Inhibitory APAs observed in several upper limb muscles prior to index tapping are shaped by supraspinal inhibitory circuits

We previously observed that index tapping is anticipated by inhibitory postural adjustments (iAPA) in the ongoing EMG of several upper limb muscles, including Biceps Brachii (BB) and Superior Trapezius (ST). Aim of the present work is to investigate the spinal and supra-spinal contribution to this effect. This has been tested by probing changes in cortico-spinal excitability, by means of TMS motor evoked potential (MEP) and changes in spinal excitability, by means of T-reflex, during iAPA development. Index tapping was triggered by an acoustic signal, while EMG from the prime mover and from BB or ST was recorded by surface electrodes. MEP or T-reflexes elicited in the relaxed postural muscle (BB or ST), with latency ranging -2000 to +300ms from index flexion, were collected and their peak to peak amplitude measured. In the various subjects (9), with the hand prone and the postural muscle contracted, a clear inhibition of both BB and ST EMG started in average 50+/-23ms before the prime mover onset; in contrast, as expected, when postural muscles were relaxed no inhibitory effect was seen. However, all MEPs falling in the iAPA temporal window were reduced in amplitude, while T-reflexes were unaffected. In each subject, statistical analysis (t-test comparing MEP or T amplitude in the iAPA window versus the responses falling prior to the go-signal) gave significance to this effect (p<0.02). Moreover a high correlation (p<0.01) was found only between the ongoing EMG amplitude and the MEP amplitude in the relaxed muscle. Lastly, on average, MEP inhibition developed 98+/-33ms before the prime mover onset, i.e. about 50ms prior to the iAPA onset. These results show i) that when motoneurons are not firing, iAPAs are still associated to the motor command although under threshold, and ii) that during the iAPA spinal motoneurons are more likely disfacilitated than inhibited. Thus, iAPAs seem to be fully sustained by inhibitory circuits located in the supraspinal centres.