Mechanism of the Electrical Silence in Shoulder Muscles during Voluntary Horizontal Adduction

Abstract

Electrical silence in the shoulder adductor muscles observed before ball impact in the tennis ground stroke was investigated in terms of the neurophysiolosical and dynamical features. Subjects employed in the experiments were 10 healthy adults including skilled tennis players of top level. Electrom yograms were recorded from the pectralis major, clavicular [Pc] and sternal [Ps] portions, and the deltoid, anterior [Da] and posterior [Dp] portions utilizing an electromagnetic oscillograph and datarecorder with surface electrodes. An electrogoniogram of the shoulder angle between the upper arm and the frontal plane, utilizing a specially constracted electrogoniometer, was simultaneously recorded with the EMGs.
The discharges of Pc, Ps and Da ceased before the ball impact in the forehand ground stroke. It did not make any significant difference whether the subjects had their eyes open or closed, and with or without ball. Horizontal adduction of the upper arm produced electrical silence in the adductors only when the swing speed exceeded a certain value (about 200 degree/s) and the shoulder position was firmly fixed.
No d istinguishable discharge in the Dp suggesting the existence of antagonistic inhibition was observed while the spike cessations occurred in the adductor muscles. During the horizontal arm swing on the fixed shoulder side, the passive backward movement at the contralateral shoulder produced clearer and faster spike cessations in the adductors-the Da, Pc and Ps- than in the control situation. On the contrary, the passive forward movement induced the partial spike inhibitions in the adductors, particularly in the Ps, and small spikes continued through the swing motion.
Backward or forward push at the contralateral shoulder during the arm swing at the fixed shoulder side produced passive lengthening or shortening of the adductors, respectively. In the case of the shortened muscular length, the latency of 34.3 ms (mean) suggested that it was caused by a spindle silence. The shortened muscular length might also release a I-B inhibition.
Therefore, in this case, the small remaining spike may be the command impulses in the central nervous system. On the contrary, it can be argued that the muscular elongation cause facilitation on spindle and I-B afferents. The clearer and faster spike cessations than in the control situation might be caused by predominantly facilitated I-B inhibitory activity which swept away all electrical activities. In the nomal tenn is ground stroke, the increased muscular activity inducing a fast swing might raise the level of the I-B inhibition enough to cancel out all electorical activities.