Key result
Creatine kinase-deficient muscle fibres displayed lower force, reduced myofibrillar Ca(2+) sensitivity, and slowed force relaxation compared to wild-type fibres.
Increased myoplasmic inorganic phosphate appears to be involved in both fatigue-induced changes of cross-bridge function and SR Ca2+ handling in the early phase of skeletal muscle fatigue.
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Implicates elevated inorganic phosphate in early fatigue mechanisms; animal data leave open translation to human muscle disorders.
Dahlstedt et al. (2001) studied Skeletal muscle fatigue. Creatine kinase deficiency (CK(-/-)) vs. Wild-type fibres was evaluated on Tetanic force, force relaxation, and myoplasmic [Ca(2+)] during tetanic contractions. Creatine kinase-deficient muscle fibres displayed lower force, reduced myofibrillar Ca(2+) sensitivity, and slowed force relaxation compared to wild-type fibres.
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