaustion-induced changes. These data provide a possible explanation at the ultrastructural level for the documented reduction in performance of the heart in the exhausted state.
通过定量光学显微镜和电子显微镜评估了成年雌性幼鼠在游至精疲力竭(STE)后心肌的完整性。心肌纤维直径、线粒体数量、大小和体积分数(VF)不受STE的影响,STE也未改变心室含水量。相比之下,在精疲力竭时,肌原纤维(MYO)VF降低,肌浆(SARCO)VF升高(两者P均小于0.05)。由于在精疲力竭时细胞和线粒体的绝对体积显然未发生变化,因此必定发生了细胞内液从MYO向SARCO空间的转移,而不影响线粒体体积。游泳训练和低蛋白饮食均未改变这些由精疲力竭引起的变化。这些数据在超微结构水平上为已记录的精疲力竭状态下心脏功能下降提供了一种可能的解释。