ライフサイエンスコーパス: eccentric contraction

1 . d(-1)) after muscle-damaging exercise (300 eccentric contractions).

2 l of ERK1/2 phosphorylation before and after eccentric contraction.

3 specific force generation and resistance to eccentric contractions.

4 eclines in in vitro EDL force after repeated eccentric contractions.

5 s are depolarized after an injurious bout of eccentric contractions.

6 on potential generation and conduction after eccentric contractions.

7 rmal pattern of ERK1/2 phosphorylation after eccentric contractions.

8 ferences were detected between isometric and eccentric contractions.

9 llowing an acute bout of maximally activated eccentric contractions.

10 tion-contraction coupling failure induced by eccentric contractions.

11 of two submaximal workloads that emphasized eccentric contractions.

12 o reverse the shift in optimum length due to eccentric contractions.

13 ic stiffness fell as a result of a series of eccentric contractions.

14 ology studies with twitch force, tetanic and eccentric contraction all being normal.

15 ntly attenuates force loss owing to damaging eccentric contractions and repetitive isometric contract

16 Both eccentric contractions and twitch potentiation reduced t

17 high susceptibility to injury with repeated, eccentric contractions as well as inflammation, resultin

18 A series of contractions with stretches (eccentric contractions) beyond the optimal length for te

19 /Ankrd2 was dramatically upregulated only by eccentric contractions, but not by isometric contraction

20 ased nuclear P-ERK1/2 localization following eccentric contractions, but the archvillin-P-ERK1/2 asso

21 GAS were delivered intravenously 48 h after eccentric contraction (EC)-induced injury of murine hind

22 ally stimulated muscles from these mice with eccentric contractions (EC).

23 following a bout of resistance exercise with eccentric contractions (EC).

24 s increased elasticity but reduced force and eccentric contraction (ECC)-mediated damage in EOMs and

25 Thirty eccentric contractions (ECs) were imposed upon rat dorsi

26 the early molecular alterations in humans to eccentric contractions (ECs), a stimulus known to induce

27 on, mouse skeletal muscles were subjected to eccentric contractions (ECs).

28 ctile overload (more specifically high-force eccentric contractions, i.e. CI) were compared side by s

29 ated with the ventral groove blubber undergo eccentric contraction in order to stiffen and control th

30 a single bout of 100 electrically stimulated eccentric contractions in vivo.

31 ion while the muscle seems more resistant to eccentric contraction induced force drop, indicating a r

32 t these mice exhibit increased resistance to eccentric contraction-induced damage and reduced fatigue

33 to measure muscle strength and resistance to eccentric contraction-induced damage.

34 The data show that eccentric contraction-induced injury causes morphologica

35 minin-binding activity and susceptibility to eccentric contraction-induced injury in skeletal muscle.

36 reas loss of in vivo torque production after eccentric contraction-induced injury is associated with

37 tetanic force and was also more resistant to eccentric contraction-induced injury than mdx4cv extenso

38 increased muscle force and protected against eccentric contraction-induced injury.

39 ction as judged by reduced susceptibility to eccentric contraction-induced injury.

40 expression is sufficient to protect against eccentric contraction-induced injury.

41 ecific force and increased susceptibility to eccentric contraction-induced muscle damage compared wit

42 ctive of this study was to determine whether eccentric contraction-induced muscle injury causes impai

43 sferlin-deficient mice significantly reduces eccentric contraction-induced t-tubule damage, inflammat

44 ch that the animals completed concentric and eccentric contractions involving the hindlimb musculatur

45 ties of muscle as evidenced by resistance to eccentric contraction mediated damage, and a reduction o

46 dicate that the activation of mTOR following eccentric contractions occurs through a PI3K-PKB-indepen

47 In situ eccentric contraction of tibialis anterior (TA) muscles

48 tion, resulting in negative velocities as in eccentric contractions of whole muscle.

49 ion, loss of torque production after in vivo eccentric contractions, or physical inactivity after mil

50 gulation plays in the biological response to eccentric contraction remains to be determined, as does

51 Additionally, a muscle injured by eccentric contractions shows a response in AChR concentr

52 actions, even though the stress level of the eccentric contractions varied over a three-fold range an

53 force was not improved but the resistance to eccentric contractions was significantly stronger.

54 cle damage and force loss following repeated eccentric contractions when compared with mdx mice.

55 During eccentric contractions, wildtype mice exhibited a 36% lo