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To explain disparate decay rates of cytosolic Ca2+ and structural changes in the thin filaments during a twitch, we model the time course of Ca2+ bound troponin (Tn) resulting from the free Ca2+ transient of fast skeletal muscle. In fibers stretched beyond overlap, the decay of Ca2+ as measured by a change in fluo 3 fluorescence is significantly slower than the intensity decay of the meridional 1/38.5 nm-1 reflection of Tn; this is not simply explained by considering only the Ca2+ binding properties of Tn alone (Matsuo, T., Iwamoto, H., and Yagi, N. (2010). Biophys. J. 99, 193-200). We apply a comprehensive model that includes the known Ca2+ binding properties of Tn in the context of the thin filament with and without cycling crossbridges. Calculations based on the model predict that the transient of Ca2+ bound Tn correlates with either the fluo 3 time course in muscle with overlapping thin and thick filaments or the intensity of the meridional 1/38.5 nm-1 reflection in overstretched muscle. Hence, cycling crossbridges delay the dissociation of Ca2+ from Tn. Correlation with the fluo 3 fluorescence change is not causal given that the transient of Ca2+ bound Tn depends on sarcomere length, whereas the fluo-3 fluorescence change does not. Transient positions of tropomyosin calculated from the time course of Ca2+ bound Tn are in reasonable agreement with the transient of measured perturbations of the Tn repeat in overlap and non-overlap muscle preparations.

The aim of this article is to review current literature on the response of soluble interleukin-6 receptor to exercise and identify a potential role for sIL-6R in skeletal muscle function. We also provide novel data on the impact of eccentric exercise on circulating levels. The aim of the research study was to investigate changes in plasma concentration of soluble interleukin-6 receptor (sIL-6R) and soluble glycoprotein 130 (sgp130) during recovery from exercise-induced muscle damage (EIMD) up to 72 h and their relationship with delayed onset muscle soreness (DOMS) and muscle function. 18 participants attended the laboratory on 4 consecutive days. On the first day, participants completed 6 sets of 10 repetitions of unilateral eccentric-concentric knee flexions at a test speed of 1.05 rad.s(-1) using a Cybex Isokentic dynamometer to induce muscle damage of the hamstrings. Prior to the eccentric exercise bout and each subsequent morning, following an overnight fast, participants had a venous blood sample taken which was centrifuged immediately and plasma frozen at -80 degrees C until later analysis. Plasma IL-6 and sgp130 were unchanged at any time point during recovery but sIL-6R was significantly reduced at 48 h and 72 h post-exercise (pless than0.05). Plasma sIL-6R was correlated with DOMS at 48 h post EIMD (r = 0.45, pless than0.05) and peak muscle torque at 24 h and 48 h following EIMD (r = -.42; pless than0.05; r = -.57; pless than0.01 respectively). Our novel finding that sIL-6R concentrations are decreased 2-3 days following a single bout of EIMD may reflect a regulatory mechanism controlling the influx of different leukocyte subpopulations into damaged tissue, although this needs to be confirmed by future studies. Our data suggests an association between sIL-6R, perception of pain and reduced peak muscle performance post-EIMD but further investigation is warranted to explore this relationship and implications for exercise performance.