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Mechanisms underlying reduced maximum shortening velocity during fatigue of intact, single fibres of mouse muscle

1998; Wiley; Volume: 510; Issue: 1 Linguagem: Inglês

10.1111/j.1469-7793.1998.269bz.x

1469-7793

Håkan Westerblad, Anders J. Dahlstedt, Jan Lännergren,

Cardiomyopathy and Myosin Studies

The mechanism behind the reduction in shortening velocity in skeletal muscle fatigue is unclear. In the present study we have measured the maximum shortening velocity ( V 0 ) with slack tests during fatigue produced by repeated, 350 ms tetani in intact, single muscle fibres from the mouse. We have focused on two possible mechanisms behind the reduction in V 0 : reduced tetanic Ca 2+ and accumulation of ADP. During fatigue V 0 initially declined slowly, reaching 90 % of the control after about forty tetani. The rate of decline then increased and V 0 fell to 70 % of the control in an additional twenty tetani. The reduction in isometric force followed a similar pattern. Exposing unfatigued fibres to 10 μM dantrolene, which reduces tetanic Ca 2+ , lowered force by about 35 % but had no effect on V 0 . In order to see if ADP might increase rapidly during ongoing contractions, we used a protocol with a tetanus of longer duration bracketed by standard‐duration tetani. V 0 in these three tetani were not significantly different in control, whereas V 0 was markedly lower in the longer tetanus during fatigue and in unfatigued fibres where the creatine kinase reaction was inhibited by 10 μM dinitrofluorobenzene. We conclude that the reduction in V 0 during fatigue is mainly due to a transient accumulation of ADP, which develops during contractions in fibres with impaired phosphocreatine energy buffering.