Effect of vibrating agonist or antagonist muscle of the reflex response to sinusoidal displacement of the human forearm.

1. The mechanical resistance of the human forearm to imposed sinusoidal movements has been determined. By means of a visual monitor, subjects maintained a steady force (typically 100 N) by flexing the elbow so as to pull with the wrist against an isometric force transducer. This was mounted upon a stretcher which displaced the forearm sinusoidally at frequencies of 7-11 Hz with a peak-to-peak amplitude of movement of about 1 mm. The average mechanical resistance over 10-40 sec of stretching was analysed into its vector components at the fundamental of the stretching frequency. Observations were made of both the normal resistance and that obtained while applying continuous vibration at 100 Hz to the tendon of either the biceps (agonist) or triceps (antagonist).2. In confirmation of Joyce, Rack & Ross (1974), at frequencies around 10 Hz the normal (unvibrated) response sometimes showed a component of ;negative viscosity' (force increasing during muscle shortening), rather than the simple ;positive viscosity' attributable to muscle visco-elasticity; this effect is attributable to the stretch reflex being appropriately delayed and of sufficient magnitude to over-ride the inherent properties of muscle. Vibration of either agonist or antagonist usually increased the extent of the ;negative viscosity' (negative quadrature component of force), as well as changing the ;elastic' stiffness of the arm (in-phase component of force).3. More commonly, the component of viscosity was initially positive. It was then normally reduced by vibration; that is, the vibration had (in formal terms) again added a component of negative viscosity.4. The vibration did not produce these effects by acting directly upon the contractile system of muscle to reduce its ;visco-elasticity'. On increasing the frequency of stretching the effect of vibration systematically shifted from being the addition of a negative viscosity, as above, to being the addition of a positive viscosity. These effects may all be attributed to an action of vibration on the stretch reflex, with the precise action of the reflex determined by the relation between the cycle time and the delays round the reflex pathway.5. In some experiments the activity of the flexor muscles was sampled by surface electromyograms from biceps and from brachioradialis; these were rectified, smoothed and averaged. For biceps, the absolute depth of e.m.g. modulation in relation to the cycle of stretching was sometimes, but not always, increased by vibration; but for brachioradialis the modulation was always reduced. Thus vibration cannot invariably produce its effects on the mechanical resistance of the arm by increasing the size (gain) of the stretch reflex. However, in all subjects the phase of the electromyographic modulation of both muscles was significantly delayed during vibration, whether of biceps or of triceps. In comparison with the normal, vibration introduced a phase lag on average of 18 degrees . In qualitative terms, this can be shown to explain the typical augmentation of ;negative viscosity'.6. The findings are discussed in relation to the genesis of tremor and to the reflex regulation of muscle contraction. They support the classical idea that afferent activity from the antagonist is as crucially implicated as that from the agonist.