SUMMARY1. We observed in a previous study on the human foot dorsiflexor muscles that the fatigue-induced decline in motor output during sustained maximal voluntary contractions (MVCs) was temporarily counteracted during the initial phase of superimposed high-frequency (150 Hz) muscle vibration, whereas prolonged muscle vibration seemed to accentuate the fatigue-induced decline in gross EMG activity and motor unit firing rates. A more extensive investigation of this late effect of muscle vibration on MVCs was performed in the present study.2. Prolonged periods of superimposed muscle vibration caused a reduction of EMG activity, motor unit firing rates and contraction force in both intermittent and sustained MVCs. This vibration-induced effect had the following main characteristics: (i) it developed slowly during the course of about 1 min of sustained vibration and subsided within 10-20 s after the end of vibration; (ii) it was much more pronounced in some subjects than in others (not age-dependent) and it was accentuated by preceding muscle exercise; (iii) it affected primarily the subject's ability to generate and/or maintain high firing rates in high-threshold motor units.3. Since the effect developed while vibration at the same time exerted a tonic excitatory influence on the a-motoneurone pool (as evidenced by the presence of a tonic vibration reflex) it is argued that the vibration-induced suppression of motor output in MVCs probably does not depend on a-motoneurone inhibition, but on a reduced accessibility of these neurones to the voluntary commands. It is suggested that contributing mechanisms might be vibration-induced presynaptic inhibition and/or 'transmitter depletion' in the group I a excitatory pathways which constitute the afferent link of the y-loop.

Microelectrode recordings were made in peroneal muscle nerve fascicles in 9 patients with traumatic spinal cord lesions at the C5 to T8 level. In 4 patients the lesion was incomplete with some sensibility but no voluntary motor function below the level of the lesion. All patients had increased tendon jerks. EMG was recorded in 5 patients and showed signs of some peripheral denervation. Simultaneous recordings from nerves to skin and to muscle were made in 2 patients and control recordings were made in 19 normal subjects. In the patients, spontaneous neural activity was sparse but after a latency of 0.5-1.1 s strong mechanical and electrical stimuli applied to the skin below the level of the lesion, stimulation of the urinary bladder and deep breaths induced bursts of efferent impulses with a conduction velocity of 0.65 m X s-1. The discharges were often followed by cutaneous vasoconstriction and/or reduction of skin resistance. It is concluded that the neural bursts contained sympathetic impulses of spinal origin. The main differences between patients and normal subjects were spontaneous muscle sympathetic activity was much lower in the patients; no evidence of arterial baroreflex modulation of muscle sympathetic activity was obtained in the patients; and in the patients a given stimulus induced sympathetic reflex discharges which occurred synchronously in muscle and skin nerve branches. Increases of intravesical pressure induced only weak increases of muscle sympathetic activity in the patients but nevertheless marked hypertensive reactions occurred. It is suggested that the excitability of decentralized spinal sympathetic neurons to muscles is usually decreased and that mechanisms other than exaggerated sympathetic outflow must be important for evoking episodes of high blood pressure in patients with spinal cord injuries.

Microelectrode recordings were made in peroneal skin nerve fasicles in 8 patients with functionally complete spinal cord lesions mainly at cervical levels. Spontaneous neural activity was sparse but deep breaths, abdominal pressure over the bladder and mechanical and electrical skin stimuli applied caudal to the spinal transection induced bursts of neural impulses after a latency of 0.5 to 1 s. The efferent discharges were conducted with a velocity of 0.75 m/s and were followed by cutaneous vasoconstruction and/or reduction of skin resistance. It is concluded that the neural bursts contained sympathetic impulses of spinal origin. No systematic changes of nerve activity were induced by changes of ambient temperature, suggesting that sympathetic thermoregulatory reflexes do not occur at spinal level in man. The vasoconstriction following a single sympathetic burst had a longer duration in the spinal patients than in normal subjects. The low level of spontaneous activity does not suggest permanent spinal sympathetic hyperactivity, but the prolonged episodes of vasoconstriction may contribute to attacks of high blood pressure in patients with spinal cord lesions.

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