ライフサイエンスコーパス: antagonist muscle

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1 nus and striking coactivation of agonist and antagonist muscles.

2 n insect legs with different arrangements of antagonist muscles.

3 stronger where they assist the weaker of two antagonist muscles.

4 ibraries from sensory neurons that innervate antagonist muscles.

5 p Ia excitatory reflexes between agonist and antagonist muscles.

6 ons to occur without increased resistance to antagonist muscles.

7 nchronous or asynchronous neuronal firing in antagonist muscles.

8 red activation of the agonist, synergist and antagonist muscles.

9 he phase difference between neural drives to antagonist muscles, a long-standing observation yet unex

10 es complement the balance of strength of the antagonist muscles acting on the joint.

11 ved botulinum type A toxin injections in the antagonist muscle at the same treatment session.

12 Continuous contraction of agonist and antagonist muscles caused by involuntary motor-unit firi

13 s resulting from coactivation of agonist and antagonist muscles driving the joints toward equilibrium

14 y there was less coactivation of agonist and antagonist muscles during the AAN paradigm.

15 in the predominant co-contraction of agonist/antagonist muscles during voluntary movement observed in

16 is stimulated by an agonist neuron, while an antagonist muscle fiber is unstimulated by a pause and s

17 ts of applying vibration to the tendon of an antagonist muscle (flexor carpi radialis) during the cou

18 les until an equilibrium between agonist and antagonist muscle force is achieved.

19 wing that, at the rest postures, agonist and antagonist muscles generated equal forces indicated that

20 Coactivation of agonist-antagonist muscle groups was observed both at rest and d

21 ity so that reciprocally acting, agonist and antagonist muscles have a stable platform from which to

22 tive finger movements, stretch of the loaded antagonist muscle (i.e., extensor) was accompanied by in

23 gether with botulinum toxin injection in the antagonist muscle improves eye alignment in comitant hor

24 Co-contraction of antagonist muscles is characteristic of spasticity arisi

25 he phase difference between neural drives to antagonist muscles is determined by the relative strengt

26 o, CA) suggested that changes in agonist and antagonist muscle lengths were responsible for the endur

27 burst was not preceded by an increase in the antagonist muscle MEP:IEMG ratio.

28 ndex related to the co-activation of agonist-antagonist muscle pairs (C-index) was modulated with tou

29 inhibitory Group Ia reflexes linking agonist/antagonist muscle pairs acting at the shoulder and elbow

30 mplified hexapedal leg geometry with agonist-antagonist muscle pairs actuating each leg joint.

31 cy inhibition and excitation between agonist/antagonist muscle pairs; inhibition was significantly mo

32 The timing of such antagonist muscle recruitment relative to the stop signa

33 During locomotion, functional antagonist muscles, TA and Sol, were coactivated both in

34 sected muscle and in the passively stretched antagonist muscle, there was a dramatic increase in the

35 on alters the control signals to agonist and antagonist muscles to change movement speed.

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