Skeletal muscle function with acute creatine kinase inhibition

Creatine kinase (CK) plays an important phosphoryl transfer role in skeletal muscle. Effects of acute CK inhibition on contractile function were investigated. Isolated canine gastrocnemius muscle in situ (n = 5; wet mass = 73.2 ± 11.6 g) was electrically stimulated to elicit four maximal tetanic isometric contractions at 1 Hz following 10 min arterial infusion of saline control (C) and 5 mM iodoacetamide (IA) to inhibit CK. Contractile characteristics between C and IA were compared by repeated measures ANOVA (α = 0.05). Peak force across all contractions was significantly greater during C (350 ± 76 N) than IA (249 ± 55 N). Peak force was significantly greater for contractions 2–4 (#2 = 352 ± 84 N; #3 = 354 ± 84 N; #4 = 354 ± 84 N) than contraction 1 (339 ± 81 N) during C, indicating a brief positive staircase effect. During IA, peak force was significantly greater for contraction 1 (286 ± 61 N) than all subsequent contractions (#2 = 247 ± 55 N; #3 = 236 ± 51 N; #4 = 231 ± 49 N) indicating an inhibitory effect. Relaxation half‐time (C = 80 ± 10 ms; IA = 130 ± 20 ms) and peak rate of force development (C = 2.5 ± 0.5 N·ms −1 ; IA = 1.6 ± 0.4 N·ms −1 ) were significantly slower during IA than C. Skeletal muscle force production and relaxation were attenuated and retarded during CK inhibition, effects that progressed with subsequent contractions. These effects were likely due to insufficient ATP buffering and/or ADP and P i accumulation during CK inhibition. Supported by: NATO LST.CLG 979220