Remodelling of the contractile apparatus of striated muscle stimulated electrically in a shortened position

J Anat. 1991 Oct;178:83-100. Remodelling of the contractile apparatus of striated muscle stimulated electrically in a shortened position. Jakubiec-Puka A, Carraro U. Source Nencki Institute of Experimental Biology, Warsaw, Poland. Abstract The aim of this study was to examine reorganisation of the contractile apparatus during adaptation to function when the length of a muscle is decreased. The rat soleus muscle was maintained in a shortened position and simultaneously stimulated electrically at a low frequency for 1-45 h. This experimental model decreased the length of the muscle and made the contractile apparatus irregular. The length of the sarcomeres decreased and became variable. The Z-line appeared wavy or fragmented. Foci, within which the sarcomeric organisation was lacking, often appeared within the contractile apparatus. These changes, occurring during the initial hours of stimulation, increased in number during the following hours. Their frequency and intensity depended on the degree of muscle shortening. In muscle moderately shortened during stimulation (up to 20%) the contractile apparatus recovered its normal appearance within 12 h of the experiment. In the muscle considerably shortened (by about 30%) the process of normalisation took much longer, in spite of recovery of sarcomere length. We conclude from these results that these changes are related to the accelerated work-induced reorganisation of the contractile apparatus whenever sarcomere number is reduced and/or when elimination of portions of the contractile apparatus occurs. These anomalies, occurring transiently in normal mature muscle when stimulated electrically in a shortened position, should be considered as adaptive phenomena. They resemble abnormalities appearing in the contractile apparatus of myopathic muscle. PMID: 1810938 [PubMed - indexed for MEDLINE] PMCID: PMC1260537 Free PMC Articl

Loss of Dystrophin and Some Dystrophin-Associated Proteins with Concomitant Signs of Apoptosis in Rat Leg Muscle Overworked in Extension

Acta Neuropathol. 2000 Dec;100(6):618-26. Loss of dystrophin and some dystrophin-associated proteins with concomitant signs of apoptosis in rat leg muscle overworked in extension. Biral D, Jakubiec-Puka A, Ciechomska I, Sandri M, Rossini K, Carraro U, Betto R. Source C.N.R. Unit for Muscle Biology and Physiopathology, Padova, Italy. Abstract This study investigated the basis for the high severity of damage to skeletal muscle due to eccentric exercise, i.e., to muscles generating force while lengthened. Fast and slow rat leg muscles maintained in an extended position were examined after 2-24 h of continuous stimulation. The treatment caused the injury to some regions of both muscles. Within the better preserved parts of the muscles, i.e., those without signs of necrotic processes, dystrophin, spectrin, and some of the dystrophin-associated proteins (beta-dystroglycan, alpha-sarcoglycan, and gamma-sarcoglycan) disappeared from sarcolemma of many fibers. The reduction or loss of dystrophin from the sarcolemma was more evident than that of other proteins examined, with sarcoglycans apparently being the most preserved. Several muscle fibers devoid of dystrophin contained apoptotic nuclei. Simultaneously, Bax, Bcl-2 and caspase-3 proteins appeared in many fibers. Our results indicate that a normal muscle overworking in an extended position undergoes the loss of several membrane skeletal proteins because of the excessive stress to the membrane cytoskeleton, which can lead to fiber death by either apoptosis or necrosis. This experimental model may represent a good model for mimicking the pathogenetic events in several muscular dystrophies. PMID: 11078213 [PubMed - indexed for MEDLINE