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Heat stress prevents overload‐induced hypertrophy of myosin heavy chain type I fiber area, but does not alter structural damage or localized patterns of cellular replication
Author(s) -
Frier Bruce Charles,
Locke Marius
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.637.7
Subject(s) - plantaris muscle , muscle hypertrophy , myosin , myod , chemistry , medicine , endocrinology , microbiology and biotechnology , anatomy , myocyte , skeletal muscle , biology , biochemistry , myogenesis , soleus muscle
Heat stress (HS) inhibits compensatory hypertrophy in the rat plantaris muscle by preventing the accumulation of myosin heavy chain type I (MHC‐I) protein. However, it is unknown whether HS also affects MHC‐I fiber area, structural changes, nuclear accumulation and localized satellite cell activation in overloaded plantaris. Thirty Sprague‐Dawley rats underwent synergistic ablation and were divided into non‐heat stressed (NHS) and heat stressed (15‐min, 42°C) groups. The contralateral limb was used as a control. Muscles were assessed after 1, 3 and 7 days of functional overload. MHC‐I fiber area was not significantly different between NHS and HS plantaris muscles after 1 day of overload (0.228 mm 2 vs. 0.172 mm 2 ,respectively); however, MHC‐I fiber area was significantly greater in the NHS plantaris compared to HS plantaris after 3‐ and 7‐days (0.364 mm 2 vs. 0.193 mm 2 and 0.442 mm 2 vs. 0.237 mm 2 , respectively). Localized Myf‐5, PCNA and MyoD suggested a similar pattern of satellite cell activation in both NHS and HS plantaris muscles on all days. Overload induced progressive structural damage and massive accumulation of nuclei in the deep portion of the plantaris regardless of a prior HS. These results suggest that HS may prevent an overload‐induced increase in MHC‐I fiber area by restricting protein expression in existing fibers, rather than via altered replication signals, tissue strain or nuclear accumulation.