Effects of lengthening contraction on calcium kinetics and skeletal muscle contractility in humans

Abstract

We have tested the hypothesis that the altered muscle contractility after lengthening contractions (LC) is caused by altered calcium (Ca2+) kinetics. Subjects (n = 8) performed 100 drop jumps and muscle contractility was measured pre- and post-exercise by maximal voluntary contraction (MVC) and transcutaneous electrical stimulation (1, 20 and 50 Hz). Muscle biopsies were analysed for muscle metabolites, rates of SR Ca(2+) uptake (CaU) and release (CaR) and myosin heavy chain (MHC) composition. The rates of torque relaxation and CaU were positively related to muscle fibre type composition (% MHC II). Muscle creatine (Cr) decreased and the ratio between phosphocreatine (PCr) and Cr increased 3 and 24 h post-exercise (P < 0.05 vs. pre-exercise). LC resulted in reduced MVC (-19%), twitch torque (-41%) and 20/50 Hz torque ratio (-30%) and a faster relaxation rate (P < 0.05). The contractile parameters recovered partially but remained altered 24 h post-exercise (P < 0.05). The average CaR was unchanged after LC (P > 0.05). However, the response varied between subjects and the relative post-exercise CaR was significantly related to the degree of LFF (post/pre 20/50 Hz force ratio) and to the decline in twitch force (post/pre twitch ratio). CaU was lower in seven of eight subjects after LC (P > 0.05). The decline in torque after LC could not be explained by metabolic factors since PCr/Cr ratio increased. The relation between CaR and fatigue suggests that the mechanism of fatigue in part may be attributed to intrinsic changes in the SR Ca2+ release channel. The faster torque relaxation after LC could not be explained by an increased rate of CaU.