Premium
Mechanisms underlying reduced maximum shortening velocity during fatigue of intact, single fibres of mouse muscle
Author(s) -
Westerblad Håkan,
Dahlstedt Anders J.,
Lännergren Jan
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.269bz.x
Subject(s) - isometric exercise , phosphocreatine , tetanus , chemistry , muscle fatigue , creatine kinase , isotonic , tetanic stimulation , medicine , endocrinology , biophysics , biology , biochemistry , energy metabolism , electromyography , excitatory postsynaptic potential , inhibitory postsynaptic potential , neuroscience , immunology , vaccination
1 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. 2 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. 3 Exposing unfatigued fibres to 10 μM dantrolene, which reduces tetanic Ca 2+ , lowered force by about 35 % but had no effect on V 0 . 4 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. 5 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.