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1 nd repetitive co-contractions 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 with feedback delay and tonically controlled antagonist muscles.
9 e spinal neurons mediating co-contraction of antagonist muscles.
10 nus and striking coactivation of agonist and antagonist muscles.
11 red activation of the agonist, synergist and antagonist muscles.
12 he phase difference between neural drives to antagonist muscles, a long-standing observation yet unex
13 es complement the balance of strength of the antagonist muscles acting on the joint.
14 ociated with large 5-15 Hz coherence between antagonist muscle activities.
15 ctromyography from task-relevant agonist and antagonist muscles, alongside transcranial magnetic stim
16 imb swing velocity.(6) In stance, minimizing antagonist muscle and joint passive forces could save en
17 ved botulinum type A toxin injections in the antagonist muscle at the same treatment session.
18        Continuous contraction of agonist and antagonist muscles caused by involuntary motor-unit firi
19 t at age 10-12 years there is little agonist-antagonist muscle co-contraction around the time of foot
20 s resulting from coactivation of agonist and antagonist muscles driving the joints toward equilibrium
21 y there was less coactivation of agonist and antagonist muscles during the AAN paradigm.
22 in the predominant co-contraction of agonist/antagonist muscles during voluntary movement observed in
23                        By preserving agonist-antagonist muscle dynamics, the AMI allows proprioceptiv
24 EMG with no significant coupling between the antagonist muscle EMGs.
25 is stimulated by an agonist neuron, while an antagonist muscle fiber is unstimulated by a pause and s
26 ts of applying vibration to the tendon of an antagonist muscle (flexor carpi radialis) during the cou
27 les until an equilibrium between agonist and antagonist muscle force is achieved.
28 wing that, at the rest postures, agonist and antagonist muscles generated equal forces indicated that
29                      Coactivation of agonist-antagonist muscle groups was observed both at rest and d
30 ed contractions, including cocontractions of antagonist muscle groups, during voluntary movements.
31 ity so that reciprocally acting, agonist and antagonist muscles have a stable platform from which to
32 tive finger movements, stretch of the loaded antagonist muscle (i.e., extensor) was accompanied by in
33 gether with botulinum toxin injection in the antagonist muscle improves eye alignment in comitant hor
34  consisting of surgically connected, agonist-antagonist muscles including muscle-sensing electrodes.
35                            Co-contraction of antagonist muscles is characteristic of spasticity arisi
36 he phase difference between neural drives to antagonist muscles is determined by the relative strengt
37 o, CA) suggested that changes in agonist and antagonist muscle lengths were responsible for the endur
38 burst was not preceded by an increase in the antagonist muscle MEP:IEMG ratio.
39 o-contraction, the inhibitory input from the antagonist muscle overcomes the additional excitatory an
40 ndex related to the co-activation of agonist-antagonist muscle pairs (C-index) was modulated with tou
41 inhibitory Group Ia reflexes linking agonist/antagonist muscle pairs acting at the shoulder and elbow
42 mplified hexapedal leg geometry with agonist-antagonist muscle pairs actuating each leg joint.
43 which surgically preserve and couple agonist-antagonist muscle pairs for the subtalar and ankle joint
44 cy inhibition and excitation between agonist/antagonist muscle pairs; inhibition was significantly mo
45                                              Antagonist muscle passive torques alone can thus control
46 ase in corticospinal excitability related to antagonist muscle recruitment could compensate for a pot
47                           The timing of such antagonist muscle recruitment relative to the stop signa
48                During locomotion, functional antagonist muscles, TA and Sol, were coactivated both in
49 sected muscle and in the passively stretched antagonist muscle, there was a dramatic increase in the
50  Subjects (n = 20) predictively co-activated antagonist muscles to adjust one component of the impeda
51 on alters the control signals to agonist and antagonist muscles to change movement speed.
52 t may occur due to the co-contraction of the antagonist muscle, which constrains PIC behaviour.