Understanding neuromuscular disorders in chronic fatigue syndrome [version 1; peer review: 2 approved] - Jammes, Ritornaz Nov 2019

https://f1000research.com/articles/8-2020

 

I'm underwhelmed by the review. It seems Jammes et al. have little new insight beyond their previous studies (which were good!).

In particular, a lack of discussion of the work of Light and colleagues on the role of sensory chemoreceptors on sensation of fatigue associated pain, nor discussion of why the power at the gas exchange threshold (VT1) on the 2nd CPET is lower than the first day.

This research group has previously shown particular interest in trying to understand the relationship between EMG signals, fatigue, sensory pathways and this ventilatory threshold. See: https://www.ncbi.nlm.nih.gov/pubmed/12914560 (though I don't agree with this conclusion.

I've just found another paper by this group which I had not read before "EMG Changes in Thigh and Calf Muscles in Fin Swimming Exercise": https://www.thieme-connect.com/products/ejournals/pdf/10.1055/s-0030-1251993.pdf]
Notably:

(I wouldn't have suggested this hypothesis at all...)

The fundamental difference between a ramped power CPET and the fin swimming test is that the power output during the ramped CPET is increased in a mostly linear manner, and since motor recruitment is mainly dependent on the force output required, this means that the neural drive must increase to match. (it is also noteworthy that perception of effort is based on the signal generated by the brain and is not altered by peripheral afferents)
Whereas during fin swimming, which doesn't have a feedback mechanism requiring constantly increasing power, a more adaptive motor response is possible namely the increase in frequency doesn't lead to a linear increase in power, if there is a reduction in force. It is notable that the VO2Peak during Fin swimming is achieved at a fairly low heart rate (145 BPM, yet the oxygen consumption at this heart rate is much higher than the equivalent during cycling), and the lack of evidence of significant anaerobic metabolism suggests the output is not limited by peripheral ox. phos. capacity, nor cardiopulmonary limits, instead the number of motor units recruited are far below maximum (reflects lower neural drive in comparison to cycling), presumably due to mechanical limitations of the activity that limits the amount of force per stroke, even at high stroke frequency. It is hard to directly compare, but the ΔRMS (%) was substantially lower during fin swimming compared to cycling.

I would argue, on balance (and I am not the first to suggest this), that the metabolic balance is a simply result of the pattern of motor units that are recruited, their firing rates and their resulting metabolic balance (based on the structure, specifically the size of the motor units, the location of the muscle fibres, the firing rate and their adapted metabolic balance). So the ventilatory threshold is ultimately an artefact of significantly increasing the amount of motor units being recruited during a ramped power exercise test. A decline in mean frequency (the optimal frequency depends on the motor unit itself, and while fatigue can alter this frequency, it can be higher for some units and lower for others) when associated with lower force output, in itself does not lead to more motor units being driven - unless there is feedback requiring power to be maintained or increased, such as during a ramped CPET.

I would have liked to see discussion of the above in the aforementioned review, but alas...

 

Me 2. Seems like a narrative review of some small and poorly replicated studies.

I hope that these French researchers are able to continue their research in ME/CFS and do some larger, more robust studies.