Calcium and the role of motoneuronal doublets in skeletal muscle control

Abstract

This work presents a novel structural model of skeletal muscle activation, providing a physiologically based account of frequency-dependent muscle responses like the catch-like effect. Numerous Ca2+ reservoirs within muscle fibers are considered, and a simplified analysis of the allocation of Ca2+ resources and the dynamics of calcium transport is proposed. The model correctly accounts for catch-like effects in slow and fast-twitch fibers during long-train stimulations and force-frequency relations in different muscle types. Results obtained from the model compare favorably to experiments showing that prolonged increases in force characteristic of the catch-like effect are not accompanied by sustained increases in free myoplasmic Ca2+. Also, in agreement with early experiments, the interspike interval in catch-inducing doublets is seen to be an important parameter for regulating the precise onset amplitude of the catch-like effect. This suggests that a plausible physiological function for the inclusion of doublets or the exclusion of individual spikes within a regular motor-neuronal spike-train is to rapidly bring skeletal muscles to predefined target forces according to prespecified motor programs in the central nervous system. This is a potentially very useful property directly mediated by the catch-like process modeled here. One further prediction of the model is that the slope of the frequency-tension profile of a given muscle is highly sensitive to changes in the efficiency and temporal characteristics of the dihydropyridine-ryanodine receptor complex. Interestingly, this is consistent with findings made on cardiac muscles, and might incidentally explain some instances of cardiac failure.

Acute Dehydration Impairs Endurance Without Modulating Neuromuscular Function

“…Additionally, no differences in TNAα were observed at any timepoint indicating a lack of DHY-induced tissue damage. While DHY did not appear to influence E-C coupling processes, we did observe a non-significant moderate effect ( g = 0.643) in the 20:VFT 3 h after DHY but not following fatiguing exercise (Table 2 ), potentially indicating a decrease in calcium sensitivity 3 h after DHY ( Binder-Macleod and Kesar, 2005 ; Nielsen, 2009 ). It is important to consider that we did not measure all components of neuromuscular function [e.g., motoneuron facilitation ( Heckman et al, 2005 ; Heckman and Enoka, 2012 )] so it is possible that some changes exist that may partly explain the loss of function.…”

A passive increase in muscle temperature enhances rapid force production and neuromuscular function in healthy adults

“…Passive heating increases the myoplasmic Ca 2+ accumulation 4,27 when muscle cells are exposed to temperatures ranging from 37−42 • C, temperature-dependently, 28 which increase the myofibrillar Ca 2+ sensitivity and isometric muscle rate of force production. 29 The sarcoplasmic ryanodine receptors (RyR) (voltage sensitivity Ca 2+ release gate) regulates the slope of the force-frequency relation responses in the muscle. 29 However, although the present study showed increased RTD after hot-water immersion during the electrically-evoked doublets, no difference was observed in the force-frequency slope relation-ship between low-and high-frequencies activation as RTD 100Hz and RTD 20Hz demonstrated similar response after passive heating (Fig.…”

“…29 The sarcoplasmic ryanodine receptors (RyR) (voltage sensitivity Ca 2+ release gate) regulates the slope of the force-frequency relation responses in the muscle. 29 However, although the present study showed increased RTD after hot-water immersion during the electrically-evoked doublets, no difference was observed in the force-frequency slope relation-ship between low-and high-frequencies activation as RTD 100Hz and RTD 20Hz demonstrated similar response after passive heating (Fig. 2A,B).…”

Interaction of posttetanic potentiation and the catchlike property in mouse skeletal muscle

“…It is an inherent property of the skeletal muscle cell and not due to changes in motor neuron excitability or neuromuscular transmission . A proposed mechanism is that high force levels produced by the high‐frequency initial pulses at the onset of stimulation may rapidly stretch the series elastic component to increase muscle stiffness compared with constant frequency stimulation, a change that might increase the transmission of mechanical force along or between sarcomeres . An alternate hypothesis is that closely spaced pulses at the onset of stimulation augment intracellular Ca 2+ levels above that experienced during constant frequency stimulation, a change which would be expected to increase force by promoting thin filament activation and thus cross‐bridge recruitment .…”