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Differential modulation of spinal and corticospinal excitability during drop jumps


Taube, W; Leukel, C; Schubert, M; Gruber, M; Rantalainen, T; Gollhofer, A (2008). Differential modulation of spinal and corticospinal excitability during drop jumps. Journal of Neurophysiology, 99(3):1243-1252.

Abstract

Previously it was shown that spinal excitability during hopping and drop jumping is high in the initial phase of ground contact when the muscle is stretched but decreases toward takeoff. To further understand motor control of stretch-shortening cycle, this study aimed to compare modulation of spinal and corticospinal excitability at distinct phases following ground contact in drop jump. Motor-evoked potentials (MEPs) induced by transcranial magnetic stimulation (TMS) and H-reflexes were elicited at the time of the short (SLR)-, medium (MLR)-, and long (LLR, LLR(2))-latency responses of the soleus muscle (SOL) after jumps from 31 cm height. MEPs and H-reflexes were expressed relative to the background electromyographic (EMG) activity. H-reflexes were highly facilitated at SLR (172%) and then progressively decreased (MLR = 133%; LLR = 123%; LLR(2) = 110%). TMS showed no effect at SLR, MLR, and LLR, whereas MEPs were significantly facilitated at the LLR(2) (122%; P = 0.003). Background EMG was highest at LLR and lowest at LLR(2). Strong H-reflex facilitation at the beginning of the stance phase indicated significant contribution of Iotaa-afferent input to the alpha-motoneurons during this phase that then progressively declined toward takeoff. Conversely, corticospinal excitability was exclusively increased at the phase of push off (LLR(2), approximately 120 ms). It is argued that corticomotoneurons increased their excitability at LLR(2). At LLR ( approximately 90 ms), Iotaa-afferent transmission as well as corticospinal excitability was low, whereas background EMG was high. Therefore it is speculated that other sources, presumably subcortical in origin, contributed to the EMG activity at LLR in drop jumps.

Previously it was shown that spinal excitability during hopping and drop jumping is high in the initial phase of ground contact when the muscle is stretched but decreases toward takeoff. To further understand motor control of stretch-shortening cycle, this study aimed to compare modulation of spinal and corticospinal excitability at distinct phases following ground contact in drop jump. Motor-evoked potentials (MEPs) induced by transcranial magnetic stimulation (TMS) and H-reflexes were elicited at the time of the short (SLR)-, medium (MLR)-, and long (LLR, LLR(2))-latency responses of the soleus muscle (SOL) after jumps from 31 cm height. MEPs and H-reflexes were expressed relative to the background electromyographic (EMG) activity. H-reflexes were highly facilitated at SLR (172%) and then progressively decreased (MLR = 133%; LLR = 123%; LLR(2) = 110%). TMS showed no effect at SLR, MLR, and LLR, whereas MEPs were significantly facilitated at the LLR(2) (122%; P = 0.003). Background EMG was highest at LLR and lowest at LLR(2). Strong H-reflex facilitation at the beginning of the stance phase indicated significant contribution of Iotaa-afferent input to the alpha-motoneurons during this phase that then progressively declined toward takeoff. Conversely, corticospinal excitability was exclusively increased at the phase of push off (LLR(2), approximately 120 ms). It is argued that corticomotoneurons increased their excitability at LLR(2). At LLR ( approximately 90 ms), Iotaa-afferent transmission as well as corticospinal excitability was low, whereas background EMG was high. Therefore it is speculated that other sources, presumably subcortical in origin, contributed to the EMG activity at LLR in drop jumps.

Citations

24 citations in Web of Science®
27 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Balgrist University Hospital, Swiss Spinal Cord Injury Center
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:16 January 2008
Deposited On:13 Nov 2008 07:56
Last Modified:05 Apr 2016 12:30
Publisher:American Physiological Society
ISSN:0022-3077
Publisher DOI:10.1152/jn.01118.2007
PubMed ID:18199811

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