Adaptations to exercise training and contraction-induced muscle injury in animal models of muscular dystrophy

被引:35
作者
Carter, GT
Abresch, RT
Fowler, WM
机构
[1] Univ Calif Davis, Sch Med, Dept Phys Med & Rehabil, Davis, CA 95616 USA
[2] Univ Washington, Sch Med, Dept Rehabil Med, Seattle, WA 98195 USA
关键词
neuromuscular disease; mdx mouse; rehabilitation;
D O I
10.1097/00002060-200211001-00016
中图分类号
R49 [康复医学];
学科分类号
100215 ;
摘要
This article reviews the current status of exercise training and contraction-induced muscle-Injury investigations in animal models of muscular dystrophy. Most exercise-training studies have compared the adaptations of normal and dystrophic muscles with exercise. Adaptation of diseased muscle to exercise occurs at many levels, starting with the extracellular matrix, but also involves cytoskeletal architecture, muscle contractility, repair mechanisms, and gene regulation. The majority of exercise-injury investigations have attempted to determine the susceptibility of dystrophin-deficient muscles to contraction-induced injury. There is some evidence in animal models that diseased muscle can adapt and respond to mechanical stress. However, exercise-injury studies show that dystrophic muscles have an increased susceptibility to high mechanical forces. Most of the studies involving exercise training have shown that muscle adaptations in dystrophic animals were qualitatively similar to the adaptations observed in control muscle. Deleterious effects of the dystrophy usually occur only in older animals with advanced muscle fiber degeneration or after high-resistive eccentric training. The main limitations in applying these conclusions to humans are the differences in phenotypic expression between humans and genetically homologous animal models and in the significant biomechanical differences between humans and these animal models.
引用
收藏
页码:S151 / S161
页数:11
相关论文
共 80 条
[1]  
ABRESCH RT, 1998, REHABIL NEUROMUSCUL, V9, P285
[2]   MODERATE RESISTANCE EXERCISE PROGRAM - ITS EFFECT IN SLOWLY PROGRESSIVE NEUROMUSCULAR DISEASE [J].
AITKENS, SG ;
MCCRORY, MA ;
KILMER, DD ;
BERNAUER, EM .
ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION, 1993, 74 (07) :711-715
[3]   Animal models for muscular dystrophy: valuable tools for the development of therapies [J].
Allamand, V ;
Campbell, KP .
HUMAN MOLECULAR GENETICS, 2000, 9 (16) :2459-2467
[4]   ECCENTRIC EXERCISE-INDUCED INJURY TO RAT SKELETAL-MUSCLE [J].
ARMSTRONG, RB ;
OGILVIE, RW ;
SCHWANE, JA .
JOURNAL OF APPLIED PHYSIOLOGY, 1983, 54 (01) :80-93
[5]  
ASMUNDSON VS, 1966, ANN NY ACAD SCI, V138, P49, DOI 10.1111/j.1749-6632.1966.tb41153.x
[6]   Ecto-ATPase activity of α-sarcoglycan (adhalin) [J].
Betto, R ;
Senter, L ;
Ceoldo, S ;
Tarricone, E ;
Biral, D ;
Salviati, G .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (12) :7907-7912
[7]   INABILITY OF MYOGLOBIN TO INCREASE IN DYSTROPHIC SKELETAL-MUSCLE DURING DAILY EXERCISE [J].
BOOTH, FW .
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 1978, 373 (02) :175-178
[8]   Rapid recovery following contraction-induced injury to in situ skeletal muscles in mdx mice [J].
Brooks, SV .
JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY, 1998, 19 (02) :179-187
[9]   Muscle fibers of mdx mice are more vulnerable to exercise than those of normal mice [J].
Brussee, V ;
Tardif, F ;
Tremblay, JP .
NEUROMUSCULAR DISORDERS, 1997, 7 (08) :487-492
[10]   ASSOCIATION OF DYSTROPHIN AND AN INTEGRAL MEMBRANE GLYCOPROTEIN [J].
CAMPBELL, KP ;
KAHL, SD .
NATURE, 1989, 338 (6212) :259-262