If you don't mind me asking, how are you sure you only have 'A' fibres? Is it purely by conduction velocity? I have never directly attempted this measurement, but it is my understanding that the axons from Ia afferents, Ib afferents, and alpha-motor neurons are all large diameter, myelinated, and have overlapping conduction velocity ranges. Some of the classic studies that looked at only Ia spindle afferents undertook a very tedious and thorough validation process including a series of multiple passive and active movements. These movements helped distinguish motor from sensory, and spindle outflow from golgi tendon organ outflow (Ib).

Motor conduction velocity to the thenar muscles, sensory A beta conduction velocity to the middle finger and mixed nerve conduction velocity of the forearm can be measured separately. The mixed nerve conduction velocity is about 3 m/s faster than the A beta conduction velocity and about 7 m/s faster than the motor conduction velocity. Thus I suppose that the mixed conduction velocity (the fastest part of the response) represents the A alpha conduction velocity (but the Ib conduction velocity may also be a part of the response). Ref: Metso AJ, Palmu K, Partanen JV. Compound nerve conduction velocity – A reflection of proprioceptive afferents? Clin Neurophys 2008;119:29-32.

Good article, thanks. In regards to your paper, are you familiar with the work by Macefield, Gandevia, and Burke? I believe they also looked at median nerve conduction velocities as well, so it may be interesting to compare your values with their findings (I only bring it up because I didn't see their work cited in yours).

Anyways, back to the original question. Is there a way for you to systematically manipulate the afferent feedback to see how it affects the compound nerve CV? Various interventions, such as prolonged stretching, prolonged vibration, or local anaesthetic influence afferent feedback. For example, prolonged stretching has been shown to greatly desensitize muscle spindles (e.g. Avela, 1999). Another possibility would be to use a local anaesthetic to the tendonious regions, which could dull the Ib afferent response.

However, both of these ideas affect the receptors themselves, not the axons directly. So they probably wouldn't have an effect on your stimulation of the axons. I wonder if there are interventions to systematically control which axons respond to the stimulation. My guess would be there isn't, but I'm no expert. I am much more of an EMG guy and have never done ENMG.

---Citations---

Macefield G., Gandevia S.C., and Burke D., Conduction velocities of muscle and cutaneous afferents in the upper and lower limbs of human subjects. Brain, 1989. 112(6): p. 1519-1532.

Avela J., Kyröläinen H., and Komi P.V., Altered reflex sensitivity after repeated and prolonged passive muscle stretching. J Appl Physiol, 1999. 86(4): p. 1283.

Thanks for the References. I do not believe that manipulation of the receptors affect the given conduction velocities. But I suppose that with needle EMG You can observe reflex effects of the Ia and II-afferents of the muscle spindle, possibly also III- and IV-afferents of muscle. This is not according to the prevailing hypotheses, but if You are interested, try to record the effect of passive stretching of a relaxed muscle to the activity of end plate spikes in needle EMG. Of course there should be an active spot (with MEPPs and EPSs) of the muscle at the focus of the recording.

Ref: Partanen J: End plate spikes in the human electromyogram. Revision of the fusimotor theory. J Physiol (Paris) 93: 155-166, 1999.

My doubt is if excentric exercise could produce any effect on muscle spindles. And I am sure it does as by example a trial of few excentric slow exercises *slow stretching during 10 sec 6 time per minute of about 5 minutes* would produce more loss of control over muscle voluntary activation or motor precision task than if we do a concentric one. Also it is known that is more energy consuming.

Now the question: Is this due to peripheral involvement (muscle spindles afferents) or central loss (of motor outflow from the cortex.. calling it central fatigue even if we do not like). Cutaneous silent period refflects A delta (pain) by text books and literature aas onset latency and motor voluntary the endset, cortical silent period shows cortical GABA involvement and what about Miexed Nerve silent period. Do you believe it may contain the brake after CMAP due to afferents from muscle spindles as onset latency...

In Metso et al 2008, you suggest that the difference between mixed nerve CV and sensory CV is represented by muscle afferent fibre participation? or that the muscle afferent conduction velocity is equal to the mixed nerve velocity?

Thank you

As far as I know A alpha fibres represent only Ia afferents of the muscle spindle.