title: Attenuated fatigue in slow twitch skeletal muscle during isotonic exercise in rats with chronic heart failure.
abstract: During isometric contractions, slow twitch soleus muscles (SOL) from rats with chronic heart failure (chf) are more fatigable than those of sham animals. However, a muscle normally shortens during activity and fatigue development is highly task dependent. Therefore, we examined the development of skeletal muscle fatigue during shortening (isotonic) contractions in chf and sham-operated rats. Six weeks following coronary artery ligation, infarcted animals were classified as failing (chf) if left ventricle end diastolic pressure was >15 mmHg. During isoflurane anaesthesia, SOL with intact blood supply was stimulated (1s on 1s off) at 30 Hz for 15 min and allowed to shorten isotonically against a constant afterload. Muscle temperature was maintained at 37°C. In resting muscle, maximum isometric force (F(max)) and the concentrations of ATP and CrP were not different in the two groups. During stimulation, F(max) and the concentrations declined in parallel sham and chf. Fatigue, which was evident as reduced shortening during stimulation, was also not different in the two groups. The isometric force decline was fitted to a bi-exponential decay equation. Both time constants increased transiently and returned to initial values after approximately 200 s of the fatigue protocol. This resulted in a transient rise in baseline tension between stimulations, although this effect which was less prominent in chf than sham. Myosin light chain 2s phosphorylation declined in both groups after 100 s of isotonic contractions, and remained at this level throughout 15 min of stimulation. In spite of higher energy demand during isotonic than isometric contractions, both shortening capacity and rate of isometric force decline were as well or better preserved in fatigued SOL from chf rats than in sham. This observation is in striking contrast to previous reports which have employed isometric contractions to induce fatigue.
authors.affiliation: Institute for Experimental Medical Research, Oslo University Hospital, Ullevål, Oslo, Norway.
authors.forename: Morten
authors.initials: M
authors.lastname: Munkvik
authors.forename: Per Kristian
authors.initials: PK
authors.lastname: Lunde
authors.forename: Jan Magnus
authors.initials: JM
authors.lastname: Aronsen
authors.forename: Jon Arne Kro
authors.initials: JA
authors.lastname: Birkeland
authors.forename: Ivar
authors.initials: I
authors.lastname: Sjaastad
authors.forename: Ole M
authors.initials: OM
authors.lastname: Sejersted
mesh_terms: D000818:Animals; D024722:Cardiac Myosins / Q000378:metabolism; D002908:Chronic Disease; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology*; D007537:Isometric Contraction; D008297:Male; D018763:Muscle Fatigue; D018482:Muscle, Skeletal / Q000378:metabolism / Q000503:physiopathology*; D018994:Myosin Light Chains / Q000378:metabolism; D010766:Phosphorylation; D010805:Physical Conditioning, Animal; D051381:Rats; D017208:Rats, Wistar
chemical_list: D018994:Myosin Light Chains; C107184:myosin light chain 2; D024722:Cardiac Myosins