Force decline due to fatigue and intracellular acidification in isolated fibres from mouse skeletal muscle.

摘要: 1. Single, intact muscle fibres from the flexor brevis foot of mouse have been fatigued at 25 degrees C by 350 ms, 70 Hz stimulation trains, initially delivered every 3.8 s and then stepwise decreasing intervals until tension was down to about 30% original (Po). Rested generated a specific force 372 +/- 8.4 kPa (mean S.E.M., n = 25). 2. Endurance, defined as time attain 0.5 Po, varied 2.5 24 min, with majority falling in range 4-8 corresponding 70-160 tetani. In all where it followed, recovery after cessation 90% or better. 3. Tetanic declined characteristic way during fatiguing stimulation: fell 0.85 Po eight fourteen tetani (phase 1), followed long period nearly steady generation 2) finally there rapid decline 3). 4. Caffeine (15 mM) caused slight potentiation tetanic rested state (4.7 0.9%, 21) slowed relaxation. No change resting seen caffeine concentrations up mM. 5. (15-25 dramatic increase when applied severely fibres: output rose 29.8 1.5 82.5 1.2% (n 13) Po. During phase 2 much smaller. 6. A 10 pause resulted large, transient imposed 3 but had little effect on production 7. Intracellular acidosis, induced superfusion Tyrode solution gassed CO2 instead normal 5% (extracellular pH 6.5 vs. 7.3), fall 7). This depression could some extent be counteracted 15 mM-caffeine, which brought back 0.90 8. It is concluded that are least two mechanisms for one manifests itself early likely related cross-bridge function another representing deficient Ca2+ handling becomes prominent later stage. For severe fatigue (0.3 Po) latter mechanism dominant.