Stimulation frequency-dependent reductions in skeletal muscle force and speed in creatine kinase-deficient mice

Citation
A. De Haan et al., Stimulation frequency-dependent reductions in skeletal muscle force and speed in creatine kinase-deficient mice, ACT PHYSL S, 166(3), 1999, pp. 217-222
Citations number
18
Categorie Soggetti
Physiology
Journal title
ACTA PHYSIOLOGICA SCANDINAVICA
ISSN journal
00016772 → ACNP
Volume
166
Issue
3
Year of publication
1999
Pages
217 - 222
Database
ISI
SICI code
0001-6772(199907)166:3<217:SFRISM>2.0.ZU;2-G
Abstract
Force and speed parameters were obtained from isometric contractions at dif ferent stimulation frequencies of creatine kinase-deficient and wildtype in situ mouse medial gastrocnemius muscles. The absence of creatine kinase di d not affect force production at higher stimulation frequencies. However, a t frequencies below 140 Hz, forces were lower than the controls (P < 0.05); at the lowest frequency applied (80 Hz) the force was reduced to approxima te to 60% compared with the wildtype muscles. In contrast, twitch force was not affected. When the contractions were preceded by a brief tetanus (50 m s), the effects of lacking creatine kinase on force production were more pr onounced; at 80 Hz stimulation isometric force was further reduced to 66.5 +/- 6.2% (mean +/- SD; n = 5) of the single contractions of the deficient m uscles and to approximate to 42% of the wildtype muscles. Twitch force was now also reduced (by approximate to 50%) after the tetanus. The speed of th e muscles was not affected in the single contractions. However, after a pre ceding tetanus, the rate of force rise was reduced by approximate to 14% at high frequencies of stimulation. With decreasing frequencies (below 250 Hz ), the reduction in speed became more pronounced; at 80 Hz the rate in the creatine kinase-deficient muscles was only 55.2 +/- 3.9% (mean +/- SD: n = 5) of the wildtype muscles. No effects of the deficiency were found for the half relaxation times. The data suggest that an impaired creatine kinase s ystem leads to lower activation levers at submaximal stimulation frequencie s, possibly by a reduction in Ca2+-release during repetitive stimulation. S imilar effects may be expected in normal fatigued muscle when phosphocreati ne is depleted.