Snow Leopard
Senior Member (Voting Rights)
When the system is working normally, it leads to more oxygen available by the cardiopulmonary system for a given level of motor drive as I stated in my previous post.
Perhaps I wasn't clear, there are many potential primary causes (some of which I mentioned), but there is some overlap in the end result (central fatigue). In the case of muscular dystrophies, the less effected motor units are driven harder, leading to increased metabolites that stimulate certain type III/IV muscle afferents. Something similar happens in the case of peripheral neuropathies since some motor units are more impaired than others.
The study I cited was to provide an example of the effect I was describing for the case of muscular dystrophies in case there was any doubt! I wasn't necessarily implying any similarity between fibromyalgia and ME/CFS.
The 2-day CPET study results (reduction of workrate at the ventilatory threshold) also likely occurs due to stimulation of those afferents, though the underlying causes can be different - hypothetically: from unusual sensitisation of those nerves, to feedback loops leading to an excess of certain metabolites, to an excess of metabolites building up due to poor oxygen uptake by some muscle fibres (as hypothesised by Systrom for example). While there are lots of hypothetical possibilities, it provides a place to start looking - and it provides a range of objective thresholds (not just the VT1, but EMG fatigue thresholds) for experimental manipulation or comparison.
