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Objective : To analyse the conditioning effects of localised acute muscle pain on power output during ipsi- and contra-lateral ballistic arm extensions. Methods : Eight male subjects performed right arm (ipsilateral) and left arm (contra-lateral) bench press movements. The power output (and force and velocity) of the concentric phase of movement was measured before and during muscle pain induced by a standardised intramuscular injection of levo-ascorbic acid in the right pectoralis major muscle (prime mover muscle) and in the lateral head of the right triceps brachii muscle (synergist). Results : The power output of ipsi- and contra-lateral arm bench press movements was significantly decreased during pain of the right pectoralis major muscle, but not during pain of the right lateral triceps muscle. The velocity and force were both affected and contributed to the decrease in power output. Conclusions : Acute muscle pain of a prime mover muscle reduces ipsi- and contra-lateral motor performance of ballistic upper limb extension. This is not a generalised or non-specific inhibitory effect on the motor system, since pain failed to modify motor performance when applied to a synergist, non-prime mover, muscle. A basically bilateral executive cortical plan for ballistic upper limb extension could explain the conditioning effect of muscle pain on both ipsi- and contra-lateral arm. Significance : The results presented here contributes to the understanding of the conditioning effects of muscle pain on movement performance.

Objective: It is known that tonic muscle pain induced by a Levo-Ascorbic (L-AS) solution injected in a foot muscle can transiently modify both regional proprioception and stimulus perception. These findings are paralleled by changes of middle-latency lower-limb somatosensory evoked potentials (SEPs). However, little is known on the behaviourally relevant aspect whether eventual SEP pain-induced changes could be partly due to a sort of ‘motor strategy’ of subjects in the frame of a self-protective reaction towards the noxious stimulus. Movement and imagery of movements are in fact known to reduce mainly pre-central SEP amplitude (i.e. gating effect). Methods: Low-threshold afferents ulnar SEPs, psychophysical pain ratings and fingers’ position sense were monitored in the time-course during L-AS injection in the right first dorsal interosseous muscle. Control experiments included SEPs (either following prevalent ulnar nerve low-threshold afferent stimulation or more conventional mixed nerve stimulation) during actual movements execution and imagery of movements of the right hand. Results: Tonic pain induced a significant reduction of the post-central N20-P25-N33 complex and a significant increase of the N18 wave. These changes, that were paralleled by distortion of the finger position sense, were delayed 2–5 min with respect to the maximal subjective pain sensation. Conversely, movement imagery tasks lead to a significant, selective, reduction of the pre-central N30 complex. This wave was even more reduced during actual movements, in combination with a reduction of those post-central components peaking after the first activation of the primary sensory cortex. Conclusions: Early sensory processing at cortical level is changed during tonic muscle pain, mainly for those components which may be theoretically involved in proprioceptive afferent elaboration. These changes are likely not due to subconscious or voluntary motor strategies of the subjects in the frame of a self-protective aversive reaction towards the noxious stimulus.

Ipsi- and contralateral patterns of lower limb nociceptive reflex responses were studied in 6 normal subjects in free standing position. Once the position was stabilized, only ankle extensor muscles showed consistent tonic activity while ankle flexors and knee extensors and flexors were virtually silent. Reflex responses, elicited by painful electrical stimuli to the skin of the plantar and dorsal aspect of the foot, were recorded from ipsi- and contralateral quadriceps (Q), biceps femoris (Bic), tibialis anterior (TA) and soleus (Sol) muscles. Plantar foot stimulation evoked a large excitatory response in the ipsilateral TA at about 80 ms and a smaller responses in Bic and Q at 70 ms and 110 ms, respectively. Ipsilateral excitatory effects after dorsal foot stimulation consisted of a Bic response at about 75 ms. In addition to excitatory effects, both plantar and dorsal foot stimulation evoked long-lasting suppression of ipsilateral Sol background activity starting at about 60 ms. Contralaterally, the only nociceptive effects after plantar or dorsal foot stimulation were a small excitatory response of Sol at about 85 ms. Evidence is provided that only excitatory responses were contingent upon nociceptive volley. The main mechanical effects seen after plantar stimulation were dorsiflexion of the foot without loss of heel contact with the floor; no withdrawal response of the foot followed nociceptive dorsal stimulation. Our main conclusion is that only reflex nociceptive responses serving to avoid the stimulus without conflicting with limb support function are expressed. The mechanisms reconciling nociceptive action and postural function of the lower limbs are discussed.