Abstract
Abnormalities in the excitation-contraction (EC) coupling of slow-twitch
muscle seem to explain the slowing and increased fatigue observed
in congestive heart failure (CHF). However, it is not known which
elements of the EC-coupling that might be affected. We hypothesize
that the temperature sensitivity of contractile properties of the
soleus muscle might be altered in CHF possibly because of alterations
of the temperature sensitivity of intracellular Ca$^2+$ handling.
We electrically stimulated the in situ soleus muscle of anaesthetised
rats that had six week post-infarction CHF using 1 and 50 Hz and
using a fatigue protocol (5 Hz stimulation for 30 min) at 35, 37
and 40 degrees C. Ca$^2+$ uptake and release were measured in
sarcoplasmic reticulum vesicles at various temperatures. Contraction
and relaxation rates of the soleus muscle were slower in CHF than
in Sham at 35 degrees C, but the difference was almost absent at
40 degrees C. The fatigue protocol revealed that force development
was more temperature sensitive in CHF, whereas contraction and relaxation
rates were less temperature sensitive in CHF than in Sham. The Ca$^2+$
uptake and release rates did not correlate to the difference between
CHF and Sham regarding contractile properties or temperature sensitivity.
In conclusion, the discrepant results regarding altered temperature
sensitivity of contraction and relaxation rates in the soleus muscle
of CHF rats in comparison to Ca$^2+$ release and uptake rates
in vesicles indicate that the molecular cause of slow-twitch muscle
dysfunction in CHF is not linked to the intracellular Ca$^2+$
cycling.
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