Why the study?
Does hindlimb unloading induce soleus muscle atrophy and pathological changes in male Sprague-Dawley rats?
Does hindlimb unloading induce soleus muscle atrophy and pathological changes in male Sprague-Dawley rats?
Hindlimb unloading in rats causes progressive soleus muscle atrophy, pathological changes, and a shift in EMG activity due to unloaded contractions, reduced use, compromised blood flow, and shortened working length.
Rat hindlimb unloading model shows rapid atrophy; hypothesis-generating for human disuse mechanisms, requiring translational studies.
Soleus muscle atrophy was induced by hindlimb unloading of male Sprague-Dawley rats (305 +/- 15 g) for 4, 7, and 10-14 days. Controls (291 +/- 14 g) were housed in vivarium cages. Soleus electromyogram (EMG) activity was recorded before and during tail suspension. Unloading caused progressive reduction in the muscle-to-body weight ratio. After 14 days, type I and IIa fibers decreased in area 63 and 47%, respectively. Subsarcolemmal mitochondria and myofibrils were degraded more rapidly than intermyofibrillar mitochondria and the cell membrane. After 10 days, 3% of the fibers exhibited segmental necrosis; affected fibers were all high-oxidative type IIa fibers. This suggested ischemic injury. By 13 days, 30% of the fibers possessed central corelike lesions involving primarily type I fibers. Video monitoring revealed abnormal plantar flexion of the hindfeet by 4 days; this posture shortened the soleus working range. Corelike lesions indicated adaptation to the shortened length. No morphological signs of denervation were detected. EMG activity shifted from tonic to phasic, and aggregate activity was 13% of normal after 7 days. These findings indicate that the atrophy and pathological changes result from unloaded contractions, reduced use, compromised blood flow, and shortened working length.
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Riley et al. (1990) studied this question.
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