Effects of ischaemia upon reflex electromyographic responses evoked by stretch and vibration in human wrist flexor muscles.

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1. The reflex electromyographic responses evoked in a wrist flexor muscle, flexor carpi radialis (f.c.r.), by forcible extension of the wrist ('stretch') and by vibration of the flexor tendon have been studied in normal subjects. Reflexes were elicited during the maintenance of a low level of voluntary flexor contraction (5% maximum). Stretch regularly produced a relatively prolonged (ca. 100 ms duration) increase in e.m.g. activity which was usually divisible into short-latency (ca. 25 ms, M1) and long-latency (ca. 50 ms, M2) peaks. Vibration produced a single, phasic peak, at short latency, with no sign of an accompanying long-latency wave comparable to the M2 stretch response. 2. Ischaemia was induced by inflation of a blood-pressure cuff around the upper arm and its effects upon the reflex patterns were studied. During ischaemia M1 stretch responses showed a more rapid and pronounced decline than did M2 responses and were abolished before voluntary power was appreciably affected. Vibration-evoked short-latency peaks changed in an essentially parallel manner to M1 stretch reflexes. During recovery from ischaemia M2 reflexes were restored before short-latency responses. 3. The patterns of reflex reductions in e.m.g. upon withdrawal of stimulation were also studied. Such troughs in activity, under non-ischaemic conditions, regularly commenced at short latency and were of relatively small amplitude. The records of several of the subjects, and particularly ones obtained during ischaemia, suggested that release of stretch (with concomitant stretch of antagonists) could elicit an additive, long-latency decline in e.m.g. The existence of any such separate, delayed component was never observed upon termination of vibration. 4. Measurements of changes in the latencies and durations of reflex components, accompanying the progression of ischaemia, indicated that depression of early reflex activity resulted in part from increases in the latencies of these initial peaks but predominantly reflected simultaneous and separate reductions in their amplitudes. 5. The generation of short-latency reflexes by stretch and vibration, both of which stimuli powerfully excite muscle spindle primary endings, and the marked susceptibility of these responses to ischaemia supports their being mediated by group Ia afferents. The contrasting behaviour of M2 stretch responses, both regarding their absence with vibration and their resistance to ischaemia, suggests that they depend crucially upon a separate group of reflex afferents.(ABSTRACT TRUNCATED AT 400 WORDS)

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