Int J Sports Med 1992; 13(3): 274-277
DOI: 10.1055/s-2007-1021266
© Georg Thieme Verlag Stuttgart · New York

Nifedipine Diminishes Exercise-Induced Muscle Damage in Mouse

J. A. R. Duarte1 , J. M. C. Soares1 , H.-J. Appell2
  • 1Department of Sport Biology, Faculty of Sport Sciences, University of Porto
  • 2Institute for Experimental Morphology, German Sports University, Cologne
Further Information

Publication History

Publication Date:
14 March 2008 (online)

Abstract

The purpose of this study was to evaluate the effects of a calcium Channel blocker (nifedipine) on the severity of muscle damage induced by intensive exercise. Male Charles River mice were assigned to four groups (8 mice/group): normal control (C), nifedipine (N), nifedipine and exercise (N + E) and exercise (E). The animals of the C group were not submitted to any exercise nor to drug administration. The animals of the N group received 1 mg·kg-1 per day of nifedipine (Adalat 10 mg, Bayer AG), per os, during 3 days. The mice of the N + E group were submitted to a treadmill run (0° slope) at 1000 m·h-1 (80% of their maximal speed) for 1 hour. In this group, the administration of the drug was under the same conditions as for the N group. The administration started 24 h before the run. The E group was submitted to the same exercise protocol as the animals of N + E group. The soleus muscle was excised for light and electron microscopic evaluation using routine histological techniques. In the C and N groups no morphological alterations were detected. In the E group the number of alterations of striated pattern was twice that in the N + E group. The number of fibres with central nuclei was 35% in the E group but only 8% in the N + E group. The total number of damaged fibres was significantly higher in the E group. The results suggest that nifedipine may give protection to exercise-induced skeletal muscle damage in mouse, probably because the blocking of Channels impaired Ca2+ influx; and the results of this study therefore confirm earlier contentions about the possible role of calcium ions in producing muscle damage after work.

    >