I see where this is coming from, but don't forget it's free calcium released from within the muscle that is an intermediate part of the muscle contraction process anyway.
As I understand it, basically what happens from nerve signal to contraction is this - when you decide you are going to contract your muscle you first send a nerve signal to that muscle. When the neuron is fired it releases acetylcholine (a neurotransmitter) into the space between the neuron and the receptors along the length of the muscle. This signals sodium to be sucked into the cell membrane (where all the receptors are) and potassium to rush out.
When this happens the muscle automatically opens calcium channels (little spaces) to let out free calcium into the free spaces between the muscle cells. This free calcium then attaches to a special protein on one of the two kinds of muscle filaments you have (the two filaments are actin and myosin and the protein sits between the two attached to the actin filaments). This 'special' protein (called troponin) is what prevents your muscles from flopping around without a nerve signal - it's only when calcium becomes temporarily attached to it that it 'gets out of the way' and allows the two muscle filament types to at first attach together and then, with the use of ATP for energy, move past each other by pushing each other away again and making the muscle contract.
So I guess the original study on which the article is based, which sites people and mice either with damaged hearts or 'exhausted by exercise' as the source of this research claim, is only referring to free calcium as a limiting factor in extreme exercise exhaustion or when there is actual damage in the first place.


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