Contractile properties of in situ perfused skeletal muscles from rats with congestive heart failure.
We hypothesized that in congestive heart failure (CHF) slow-twitch but not fast-twitch muscles exhibit decreased fatigue resistance in the sense of accelerated reduction of muscle force during activity. Experiments were carried out on anaesthetized rats 6 weeks after induction of myocardial infarction or a sham operation (Sham). Animals with left ventricular end-diastolic pressure (LVEDP) > 15 mmHg under anaesthesia were selected for the CHF group. There was no muscle atrophy in CHF. Force generation by in situ perfused soleus (Sol) or extensor digitorum longus (EDL) muscles was recorded during stimulation (trains at 5 Hz for 6 s (Sol) or 10 Hz for 1.5 s (EDL) at 10 or 2.5 s intervals, respectively) for 1 h in Sol and 10 min in EDL at 37 degrees C. Initial force was almost the same in Sol from CHF and Sham rats, but relaxation was slower in CHF. Relaxation times (95-5 % of peak force) were 177 +/- 55 and 131 +/- 44 ms in CHF and Sham, respectively, following the first stimulation train. After 2 min of stimulation the muscles transiently became slower and maximum relaxation times were 264 +/- 71 and 220 +/- 45 ms in CHF and Sham, respectively (P < 0.05). After 60 min they recovered to 204 +/- 60 and 122 +/- 55 ms in CHF and Sham, respectively (P < 0.05). In CHF but not in Sham rats the force of contraction of Sol declined from the second to the sixtieth minute to 70 % of peak force. The EDL of both CHF and Sham fatigued to 24-28 % of initial force, but no differences in contractility pattern were detected. Thus, slow-twitch muscle is severely affected in CHF by slower than normal relaxation and significantly reduced fatigue resistance, which may explain the sensation of both muscle stiffness and fatigue in CHF patients.
Lunde
Per Kristian
PK
Institute for Experimental Medical Research, University of Oslo, Ullevaal University Hospital, N-0407 Oslo, Norway.
Verburg
Esther
E
Eriksen
Morten
M
Sejersted
Ole M
OM
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000096:biosynthesis / Q000378:metabolism; D015153:Blotting, Western; D004558:Electric Stimulation; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D008297:Male; D009119:Muscle Contraction / Q000502:physiology; D018763:Muscle Fatigue / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism / Q000503:physiopathology*; D010477:Perfusion; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D012519:Sarcoplasmic Reticulum / Q000378:metabolism
D012333:RNA, Messenger; D009320:Atrial Natriuretic Factor