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1 . d(-1)) after muscle-damaging exercise (300 eccentric contractions).
2 l of ERK1/2 phosphorylation before and after eccentric contraction.
3 otected muscle against force loss induced by eccentric contraction.
4  specific force generation and resistance to eccentric contractions.
5 eclines in in vitro EDL force after repeated eccentric contractions.
6 s are depolarized after an injurious bout of eccentric contractions.
7 on potential generation and conduction after eccentric contractions.
8 rmal pattern of ERK1/2 phosphorylation after eccentric contractions.
9 ferences were detected between isometric and eccentric contractions.
10 llowing an acute bout of maximally activated eccentric contractions.
11 tion-contraction coupling failure induced by eccentric contractions.
12  of two submaximal workloads that emphasized eccentric contractions.
13 o reverse the shift in optimum length due to eccentric contractions.
14 ic stiffness fell as a result of a series of eccentric contractions.
15 ology studies with twitch force, tetanic and eccentric contraction all being normal.
16 ntly attenuates force loss owing to damaging eccentric contractions and repetitive isometric contract
17                                         Both eccentric contractions and twitch potentiation reduced t
18 high susceptibility to injury with repeated, eccentric contractions as well as inflammation, resultin
19     A series of contractions with stretches (eccentric contractions) beyond the optimal length for te
20 /Ankrd2 was dramatically upregulated only by eccentric contractions, but not by isometric contraction
21 ased nuclear P-ERK1/2 localization following eccentric contractions, but the archvillin-P-ERK1/2 asso
22 ignificantly milder force deficits after the eccentric contraction challenge (15% and 14%, respective
23  GAS were delivered intravenously 48 h after eccentric contraction (EC)-induced injury of murine hind
24 following a bout of resistance exercise with eccentric contractions (EC).
25 ally stimulated muscles from these mice with eccentric contractions (EC).
26 s increased elasticity but reduced force and eccentric contraction (ECC)-mediated damage in EOMs and
27                                       Thirty eccentric contractions (ECs) were imposed upon rat dorsi
28 the early molecular alterations in humans to eccentric contractions (ECs), a stimulus known to induce
29 on, mouse skeletal muscles were subjected to eccentric contractions (ECs).
30 ctile overload (more specifically high-force eccentric contractions, i.e. CI) were compared side by s
31 ated with the ventral groove blubber undergo eccentric contraction in order to stiffen and control th
32 a single bout of 100 electrically stimulated eccentric contractions in vivo.
33 sisting of a series of four strain-producing eccentric contractions in vivo.
34 ion while the muscle seems more resistant to eccentric contraction induced force drop, indicating a r
35 ombinant human MG53 protein protects against eccentric contraction-induced acute and chronic muscle i
36 t these mice exhibit increased resistance to eccentric contraction-induced damage and reduced fatigue
37 to measure muscle strength and resistance to eccentric contraction-induced damage.
38                           The data show that eccentric contraction-induced injury causes morphologica
39 minin-binding activity and susceptibility to eccentric contraction-induced injury in skeletal muscle.
40 reas loss of in vivo torque production after eccentric contraction-induced injury is associated with
41 tetanic force and was also more resistant to eccentric contraction-induced injury than mdx4cv extenso
42 increased muscle force and protected against eccentric contraction-induced injury.
43 ction as judged by reduced susceptibility to eccentric contraction-induced injury.
44  expression is sufficient to protect against eccentric contraction-induced injury.
45 ecific force and increased susceptibility to eccentric contraction-induced muscle damage compared wit
46 ctive of this study was to determine whether eccentric contraction-induced muscle injury causes impai
47 sferlin-deficient mice significantly reduces eccentric contraction-induced t-tubule damage, inflammat
48 ch that the animals completed concentric and eccentric contractions involving the hindlimb musculatur
49 ties of muscle as evidenced by resistance to eccentric contraction mediated damage, and a reduction o
50 dicate that the activation of mTOR following eccentric contractions occurs through a PI3K-PKB-indepen
51                                      In situ eccentric contraction of tibialis anterior (TA) muscles
52 tion, resulting in negative velocities as in eccentric contractions of whole muscle.
53 ion, loss of torque production after in vivo eccentric contractions, or physical inactivity after mil
54         When applied to muscles of mdx mice, eccentric contraction produced an acute 27% reduction in
55 gulation plays in the biological response to eccentric contraction remains to be determined, as does
56            Additionally, a muscle injured by eccentric contractions shows a response in AChR concentr
57  protocol induced by electrically stimulated eccentric contractions triggering regenerative processes
58 actions, even though the stress level of the eccentric contractions varied over a three-fold range an
59 ereas mTORC1 activation by growth factors or eccentric contractions was preserved.
60 force was not improved but the resistance to eccentric contractions was significantly stronger.
61 cle damage and force loss following repeated eccentric contractions when compared with mdx mice.
62                                       During eccentric contractions, wildtype mice exhibited a 36% lo
63 ive fibers (membrane damage indicator) after eccentric contractions with both genotypes (stimulation: