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Ann Thorac Surg 1995;59:1038
© 1995 The Society of Thoracic Surgeons
Department of Muscle Physiology, Carl-Ludwig-Institute of Physiology, University of Leipzig, Liebigstr 27, 04103 Leipzig, Germany
Clinic for Heart Surgery, University of Leipzig, Russenstr 19, 04289 Leipzig, Germany
To the Editor:
We are grateful for the response shown our article. We recognize Dr Salmons' critical remarks, but we believe that the way this criticism was stated is not particularly appropriate for the caliber of this journal.
To start out with, we would like to thank Dr Salmons for his correct criticism on the fact that we did not give the standard deviation according to the percentage of the fiber type distribution. We omitted these data because the results were so obvious that we did not find it necessary to show it in detail. We most certainly determined the standard deviation. The particular data required by Dr Salmons are the following: unstimulated controls, 20% ± 4.5%; stimulated latissimus dorsi without anabolic steroids, 65.6% ± 3.3%; and stimulated latissimus dorsi with anabolic steroids, 96.7% ± 3.8% type I fibers.
Doctor Salmons stated that one part of the fibers was not completely transformed and therefore it could express both types of myosin isoforms. But as written in the Material and Methods section, we studied myosin adenosine triphosphatase activities after acid and alkaline preincubations. We paid close attention to finding transitory type IIC fibers with positive reactions in both stainings. The number of these fibers is less than 2%, and therefore we stated that the transition of the muscle fibers was complete at the time of the investigation. We did not find it necessary to take up space in this article to report unnecessary data.
Another problem refered to by Dr Salmons is that part of the muscle was irreversibly damaged and replaced by fibers or fatty tissue. As written in the methods we also performed classic histological stainings (hematoxylin and eosin staining; staining after van Gieson). We did not find any signs of inflammation, fatty degeneration, or increase of connective tissue. Furthermore, we did not experience a higher incidence of fibers with central nuclei or other signs of generation of new fibers, despite the fact that we took special care to look for it. We also used a monoclonal antibody against the neonatal myosin isoform and found a negative result, supporting the idea that at the time of investigation no significant regeneration took place in the muscle.
According to Dr Salmons' criticism on our experimental protocol we have to add that we carefully followed the stimulation patterns used in clinical practice. Therefore we strictly followed the use of burst stimulation at a submaximal level to prevent overstimulation. In this way we did exactly what Dr Salmons suggested in his commentary. It is quite clear that by using burst stimulation one can determine only the ``contraction time'' of a tetanic contraction.
In contrast to Dr Salmons' statement that we had dismissed the large body of literature about side effects of anabolic steroids, we must point out that we carefully studied the side effects of anabolic hormones in general and took special care in the selection of the steroid that we used. In this matter we received help and advice from the physiologists of the former Institute of Physical Culture and Sports in Leipzig, East Germany. It is important to recognize that, especially for the steroid used in this study (metenolone; a 17-ß-ester derivate), no serious or irreversible side effects are known. This is not the case for 17-
-alcylated steroids, which often were misused by athletes. In our opinion the comparison of undesired side effects of metenolone on one hand and the theoretical benefit in the context of cardiomyoplasty on the other hand appears to us to be reason enough to investigate the use of this drug in such studies.
Finally we have a comment to Dr Salmons' remarks in his fourth paragraph, beginning ``Figure 4 is highly misleading. . .''. According to our protocol, both the data obtained for the contraction amplitude under a 7.5 V and a 10.5 V stimulation are correct. We cannot follow Dr Salmons' criticism as to why the 10.5 V reading should be the only reliable data. Recalculating the whole body of our data concerning the muscle weight of all latissimus dorsi muscles of both the first and second study, the result is significant in paired Student's t test (t = 1,773; p < 0.05). Therefore the statements that ``via a significant increase in muscle mass (amounting to 80%)'' and ``the demonstrated increase in muscle mass due to administration of anabolic steroids'' are definitely with foundation.
Related Article
Ann. Thorac. Surg. 1995 59: 969-970.
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