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• W2077246538 abstract "RESPONSE Dear Editor-in-Chief: The main concern of the above letter involves an article by Nash et al. (6). Unfortunately, we cited the reference for this article incorrectly. In reconsideration of this point, it was found that the discussion of our article contains a misrepresentation concerning the results of these investigations. We are grateful to Drs. Nash and Jacobs for pointing out this mistake. However, in our opinion the conclusions made in our article are not substantially affected by this inadvertent error. As specified in the letter by Nash and Jacobs, untrained subjects with paraplegia display a smaller stroke volume and a higher heart rate in comparison with non-handicapped untrained subjects. It has been found that the left ventricular stroke volume correlates positively with the left ventricular end-diastolic dimension (3). Further, a positive linear correlation exists between the left ventricular stroke volume and the V˙O2peak(8). These relationships support our findings that untrained subjects with paraplegia have smaller left ventricular dimensions than untrained non-disabled subjects, particularly since the average left ventricular end-diastolic dimensions obtained in our study correspond with previous measurements from Kessler et al. (5) and Davis et al. (1). As cited by Nash in a training study from Davis et al. (1), untrained subjects with paraplegia completed a predominantly aerobic arm-cranking ergometry training program over a 16-wk period(3 times per wk for 20 to 40 minutes, maximum). No increase in the left ventricular end-diastolic dimensions and the left ventricular stroke volume was established at the end of the training period. Another study of wheelchair athletes at the regional and national level (exclusively paraplegics) showed contradictory results (2). Stroke volume, determined by indirect Fick principle, and VO2peak, measured with a spirometer, were approximately 40% higher in paraplegic athletes compared with an untrained control group. An echocardiographic assessment of left ventricular dimensions was not performed in this examination. The data from this study indirectly indicate a training-induced increase in left ventricular dimensions in longterm wheelchair-trained paraplegic athletes. In our examination (4), internationally successful wheelchair-trained paraplegic athletes from the German Paralympic Teams showed a much higher training level in comparison with the paraplegic athletes in the above mentioned study from Davis et al. (2). The weekly schedule averaged 6 to 15 hours of endurance training in various sports, mainly cross-country sleeding and wheelchair racing. In consideration of the method restrictions presented by Nash, the echocardiographic measurements from Washburn et al. (9) indicate that significant structural training adaptations of the heart first occur in subjects with tetra- and paraplegia when a level of physical activity >3000-4000 kcal/wk is reached. However, the subjects with paraplegia in the training study from Davis et al. (1) reached a maximum metabolism of approximately 800-1000 kcal/wk with the training protocol. Therefore, significant structural cardiac adaptations in the subjects with paraplegia examined in the study from Davis et al.(1) were not to be expected. In contrast, the wheelchair-trained high performance paraplegic athletes examined by us had an established weekly metabolism of minimal 3000 kcal over the past several years. Consequently, the differences in the left ventricular dimensions between the untrained and trained subjects with paraplegia in our study are explainable and do not contradict the above mentioned results. As far as we know there are no existing echocardiographic findings for comparably trained subjects with paraplegia. The additional comments in the letter from Nash et al. concerning the recorded differences in relation to heart rate and stroke volume at rest as well as the maximum heart rate and the V˙O2peak in wheelchair ergometry between trained and untrained subjects with paraplegia in comparison with the non-handicapped control group provides an important supplement to our discussion and have been confirmed (7). We agree with Nash et al. that owing to the inhomogeneous levels of lesion in the examined subjects with paraplegia, the demonstrated differences cannot be clearly attributed to a training effect. However, the distribution of the levels of lesion in untrained and trained subjects with paraplegia is comparable in our study such that the group differences should not be affected. Martin Huonker, M.D. Klinikum der Albert-Ludwigs; Universität Freiburg; Germany" @default.
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• W2077246538 date "1998-08-01" @default.
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• W2077246538 title "CARDIAC STRUCTURE AND FUNCTION IN EXERCISE TRAINED AND SEDENTARY PERSONS WITH PARAPLEGIA" @default.
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• W2077246538 doi "https://doi.org/10.1097/00005768-199808000-00025" @default.
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