The Journal of Neurophysiology Vol. 84 No. 1 July 2000, pp. 184-188
Copyright ©2000 by the American Physiological Society

Long-Latency Component of the Stretch Reflex in Human Muscle Is Not Mediated by Intramuscular Stretch Receptors

School of Biological Sciences, Royal Holloway, London University, London TW20 0EX, United Kingdom

Corden, D. M., O.C.J. Lippold, Katie Buchanan, and Caryll Norrington. Long-Latency Component of the Stretch Reflex in Human Muscle Is Not Mediated by Intramuscular Stretch Receptors. J. Neurophysiol. 84: 184-188, 2000. Reflex responses to mechanical stimulation of muscle (brief imposed movement) were investigated. Reflexes were elicited in the forefinger, recording from the first dorsal interosseous (FDI), and in the foot, recording from soleus. These responses typically consisted of a short-latency component (M1) and a long-latency component (M2) at 33 ms and 53 ms, respectively, after the stimulus in the case of FDI, and 37 ms and 68 ms, respectively, in soleus upon stimulation of the sole of the foot. Normally, when a muscle is stretched by a mechanical stimulus (either naturally or by an experimentally imposed movement), both skin receptors and muscle stretch receptors are activated. It is possible, however, to devise stimulation parameters where this is not the case. Fixating the finger with plasticine enables the effects of skin stimulation to be studied without stretching the FDI muscle. On the other hand, tapping a long tendon allows muscle stretch receptors to be activated without involving skin or subcutaneous structures. Component M1 was always abolished by finger fixation in 40 trials on 10 subjects, with M2 being essentially unchanged in latency, duration, or amplitude. Reflex responses were obtained in soleus muscle in nine experiments by prodding the sole of the foot (thereby stimulating both skin and muscle stretch receptors). Alternatively, the tendo achilles was prodded (which solely activates stretch receptors in the muscle). In the former, M1 and M2 were generated. In the latter, only M1 was produced. It is concluded that the long-latency component of the stretch reflex, M2, originates in skin and/or subcutaneous nerve terminals and that no part of M2 originates in muscle stretch receptors.