Premium
Cellular adaptations in soleus muscle during recovery after hindlimb unloading
Author(s) -
Oishi Y.,
Ogata T.,
Yamamoto K.i.,
Terada M.,
Ohira T.,
Ohira Y.,
Taniguchi K.,
Roy R. R.
Publication year - 2008
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2007.01747.x
Subject(s) - soleus muscle , myosin , hindlimb , endocrinology , medicine , atrophy , heat shock protein , apoptosis , muscle atrophy , mitochondrial biogenesis , cytochrome c oxidase , biology , chemistry , mitochondrion , skeletal muscle , microbiology and biotechnology , biochemistry , gene
Aim: We used a model of chronic unloading followed by reloading to examine the apoptotic responses associated with soleus muscle atrophy and subsequent recovery. Methods: Male Wistar rats were subjected to hindlimb unloading (HU) for 2 weeks and subsequent reloading for 0, 3, 7 and 14 days. One‐half of the HU‐reloaded rats were administered cyclosporine A (CsA), a calcineurin (CaN) inhibitor. Results: There was fibre atrophy (73%) and a decrease in slow type I fibre/myosin heavy chain (MyHC) composition in the soleus muscle after 2 weeks of HU. Fibre size and type I MyHC composition recovered to near the age‐matched control levels by recovery day 14 in non‐treated, but not in CsA‐treated, rats. Myonuclear number was lower and the number of apoptotic nuclei higher in 2‐week HU than control rats. These values returned to control levels after 7 and 14 days of recovery, respectively, in both HU‐recovery groups. After 2 weeks of HU, the levels of heat shock proteins (Hsp) 60 and 72, mitochondrial cytochrome c oxidase subunit IV (Cox IV), and peroxisome proliferator‐activated receptor gamma coactivator 1 (PGC‐1) proteins were lower than control. The levels of all of these proteins gradually increased to or above the control levels during cage recovery in both groups. Conclusion: Our results indicate that apoptotic mechanisms are involved in the modulation of myonuclear number during chronic unloading and subsequent reloading. Furthermore, it appears that CaN is related to fibre size and phenotype adaptations, but not to apoptotic responses.