Abstract

Skeletal muscle fatigue develops during physical exercise. Most reports on skeletal muscle fatigue use isometricfatigue protocols with a fall in force production as a measure of fatigue. However, most muscles shorten during normal use and we propose that the fatigue mechanism will be different during dynamic contractions as compared with isometric contractions. Methods: Fatigue was induced in rat soleus muscles from post infarction heart failure (HF) rats and controls (SHAM) by in situ isotonic shortening contractions (1s at 30Hz every 2s for 15min). The muscles were allowed to shorten isotonically against a load (AL) corresponding to 1/3 of maximal isometric force. After 15min recovery period the muscles were stimulated with a similar protocol. MLC2s phosphorylation and metabolites were measured at different points of time. Results: During 1st protocol, fatigue development was confirmed by a significant fall in shortening in both SHAM and HF. After 100s of stimulation soleus from SHAM showed an increase in baseline tension (Tbl) between stimulation trains, which was much less pronounced in HF (p<0.01). At this time there was a significant higher lactate concentration in SHAM muscle compared with HF. The increase in Tbl at 100s was correlated to both isotonic and isometric relaxation rate. At 100s in 2nd protocol, the isotonic and isometric relaxation rates were nearly recovered leading to almost no rise in Tbl in both SHAM and HF. There was a linear correlation (p=0.99) between maximal shortening and MLC2s phosphorylation in protocols with variable AL. We propose that MLC2s phosphorylation participates in the regulation of shortening, while metabolites (especially lactate) may contribute to the reduced relaxation rates leading to increased Tbl.

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