The ‘late’ reflex responses to muscle stretch: the ‘resonance hypothesis’ versus the ‘long‐loop hypothesis’

Abstract

SUMMARY1. Experiments were performed to check the validity of previous claims concerning the 'long-loop' aetiology of 'late' reflex electromyogram (e.m.g.) responses to muscle stretch in man. The primary aim was to investigate whether observations previously presented in favour of the 'long-loop hypothesis' are explicable also in terms of the 'resonance hypothesis', according to which the 'late' reflex components represent spinal, short-latency responses to intramuscular oscillations initiated by the impact.2. The contracting wrist flexors of healthy subjects were exposed to trains of recurrent 25-50 Hz stretch stimuli (wrist torque pulses). Each of the initial two or three pulses in the train was followed by e.m.g. peaks with a latency of 20-25 msec. The e.m.g. peaks driven in this way had the following characteristics in common with the successive two or three e.m.g. peaks which were induced by single ramp stretches or tendon taps. (a) Changes in stimulus parameters which altered the strength of the initial e.m.g. peak often had an opposite effect on the strength of the succeeding peak(s). Muscle vibration which attenuated the initial peak often enchanted the succeeding one(s). (b) The initial e.m.g. peak was less affected than the succeeding peak(s) by the subjects' attempts to respond with rapid 'resist' or 'let go' reactions.3. Intramuscular oscillations (monitored by a needle accelerometer) and e.m.g. responses evoked by single ramp stretches and/or tendon taps were also studied in the long thumb flexor, the calf muscles and the masseter muscle. In the thumb flexor, the initial accelerometer deflexion was only rarely succeeded by a short latency e.m.g.peak, but the succeeding wave in the needle accelerogram was followed by such a peak, appearing about 40 msec after stimulus application. By contrast, the calf muscles and the jaw elevators exhibited a high amplitude, short-latency e.m.g. response to the first but only rarely to the second intramuscular oscillation wave.4. The interval between initial and second e.m.g. peaks following tendon taps was longer for calf muscles than for wrist flexors and longer for wrist flexors than for jaw elevators. Similar differences were observed with respect to the intervals between the damped intramuscular oscillations initiated by the impacts.5. Without denying the existence of 'long-loop reflexes' it is concluded that the characteristics of the 'late' reflex responses to muscle stretch in man are explicable also in terms of the 'resonance hypothesis'.

Effect of cutaneous nerve stimulation on voluntary and stretch reflex electromyographic activity in wrist flexors in humans.

“…activity was inhibited more during long latency (M2) reflex components than during Ml reflex components. If the M2 reflex component resulted from mechanisms essentially similar to those which generate M 1, as suggested by Eklund et al (1982) (Bawa & Tatton, 1979), later more detailed studies in man have shown that a given motor unit can contribute to either the M 1 response, the M 2 response, or both, depending upon the experimental conditions used (Calancie & Bawa, 1985). Nevertheless, under any given experimental condition, M2 does tend to result from activity in larger higher threshold motor units than M 1 (Calancie & Bawa, 1985).…”

“…The long latency component has attracted considerable attention in recent years and its origin is still a matter of controversy. Some investigators propose that it may be mediated entirely at the spinal level (Ghez & Shinoda, 1978; Tracey, Walmsley & Brinkman, 1980;Miller & Brooks, 1981;Eklund, Hagbarth, Haaglund & Wallin, 1982) while others have argued in favour of a 'long loop' transcortical W. J. BECKER AND OTHERS reflex (Marsden, Merton & Morton, 1972;Lee & Tatton, 1975). It is possible that both mechanisms may contribute (Lee, Murphy & Tatton, 1983).…”

Electromyographic reflexes evoked in human wrist flexors by tendon extension and by displacement of the wrist joint.

“…skin, joint) are likely to be simultaneously activated. Indeed, M2 responses, of different muscles, have been alternatively attributed to the reflex action of muscle spindle group I a (Phillips, 1969;Marsden, Merton & Morton, 1972;Eklund, Hagbarth, Hagglund & Wallin, 1982) or group II (Matthews, 1984) afferents, both muscular and nonmuscular (cutaneous and possibly joint) afferents (Marsden, Merton & Morton, 1985) and solely cutaneous afferents (Darton, Lippold, Shahani & Shahani, 1985). Furthermore, joint displacement usually causes combined extension of several synergistically operating muscles and reciprocal release of their antagonists.…”

Modelagem e simulação do sistema neuromuscular responsável pelo controle do torque gerado na articulação do tornozelo.

“…Uma possibilidade é que o MLR seja originado pela atividade sustentada das próprias aferentes Ia que causariam uma reativação dos MNs após uma primeira salva de disparos síncrona (Berardelli et al, 1982;Eklund et al, 1982;Meskers et al, 2010;Schuurmans et al, 2009 Estudos conduzidos em seres humanos durante a manutenção da postura ereta quieta sugerem que outra possibilidade para a gênese do MLR é a atividade das aferentes do tipo II dos fusos neuromusculares, pois estas fibras sensoriais possuem uma menor velocidade de condução axonal e percorrem uma alça de realimentação mais longa, o que aumenta o atraso para a excitação dos MNs (Bove et al, 2003;Nardone et al, 1990;Nardone;Schieppati, 1998; (Matthews, 1989;Shemmell et al, 2009;Shemmell et al, 2010). Porém, para músculos dos membros inferiores esta hipótese é menos plausível devido às estimativas de latências obtidas com as técnicas de estimulação magnética…”

“…O reflexo de estiramento do Tríceps Sural foi simulado pela variação em rampa de θ A , similar ao realizado em protocolos experimentais em seres humanos (Bove et al, 2003;Cronin et al, 2008;Kawashima et al, 2004;Nardone et al, 1990;Nardone;Schieppati, 1998;Nardone et al, 2000;Obata et al, 2010;Sinkjaer et al, 1999;Toft et al, 1991 (Lemon, 2008;Windhorst, 2007 (Berardelli et al, 1982;Eklund et al, 1982;Schuurmans et al, 2009). Neste caso, excluiu-se do modelo tanto as aferentes tipo II quanto os INs do grupo II.…”