AJP - Cell Physiology, Vol 258, Issue 4 C589-C592, Copyright © 1990 by American Physiological Society
Effects of elevated temperature on protein breakdown in muscles from septic rats
M. Hall-Angeras, U. Angeras, P. O. Hasselgren and J. E. Fischer
Department of Surgery, University of Cincinnati Medical Center, Ohio 45267-0558.
Elevated temperature has been proposed to contribute to accelerated muscle
protein degradation during fever and sepsis. The present study examined the
effect of increased temperature in vitro on protein turnover in skeletal
muscles from septic and control rats. Sepsis was induced by cecal ligation
and puncture (CLP); control rats were sham operated. After 16 h, the
extensor digitorum longus (EDL) and soleus (SOL) muscles were incubated at
37 or 40 degrees C. Protein synthesis was determined by measuring
incorporation of [14C]phenylalanine into protein. Total and myofibrillar
protein breakdown was assessed from release of tyrosine and
3-methylhistidine (3-MH), respectively. Total protein breakdown was
increased at 40 degrees C by 15% in EDL and by 29% in SOL from control
rats, whereas 3-MH release was not affected. In muscles from septic rats,
total and myofibrillar protein breakdown was increased by 22 and 30%,
respectively, at 40 degrees C in EDL but was not altered in SOL. Protein
synthesis was unaffected by high temperature both in septic and nonseptic
muscles. The present results suggest that high temperature is not the
primary mechanism of increased muscle protein breakdown in sepsis because
the typical response to sepsis, i.e., a predominant increase in
myofibrillar protein breakdown, was not induced by elevated temperature in
normal muscle. It is possible, however, that increased temperature may
potentiate protein breakdown that is already stimulated by sepsis because
elevated temperature increased both total and myofibrillar protein
breakdown in EDL from septic rats.
